Letters
TWiV regularly receives listener email with corrections, comments, suggestions for show topics, requests for clarification, and additional information. A selection of these is archived on this page.
TWiV 96
Connor writes:
My name is Connor and I am an undergraduate (soon to graduate) Microbiology student at Oregon State University. I’ve recently discovered your show and I love listening to it. Especially now that it’s featured on Stitcher, making it much easier for me to listen to when I’m walking around campus or taking a road trip. I am taking an immunology course this term and I wanted to discuss the article you brought up about HIV and HLA class 1 (which I’ll call MHC 1 from here on out, so as not to confuse myself). You expressed some confusion, and I thought I’d try to explain it. Try is the key word here since I am only a student on this and I’m actively trying to figure this out as I’m writing.
MHC class 1 molecules present peptides from a cell’s cytosol on its surface. T-cells can then bind these molecules. If the peptide bound to the MHC is recognized as self by the T-cell receptor, the T-cell will receive a negative signal and leave the cell alone. When recognized as pathogenic, the T-cell will get a positive signal that will tell it to kill the MHC presenting cell. This is pretty basic and I’m guessing you already know this but I thought I would give some background.
Now the problem with this is preventing T-cells from recognizing self peptides. The thymus is very important for this. Cells in the epithelium of the thymus express MHC 1 (and 2), and using what is known as the AIRE transcription factor, tissue-specific peptides found all over the body can be expressed by these thymic epithelial cells and presented on their MHC’s. Positive and negative selections occur to get rid of nonfunctional and self-reactive T-cells. Now here is where the paper comes in.
Since there is so much allelic diversity from MHC’s, they can vastly differ between individuals. Here the paper mentions HLA-B 57 specifically. They say this MHC can bind far fewer peptides in the human proteome than others. This should cause thymic epithelial cells to present fewer self-peptides to T-cells and decrease negative selection. As a result the diversity of T-cells would increase, and they would be able to recognize a greater variety of peptides as foreign. However, I believe this would increase risk of self-recognition and ultimately autoimmunity.
My guess is that as HIV mutates, it may begin to express sections of peptide that may be similar to some of those found in the human proteome. So in most cases a regular diversity of T-cells will recognize these peptides as self and no or little response will be elicited. But in the case of thymic cells expressing HLA-B 57, less negative selection occurs in the thymus, a greater variety of T-cells persist in the body, and your immune system has a greater chance to recognize HIV as a pathogen even after mutation.
This is purely speculation, but I’d be interested in hearing what you have to say about this. I hope I explained it well (and correctly, my immunology professor would be disappointed if I didn’t). If I confused you I apologize. You guys do an awesome job and I look forward to each new episode. Thanks again,
Connor
Sergio writes:
Dear Twivers:
This is the second time I write and the previous was like two years ago. I had stumbled on twiv searching for microbiology related podcasts for my then brand new ipod. Now the ipod is pretty worn out and twiv is one of my favorites….i never miss one. I am a plant pathologist/microbial ecologist about to finish my Ph.D. work in bacterial plant pathogens, but I am so into molecular biology that plant virology is very attractive and probably I will [do] some plant virology in the future.
Now that all of you have been showing interest in RNA interference and related topics I thought this would be the perfect moment to ask you something that has been around my head for some time. A few years ago in my plant virology class my professor explained his research on new plant varieties resistant to viral infections. There are 2 main approaches: Infection of plants by mild virus strains to generate what is known as “cross protection” (something like a “vaccine” for plants, without the immune system) and transgenic plants where a viral gene (set of genes?) is insterted into the plants. Then he started to explain the rationale and the theoretical basis of these two methods and their relationship to “gene silencing” or RNAi. That’s where he lost me!!! I have been going around this in my (little) free time and I kind of get the “cross protection” stuff, but the transgenic stuff is beyond me, needless to say I don’t get the relationship to RNAi. I know you are specilized in animal viruses but you are my best source of info on viruses so I thought I would give it a try.
Now that I am about to go back home and hopefully work as a researcher in a university I also thought you could give me some advise on getting funded. You see…I am from Bolivia and public universities there are completely free (as in beer) so there is no money for research. Most of the budget goes to infrastructure and salaries so serious researchers must get their funds mostly from foreign cooperating agencies or multinational organizations. I thought this was because we were a developing country and being so poor simply there was no money for research, but I learned that the situation is not so different in the US. Researchers have to compete very hard to get funded and if they don’t….well….it’s over. Since in Bolivia the money comes from cooperation there is a natural skew towards applied research and mostly oriented to development, but I believe (I hope I am not being naive) that if you get funded and get some materials and equipment for applied research, some basic research “made in the developing world and for the developing world” is possible. What do you think? Do you think it is better to stay in the applied field solving the many problems we have in the developing world or is it a good idea to try to perform basic research and add new knowledge for the sake of science from the developing world (would a paper be published even if it is from a small Bolivian university?). An if you were from a cooperating agency..what would I have to write to convince you to fund some research. By the way, I forgot to mention that I am studying in Japan, where as soon as you get a scholarship the reserach is automatically funded by the Japanese Gov. and each lab has a budget directed to research that seems enough at leats to fund students’ research.
I know my questions are too detailed and probably out of the scope of twiv, but hey….better safe than sorry right. Once again tahnks for twiv and twip….and hopefully very soon for twib. Sincerely,
Sergio
Eric’s response:
This is one way post-transcriptional gene silencing was first observed: people were trying to make more intense colors of petunias using transgenes encoding pigment enzymes. What they wound up with instead were flowers with white sectors where not only wasn’t the extra pigment made, but the endogenous gene was silenced. So the same principle applies to viruses: make a transgene expressing some (but not all) virus genes. If the plant gets infected, there are already pre-loaded RISC complexes with siRNAs ready to cleave the virus’s RNA. The phenomenon of transgene-induced virus resistance was known before the discovery of RNA-interference, but the mechanism wasn’t known. What happens is that multicopy transgenes produce a sufficient amount of dsRNA to engage the RNAi machinery. Plants (and some other creatures) have the ability to replicate dsRNA via RNA-dependent RNA polymerases. (Mammals don’t seem to have RDRPs—except whatever copies Delta.) RNAs homologous to virus sequences can be maintained (and transported from cell to cell, I think) and act as siRNAs, thus conferring resistance.
I guess that’s what people mean by “immunity” in plants. The technical term used in the literature is “cross protection,” which refers to a phenomenon that is entirely RNAi-based. The persistence of the protection is due to the propagation of the virus-specific RNA by RDRPs.
TWiV 95
Jim writes:
Some listeners might benefit from reading “The Treatment; why is it so difficult to develop drugs for cancer” in the May 17, 2010 issue of The New Yorker, a nine page article (pp 68-77).
This link goes to the digital edition ( http://archives.newyorker.com/?i=2010-05-17#folio=076 ), but you have to be a subscriber ($) to access it.
One part of the article describes the mass screening of chemicals for potential compounds and points out that although industrial research labs like Kodak and Fujifilm have millions of chemicals in their vaults, Pfizer was screening only 600,000 and Merck about 500,000. One researcher obtained a grant and purchased 22,000 chemicals from Russia and Ukraine at $10 each [AD: I have an aside about these Russian libraries], then screened them ninety-six at a time and a hundred batches a day with automatic equipment to find some suitable candidates for clinical tests that eventually produced elesclomol. They never explained why Kodak and Fujifilm were not approached. Has anyone made an effort to locate where such chemicals are assembled and how they might be accessed?
Another interesting point was the importance of the Kaplan-Meier curve that is the turning point of any clinical trial in determining its success. Interesting insight.
Jim
VA
Ricardo writes:
Hello TWIV Professors,
Please read the answers or at least the winning answer of the DROBO Contest part 2 (Influenza replication in bacteria) so all listeners can learn with the winner of the contest.
Thank you,
Ricardo
Brazil
This is the winning answer (from Jeff):
Would it be possible to genetically engineer influenza virus so it could replicate in bacteria? Why or Why not?
First, this depends on the definition of “replication”. But there are lots of reasons why flu cannot infect and replicate in E. coli.
1. E. coli doesn’t have the required receptor proteins to bind flu.
2. E. coli doesn’t have a mechanism to internalize flu through it’s cell wall.
3. E. coli doesn’t have capped mRNAs which are needed to create flu mRNAs through the “cap-stealing mechanism”.
4. E. coli doesn’t have a mechanism to splice flu mRNAs to produce the full complement of flu proteins; this normally takes place in the nucleus of eukaryotic cells.
5. E. coli doesn’t have an environment equivalent to the acidic endosome needed to allow escape of the nucleocapsid.
6. E. coli doesn’t have ER/Golgi (or enzymes) to produce N-linked glycosylated proteins.
7. Flu HA and NA proteins would not be directed to inner membrane of E. coli; signal sequences wouldn’t work; therefore virus would not assemble on inner membrane.
8. E. coli doesn’t have protease to activate flu HA to make the protein competent to trigger fusion.
9. Even if flu mRNAs were made (with or without CAPs) they couldn’t be translated in E. coli (no ribosome binding sites).
10. A different codon-usage bias may interfere with protein translation.
11. Formyl-methionine would be placed at the N-term of flu proteins, may interfere with function.
12. Proteins may not fold properly in E. coli and they may interact (bind) to E. coli proteins inappropriately, reducing their effective concentration. For example basic domains used as Nuclear Localization Signals in mammalian cells may cause problems.
However, perhaps we can use a less stringent definition of “replication”.
Perhaps it’s possible to try and engineer a system to replicate the viral RNAs in E. coli. This would be similar in some aspects to the reverse genetics systems used for flu in mammalian cells.
Instead of trying to express all the proteins of flu, we could limit ourselves to the proteins required to replicate a flu genome segment. The flu proteins would need to be under E. coli transcription/translation control. For replication would need PB1, PB2, PA and NP proteins. It should also be possible to use plasmids with two promoters (opposite orientation) to get 1 or more of the flu genome strands (opposite of the mRNA) made to act as template for the replicase.
Maintaining everything in E. coli, is a little tricky; plasmids with different compatibility groups (plasmid maintenance in E. coli) and antibiotic resistance for selection would be needed. This problem would go away if an in vitro transcription/translation (still prokaryotic) were used.
One further obstacle to this system is generating the proteins in correct amounts; would need a lot more NP than replication enzymes.
TWiV 94
Kate writes:
Is it possible that disease stage makes a difference in detection of XMRV and have any XMRV studies tested patients for the virus at several different points over a period of time?
Cort writes:
How different or similar are your methods from the Science paper or the amended version of the WPI’s methods http://www.iacfsme.org/BULLETINSPRING2010/Spring2010MikovitsLetter/tabid/427/Default.aspx
Since the Science paper was published at least six papers have been published that were unable to find it and several other studies have reportedly failed. Have there been other retrovirus (or virus) studies which the scientific community initially experienced a similar degree of difficulty validating but later did validate?
What new information will your study bring to the table? When do you expect it to be published?
Are your results validated against a positive human sample?
Did you receive XMRV samples from the WPI and if so were you able to validate the presence of XMRV in them?
Our understanding is that you gathered samples from patients rather than used stored samples. Is this important and why?
Flowerancy writes:
1. Do you think that XMRV is the result of vaccines (either human or pet) contaminated with animal retrovirus?
2. Do you think that XMRV could have “dropped into” or “piggybacked onto” a herpes virus like HHV-6 or EBV, which allowed it to be spread casually?
3. How can cluster outbreaks of CFS be explained?
4. Could an escaped engineered virus be the cause of XMRV?
5. Can you please explain how XMRV affects the female urogenital system?
Gay writes:
In your studies of XMRV, what kind of tests have you found to be most successful at finding XMRV in blood? Do you think culturing the virus makes a difference?
XMRV growth is stimulated by androgen. If XMRV should be shown to be the cause or a co-factor in chronic fatigue syndrome, why are most (like 4 to 1) CFS patients women? And related to that, the macaque monkey studies showed that XMRV has a tropism for prostate tissue; do we know what tissues it prefers in women?
Could XMRV cause immunosuppression, and if so, how?
In the studies on macaque monkeys, XMRV viremia in the blood cells peaked at about day 8 after infection, and after a couple of weeks it was almost gone from the blood. Since finding XMRV in the blood seems to be difficult, is there somewhere else we should test for it? Like maybe saliva or respiratory secretions?
Kate writes:
My question for the brilliant Dr Singh is,
If xmrv is it! then when would drugs be available to treat us, if everything went to plan! (months, Years or decades?)
Jackie writes:
I was very encouraged to hear that you are engaged in a major study of the XMRV in Chronic Fatigue Syndrome with Dr Bateman and Dr Light.
1. Could you give any indication please of just how close you and your colleagues might be to proving that the XMRV causes CFS, or whether we are still at the stage of proving strong association only?
2. If strong association only, what kind of studies do you think we might need to discover whether there is causation?
3. Where in your view is the most likely reservoir for XMRV in CFS patients, other than in the peripheral blood?
4. Is the reservoir likely to be the most practical location from which to harvest XMRV samples and develop tests for use in a clinical setting (ie clearly saliva or blood tests are more practical, but what if the main reservoir is the brain or the nervous system?)
Thank you both very much!
The UK may seem a world away to you all at this present time, but I can assure you that CFS labelled patients over here are enthusiastically following all promising scientific developments in this field worldwide and are very grateful to you and your colleagues for undertaking this groundbreaking research and for your scientific curiosity.
Rebecca writes:
In treating XMRV, some of us are considering getting stem cell treatments. Do you think HAART would hurt the new stem cells we get?
Katrina writes:
What can you tell us about the XMRV assay being used for the Stanford/Columbia study?. How is it similar or different from others?
Thanks so much, and for all of your work on XMRV/CFS, especially!
Terry writes:
I was wondering if Dr. Singh could comment on your show if XMRV may be present in cancers other than prostate cancer. I am interested to know specifically if it may be a factor in the development of cervical cancer in women. Is there any chance XMRV could act as a trigger and interact with a person’s genes and HPV (and factors like smoking) to create cervical tumours? Also, if there is time could Dr. Singh comment if XMRV triggers the expression of Herv’s (endogenous retroviruses) in cancer and other disease?
Thank you for covering this important topic on Twiv. I am a new fan.
Eric writes:
- Can you provide us with a rough indication about when we can expect the publication of your XMRV/CFS study?
- In case XMRV causes CFS, to what degree do you expect people with CFS to recover, given the right treatment (not the treatment available now, but any future one)?
Michael writes:
Would it be expected that XMRV would have a similar disease effect as the related viruses in mice (SFFV, MULV).
If that is true, could we expect that the reason we see various outbreaks and susceptibility to XMRV be the same as in mice?
For example in mice (as summarized by http://jvi.asm.org/cgi/content/full/83/21/11211) SFFV vulnerability can be either genetic or affected by a co-infection. If XMRV also turns out to facilited by a co-infection could that cause the observed clusters? For example some other virus (most likely one of the ones people have thought actually caused the disease over the last 20 years) infects a bunch of people in an area and as a result a group there who are already carrying XMRV now get CFS?
Also given that there seems to be a high rate of thyroid problems and perhaps thyroid cancer in people with CFS could this also be a result of the virus. For example if certain people have a genetic variance of MET it could be activated by XMRV and cause cancer to kick off?
TWiV 93
Joyce writes:
Love the pod cast!
I once went into a very large bookstore and asked the clerk if they had any books on parasitology. She said that they did and pointed in the direction ofa large case of colorful books which on closer examination turned out to have titles such as “Unbelievable Investigations Into Ghosts”, “Area 51 Revealed” and “Recalling a Past Life” Nothing about ascarids or mosquito born disease. Oh, well.
It is wonderful to hear people who are enthusiastic about the history and future of their special fields. I listen to both TWiV and TWiP. I am decidedly a non-scientist. My science education consists of closely reading the last three editions of the Merck Veterinary Manual and raising livestock for most of my life. I appreciate any the references to remedial reading sources in Virology and Parasitology.
As a non-scientist I would love more information about lab procedures and technology. How do you “extract a protein”? What is involved in “setting up a lab”? How have these things changed?
Keep up the excellent work, gentlemen. And could you scare up a few more gentlewomen scientists?
Joyce
Peter writes:
Since I last emailed you I’ve been able to ascertain that there is a program to serosurvey imported captive Pteropid fruit bats held in American facilities e.g.zoos etc , which is being facilitated through the Lubee Bat Concervancy’s Allyson Walsh and CDC’s Tom Kiaszak.
As far as a survey of native North and South American and Caribbean bats, nothing is apparently known yet on the status of henipaviruses, but Jon Epstein from The Consortium for Conservation Medicine in New York advises that they have received funding from the NIH to survey native new world bats for unknown and known viruses including henipaviruses, in a program to be headed by Peter Daszak.
Let me know when you’re planning to do the show and I’m only too happy to talk with you on Skype. Keep up the good work.
Kind regards
Peter
Equine Veterinary Surgeon
Jamie writes:
Hello everyone!
First I want to say that you truly add an educational ray of sunshine to my day!
I’m an animal technician with a reputable university and fortunately we are allowed to listen to iPods while we work. I discovered TWiV via TWiP (I have to add that I most definitely would appreciate more frequent TWiP’s). The length of the podcast gets me through my morning of checking and changing and then I move on to iTunesU courses.
I do have a question, or rather a request.
One of the rooms that I work in is considered a biohazard level 2 (BL2). The posting on the door reads “hazardous agents: Influenza, Adenovirus, Lentivirus”. After listening to all the TWiV’s, I feel I understand Influenza. However, I don’t know much about Adenovirus and Lentivirus.
As an animal technician, I try to solicit information from the investigators about their study so that I can be sure the animals get the utmost care. I know what side effects to be prepared for (particularly with this lab’s mice), I guess I’m looking for the “why”. Of course these viri may or may not have to do with the side effects that I am mindful of, I wholeheartedly appreciate any insight.
Keep up the titillizing podcasts, I look forward them!
Regards,
Jamie
Ken writes:
During episode 87, Vince and Graham both used a word that microbiologists have been urged to purge from their vocabularies: Prokaryote.
The initiative is from Norman Pace, a pioneer of molecular microbial ecology. Pace argues, persuasively in my opinion, that, while the word “eukaryote” can be used to refer to a phylogenetically coherent group of organisms, “prokaryote” cannot. Using the word can mislead students into thinking that cellular life is divided into two main groups.
Pace gives a good exposition of his argument in a short essay published in 2006.
http://www.nature.com/nature/journal/v441/n7091/full/441289a.html
It may seem silly, but it’s a good lesson in thinking phylogenetically.
By the way, the best virus joke is attributed to comedian Brian Malow:
A virus walks into a bar.
The bartender says, “We don’t serve viruses in this bar.”
The virus says, “Now we do.”
Sophie writes:
Hello to all the great people on twiv and twip people.
I listened to the ER twiv and the question about why we don’t have any active ER viruses. Could it be because our immune system are more active/better than for example a hen’s? I’m aware that this probably wouldn’t explain the difference between us and other mammals – but could the differences between our immune systems be big enough.
At last, but not least I want to thank you for telling me about drobo – it’s exactly what we need – especially school notes and pictures – just too bad that the promotion code doesn’t work for us danes 
Sincerely Sophie
Welkin’s reply:
My first reaction is that our immune systems should be no better or worse, but then there’s the caveat that most active ERVs probably come from heavily domesticated/inbred animals – chickens and mice – so maybe there’s something to it. Not worse, but less diverse.
Perhaps another, purely speculative, possibility is behavioral- humans recently developed weapons and cooking, so could we be less likely to come into direct physical contact with infectious, retrovirus-containing material from other species?
A tangential but similar question, that has bothered me for sometime, is why there are no known retroviruses of dogs? Cats have several, so do humans, horses, cows, mice, chickens, sheep – why not dogs?
Jim writes:
Will the Ipad change the way you teach and communicate by allowing textbooks that incorporate interactive apps, motion, audio files, games, and faster/more frequent revisions?
Will use of the touch screen devices, such as the Ipad, improve sanitation by promoting cleaner hands?
Will the Ipad represent sand or pebbles? – - haw, haw
Jim
Chris writes:
Dear Drs. Racaniello and Despommier:
I just wanted to thank you so much for taking the time to make my birthday gift possible–via Dr. Jean Lim. It meant more than you could possibly imagine to have so many people take the time out of their schedules over something so silly as a 23rd birthday. I know even as a first year graduate student I find that time seems to be the resource that dries up the most quickly, and it’s very inspiring to someone who is just beginning to dream of spending their life in science to have those way ahead of them take the time to lend a hand on the way up.
I know you get this sort of feedback a lot via email, but perhaps there is never too much–thanks for taking the time to do TWiV. It’s proven to be so much more than great entertainment while working out at the gym (I love that they keep getting longer, too–I’m doing much longer workouts so I can finish listening!), but has really helped me to challenge my professors actively in virology and pathogenesis–which I think they like even more than I do. Also, some of the stories and ideas you bring up on TWiV have helped to fuel entire science discussions over food and beer between groups of graduate students and post-docs here (we all follow TWiV compulsively, haha) which is where I think all the best thinking is done.
I appreciate all the time and effort you both (and Dr. Dove and Dr. Condit and guest-of the week…) do to help make our training experience so much fun, and I hope it shall continue for future students for a long time.
Chris
Peter writes:
Dear TWiV hosts (this includes Rich, since I am not regarding him as a guest anymore),
What a week!
Monday (It’s Monday for me here in Korea, when it’s still Sunday for you) the interview with Adolfo Garcia-Sastre; Wednesday FiB #56 about New Antiviral Strategies with Karla Kirkegaard and Thursday a tape worm long TWiP #6 and MTS #46 with Curtis Suttle titled It’s a Virus World and We Just Live On It
From me just four news items, I would like to hear discussed by you (if you haven’t done so already):
1.) Well, not really news, since more than a month old, I attached the 8+ min section of the interview with Harriet Robinson (Senior VP, GeoVax Labs) on a combined new two component HIV vaccine. Sounds promising to me.
2.) 2 min of Mark Crislip from the most recent Puscast for the first two weeks of March
As he says it’s cool. I remember you mentioning Rinderpest as being a potential candidate for the second eradicated infectious disease, but did you discuss the relation to measles?
As a German, of course I like you using German words like Schmutzdecke and Rinderpest.
I should have known the origin of the name of toll-like receptors, but I learned it from TWiV. Don’t ask me why, but I always associated it with (highway) toll-gates.
3.) Vaccine delivering mosquitoes
From the latest Science podcast and a potential way to keep vaccination campaigns of cattles up and running.
4.) And last but not least and always of interest to me working the biopharmaceutical industry – product safety – here ‘PCV1 virus DNA found in GSK’s Rotarix vaccine’: http://www.in-pharmatechnologist.com/Processing-QC/PCV1-virus-DNA-found-in-GSK-s-Rotarix-vaccine/?c=EhWMkLwu2mysBysCtgNUDA%3D%3D&utm_source=newsletter_weekly&utm_medium=email&utm_campaign=Newsletter%2BWeekly
Thank you for TWiV and TWiP,
Kind Regards from Korea,
Peter
Jeffry writes:
Hi Vincent-
Perhaps I haven’t listened to a specific TWIV addressing this, but what is your opinion on viruses having a role in autism spectrum disorders?
http://www.autismone.org/content/episode-8-viruses
Dr. Stewart and Lisa discuss viruses and their effect on children in the Spectrum. As always you can submit your questions for next months Podcast by sending them to questions@drkendalstewart.com
Is it possible to have a TWIV with Dr. Stewart as a guest?
Also, before you speak about the possibility from your perspective, could you also answer what we can test for to rule out viral infections? How do we know what we don’t know or test for?
Even though I do not agree with everything you speak of, I do find your twivs educational. Thanks for the info as always.
Respectfully,
Jeffry in Colorado
Amy writes:
Hi Professor Racaniello,
I’m an undergraduate student in your class, and I have a question about episode 67.
Of all the extreme sterilization methods that you discussed in this podcast, why is phenol the only one that can alter or destroy prions? What mechanisms does this chemical use to alter the particle, and do you think it is possible to use phenolic derivatives to treat prion diseases or are they too toxic?
Thanks!
~ Amy
Radhika writes:
Hi,
This really does not have to do with viruses but rather prions. How did prions originally form, is it just a mutation in peptide structure, and are there any links between prions and degenerative brain diseases such as Alzheimers?
Thanks,
Radhika
Mark writes:
Hi Vince et al,
I was interested to hear you talking about people using calorimetry to measure energies of viral processes.
On a bit of a tangent I wonder if you are aware of a paper published in June 2009 ago where researchers measured the energies required to cleave the von Willebrand’s protein by molecular manipulation using laser tweezers:
X. Zhang*, K. Halvorsen*, C.-Z. Zhang, W.P. Wong^, and T.A. Springer^, “Mechanoenzymatic cleavage of the ultralarge vascular protein, von Willebrand Factor,” Science 324 (5932), 1330-1334 (2009).
I’ve long thought that quantum approaches could be applied to biological processes, perhaps that specific frequencies of electromagnetic radiation (read photon energies) could be applied to enhance or inhibit specific biological processes. Are you aware of any research in this area?
Thanks for all that wooshing noise above my head
Mark
Adam writes:
Does the fact that Mimivirus and other similar DNA viruses that also replicate in the cytoplasm without directly sending nucleic acids to the nucleus mean that like the evolution of eukaryotic cells into different species and types of cells from one eukaryotic cell ; viruses are also one step closer to moving away and evolving into something we can call a life form? Is it possible that the virus over the course of time will keep moving farther and farther from the nucleus needing it less and eventually moving away completely from the host cell itself due to new progeny being mutated through exposure to differrent environments and by picking up more host proteins/ machinery/ nucleic acid through time?
? writes:
I thought this would be an interesting article to discuss. It covers a study where M13 virus was used to split water, which may be a potential method for production of Hydrogen for fuel cells. I know these aren’t “the kind that make you sick,” but it would be an interesting aside.
http://www.sciencedaily.com/releases/2010/04/100411143403.htm
Sheldon writes:
If you use Windows and your eyes aren’t as good as they once were, you need to zoom in on the page. But that doesn’t work for all programs.
Using itunes can be difficult
So why not change the resolution of your monitor. The problem is that you have to get all the way into monitor settings. Wouldn’t it be nice to have two quick launch icons one to lower the resolution (zooming in) and the other to reset the resolution to your normal favorite.
That’s where nircmd comes in. Search for it and read down for the command for creating a shortcut that changes the resoluton. Download it, extract it and a few minutes of playing around and it works fine.
If you accidentally create a shortcut that your monitor doesn’t support, don’t worry — nothing happens.
Now I can read itunes.
Sheldon
Toronto
Jason writes:
Hi TWIV fellows,
Firstly my congratulations on a wonderful podcast. TWIV is the first podcast I have ever listened to and now find it a pre-requisite for my daily 100klm (60mile) round trip to and from the lab. I am still listening to the TWIV archives (25 more to go) and intend to listen to them all again, just in case I missed something. I also recommend that our students sign up to your mailing list as I think it is a valuable tool for their education.
Anyway, I have been watching the Tajikistan poliovirus importation event and have to say I am concerned. Currently there are over 270 cases of AFP with more than 50 of these confirmed as wild type 1 polio with more to come no doubt. Given a conservative AFP to asymptomatic infection ratio of 1:100, there appears to be in excess of 27,000 case of polio infection in a community with a vaccination coverage of around 90%. I would really appreciate hearing the TWIV teams viewpoints on this.
Also I found this paper very interesting (and concerning), any thoughts?
Asymptomatic Wild‐Type Poliovirus Infection in India among Children with Previous Oral Poliovirus Vaccination Grassly NC et al.
http://www.journals.uchicago.edu/doi/abs/10.1086/651952
Keep up the good work, and thankyou for helping me keep up to date with viruses other than enterovirus during my daily commute.
Kind regards,
Jason
TWiV 92
Destainie writes:
Hi Vincent et Al
I am an avid listener of both Twiv and Twip and am very grateful that you all take the time each week to create these wonderful podcasts, they are a great learning tool! I did have several questions I’d like to ask. My first has to do with HIV. It is my understanding that currently doctors use combinations of three different anti-virals to treat and manage the infection and this is due to HIV ability to evolve quickly and become drug resistant. My question is why does HIV evolve so quickly compared with other viruses? Or does it only seem faster because the immune system can’t fight it off? What would happen if you increased the combination to 4, 5 or even 10 antivirals?
My second question is since we know that viruses evolve and become drug resistant is there any way to try to predict the way a certain virus will evolve such that we can try to prevent or prolong drug resistance? My guess is probably not but it would be nice if we could.
My last and final question (for now) has to do with a podcast I heard a while back where you mentioned that a lot of Immunologist and/or Virologist are retiring soon. I am in the process of studying for the GRE and I plan on applying this fall for Immunology programs… since you know the field better than I which ones would you recommend? I should mention that my interests right now would be for a Immunology program with an emphasis in virology if I could and I actually would absolutely love if I could become a double doctor and combine this degree with an MD. I find the human body’s ability to fend off invaders and heal completely fascinating, such that I would be more than happy to devote my life to studying it!
Thank you for all that you do,
Destanie
Merry writes:
Hi, Vincent & TWIV,
I particularly enjoyed this week’s chat with Graham Hatfull as I am a phage enthusiast. He certainly gave the phage their rightful due! And I appreciated the mention of the blog that Elio Schaechter and I write, Small Things Considered, as well as Graham selecting Forest Rohwer’s book (Coral Reefs in Microbial Seas) as his pick-of-the-week.
Also in the pick-of-the-week, you enthusiastically praised the great breadth of information contained in John Ingraham’s recent book, March of the Microbes. I have my own copy close at hand here. When I received it, I turned eagerly to Chapter 10, Viruses — my favorite topic. He, like TWIV, focuses on those that make us (or other animals) sick. Not a word in that chapter about the phage. Of course, he has to be selective as he is covering a vast territory in one book. However, he does not simply ignore them. On the first page of that chapter he sets the tone by quoting two Nobel laureates. First, David Baltimore, who said about viruses: “If they weren’t here, we wouldn’t miss them.” That is followed by Peter Medawar’s quip describing a virus as “a piece of bad news wrapped in a protein.” Both highly quotable quotes.
But considering the ecological and environmental role of viruses in general, and phage in particular, his view of viruses seems incomplete. Would you, Rich, and Alan care to share your thoughts about this?
All the best,
Merry Youle (Small Things Considered)
Jack writes:
Hello Vince,
I discovered TWIV recently and I have become a big fan – keep it up. I have been teaching an undergraduate Introductory Virology course for over 30 years – initially for 10 years at UC Berkeley and now at Nebraska. TWIV will become a requirement for my course this Fall. We have some excellent virology programs here. We recently consolidated all human, animal, algal & plant virology into one building – check out www.unl.edu/virologycenter. I just added a link to your Blog on our website.
I have been going through all of the TWIV episodes this summer. I am a plant virologist and I recall one episode in which the discussion focused on innate immunity. It turns out that plants have an innate immune system with toll-like receptors and MAP kinase cascades. There is also an adaptive immune layer – RNA silencing. This is what we work on. It might be a fun topic for a future TWIV.
I am also interested in Dick’s enthusiasm in “vertical farming”. I read his essays and it all sounds quite promising. What struck me, somewhat ironically, is the potential virology connection. One of the major threats to greenhouse food production are plant viruses. Commercial operations have gone bellyup because they have not been able to successfully control the spread of viruses. Most problems result because the viruses are contact transmitted through roots and soil. Interestingly, some of these viruses like Tomato Bushy Stunt (the 1st icosahedron to be structurally resolved by Steve Harrison) pass right through the human gut and become contaminates in waterways used for irrigation. All quite interesting biology.
Keep up the good work. You are doing a great service to the discipline.
T. Jack Morris
Distinguished Professor
School of Biological Sciences
University of Nebraska
Caleb writes:
Hello TWiV guys,
I’m in 6th grade and I love your podcast. I have a few questions. What is the biggest virus? What are viriods and prions and virophages? Thanks for all your time and for the great podcast.
Caleb W.
[Caleb: check out TWiV #23 on the biggest and smallest viruses and virophages, TWiV #24 on viroids, and TWiV #12 and #67 on prions]
TWiV 91
Darrick and Scott write:
Hello Professor Racaniello,
We are two graduate students from the University of Guelph in Canada studying oncogenic sheep betaretroviruses and we are big fans of the show. Part of the reason we like the show so much is that we can use it to keep up to date on the latest virology events and in addition expand the breadth of our virology knowledge. We will be attending ASV in July and we hope to see you there at the live podcast.
P.S. We have put together a few rap songs using clips from some of your past podcasts that I think you and the rest of the twiv crew will enjoy. We put together the songs using audacity and free rap beats from http://www.20dollarbeats.com/.
Sincerely,
Darrick and Scott
T-Number Index by G-Unit (mp3)
Vincent (mp3)
(the) Acrophobic Antediluvian writes:
The May 25 episode of the “To The Point” podcast from KCRW had a segment titled “Synthetic Cells: Momentous Breakthrough or Ethical Morass?” http://www.kcrw.com/news/programs/tp/tp100525is_synthetic_biology
This was a fascinating listen, and to me illuminated a problem that you have discussed before on Twiv; specifically, that it is common for Science stories to be distorted or sensationalized by the media.
This instance is however clouded by the fact that David Baltimore and Craig Ventor completely disagreed and had what seemed to me a tense argument.
One said a breakthrough in creating life occured in a laboratory, the other said it really is nothing new and is not a paradigm shift.
So, whose story do we accept? How should we listen to a conversation like this and decide who is in the right? Should we go by the credentials (number of Nobel Prizes won,etc.)? It seems as if the issue is split down the middle.
Can you comment? Is there consensus in the scientific community? Are the Twiv hosts on one side of this? I urge you all to listen.
Sincerely,
(the) Acrophobic Antediluvian
TWiV 90
Eric writes:
Hi Vincent,
After 86 episodes of TWiV, I am still loving every minute of the podcast and I am constantly impressed with how much I learn. For example, I have been mentoring an undergraduate student in the lab and we have had a rough two week stretch where none of her experiments have worked. I was racking my brain, trying to come up with some things that would help boost her confidence. On my way in to the lab on Thursday morning, I listened to you and Rich and Dr. Kiki; and Rich described how a good mentor guides the student in a direction that will allow them to succeed. I took that approach with her that morning and we had a great discussion about the project, what additional experiments she could try, and I was able to assure her that it was not her skills that were lacking. On Friday, she had two great successes that really boosted her confidence, and I felt like a good mentor! Thank you TWiV!
Tonight, I listened to Dark Matter with Eric Delwart, and I loved it. I have been experiencing many of the same things that Dr. Delwart described, and in fact I have 100s of hours of eyeball time invested in the bat virome project.
Thanks for your continued work with the podcast. I find it extremely helpful to hear about different viruses that I would normally have no exposure to.
Thanks,
Eric
David writes:
TWiV gang,
Several emails you’ve received have addressed the question, can computer viruses mutate? My take on this question is a qualified yes, but in a different way than biological viruses.
If I remember correctly, one of the emails you received answered this question as no, because randomly changing bits of a computer program almost invariably result in a broken program. I can vouch that this is true – I work in a group that designs computer chips, and any single bit change will cause the mutated program to go out into the weeds. However, mutations in biological systems, and as well as those that computer viruses undergo, happen at a different level.
By my way of thinking, changing a single bit in a computer program would be like changing a single atom in a biological compound. If you replace a Carbon atom with a Gold atom in Adenine, what you’ll probably end up with is an expensive non-functional molecule. Instead, mutations in DNA and RNA seem to happen at the molecular level, for example where an Adenine gets replaced by an Guanine, in the case of single nucleotide polymorphisms. Other mutations, such as copy number variations, occur at the level of a large collection of molecules. The point is that biological mutations occur at a higher level of organization than “bits”. This greatly increases the probability that the resulting mutants are viable (and sometimes “fitter”) than the original.
For computer viruses, I’m unaware of any comparable higher level of mutation inherent in computers. I’m not exactly how accurate computer based copying is, but I’ll hazard a guess that it is more accurate than biological copying. Errors in computer copying that I’ve typically encountered have been due to equipment failure (queue Drobo promotion here ). Because of this, when computer viruses change, it is because the computer virus itself purposely inserts variation into its offspring as they are created.
One way antivirus programs detect viruses is to look for virus signatures, sequences of bits in viruses that are characteristic of a virus or family of viruses. To evade detection, one tactic newer viruses use is to modify (“mutate”) their children to be unrecognizable to the antivirus software. The viral code is modified at a higher level of organization than bits, such as reordering instructions (analogous to SNPs, perhaps). In this way, some computer viruses do change (mutate if you will), but they self-mutate, rather than let nature do the mutating. For some more background, see http://en.wikipedia.org/wiki/Computer_virus#Stealth.
The Tierra program mentioned in one episode, mutates at both at the bit level and at a higher level of organization (swapping segments of code). The Tierra virtual environment does the mutating in this case.
This does beg one question – are there any biological entities that you are aware of that actively self-mutate?
Keep up the good work. I listen to several podcasts, and TWiV (and TWiP) are among the few that I make sure I have time and concentration to really listen to. I get a lot out of these podcasts.
– David
P.S. I guess the moral of the story is don’t mutate the bits, mutate the organization
TWiV 89
Andreas writes:
Hello professors,
I would just like to start by saying thank you for the wonderful podcast.
Today I found this article on npr which seems to describe a remarkably effective antiviral treatment for ebola.
The article has virologist Heinz Feldman expressing concerns that the drug – though very effective – is unlikely to be brought to market due to the lack of financial incentives.
What’s your take on this?
Regards
Andreas
Ken writes:
Hello DRs.V.R.A.D,
My Name is Agyeman-Badu, a graduate student in Ghana and a regular listener to TWiV and TWiP. I came across a paper by Zhang et al and I have a question about priming of non-enveloped viruses before cell entry. If viruses are really particles before cell entry and hijack the cell machinery to act as living and replicate, how is it possible for non-enveloped viruses like the B19 viruses, Adenoviruses, Rhinoviruses, coxsakieviruses and even the Hepatitis Delta virus to prime from a dormant state to a metastable state by shedding off protective proteins before cell entry? How can a viral particle release proteins if it is not in a cell? I tried reaching the original authors but couldn’t and hope you geniuses could help me answer this question. Maybe there is something i don’t know and i would like you to fill the gap in my knowledge like okazaki fragments. Thanks and keep up the good work, you are really helping some of us now coming in the molecular research field.
Ken
Damon writes:
Dear Professors,
I am writing to more or less ask for a sanity check on the topic of flu vaccination. When my company began operation of a flu laboratory, our medical director mandated twice yearly flu vaccinations. Now, these are the normal seasonal vaccines, not the strains we are working with, but the hope is that there would be some cross-protection. That I can buy as a risk mitigation approach. However, I originally assumed that the vaccine we receive in the spring was the southern hemisphere vaccine, which would give us even broader influenza immunity. I recently learned that is not the case. In the spring we receive another shot of the same vaccine we were given the preceding fall. The justification for this is ostensively that the repeated shot will compensate for waning immunity.
I am tempted to call shenanigans on this, because I can find no evidence that flu immunity provided by a vaccine wanes, especially over a time period as short as six months. In fact, flu immunity against particular stains seems to be lifelong, as evidenced by the finding that people exposed to a similar flu decades ago had resistance to the latest H1N1.
What are your opinions on this? Is there any benefit to receiving an identical flu shot twice in a row?
A related question: Why is it that pets need to be revaccinated yearly, when most human vaccines provide lifelong immunity?
Thanks for all the fulfilling commutes provided by TWiV!
Best regards,
Damon
Dan writes:
Twiv crew:
Your recent interview with Dr. Kiki that touched on press releases and sometimes missconstrued information by the media relates well to this story in Wired Magazine. I am including the URL here as well as attaching a PDF with this email if for some reason the article ages off the site. You might want to consider a short mention of it on your program.
As a meteorologist, I now find myself in a field where the public’s perception of the science is now heavily influenced by politics and public opinion (case in point – global warming/climate change). It used to be that a meteorologist only had to worry about a forecast, improving a numerical model, or better ways to assimilate or improve data for analyses and models, but now we have to fend off a growing upset public that have received erroneous information about climate change. It is ironic that I chose this field to help humanity. I figured a better forecast could only help mankind make better decisions that would benefit everyone. But because of strong opinion, some of my colleagues are now more worried about a direct physical assault on their own person or families than the science. The improvement in communication is a two-edged sword, not only does it allow for the wonderful opportunity of “free access” to knowledge (even perhaps cutting edge information such as presented on your podcast) a dream that I share with you, but it also allows for the uneducated to voice an “equal” opinion.
We all know funding dollars for research grow more valuable to us every day. I would hate to have to spend my research dollars on PR, but it might be necessary as science becomes more political and opinions more polarized. In virology you have your own nemesis – the anti-vaccinators, look how much damage one or two unscientific articles affected many people to question real science, and in your case you don’t have the resources of giant corporations that might have something to gain if vaccines were rejected by the public fighting against your cause (or maybe there are, please educate me on that point if there is). We share a common problem even though we are in different fields. I value your collective opinion on how to best deal with this problem and your reaction to science PR. To a degree you folks are doing what this article advocates, your audience is wide open and you do a great job of taking the science to the lay-person’s level. But to what extent do we go? and what is the best way to reach those who have open minds before they meet the entity that has an apparent agenda to coerce their beliefs so they will perhaps vote a specific way in the next election that might very well have a bearing on research funding for basic science?
I value your comments, candor, and intelligent discourse; I always look forward to listening to your show during my daily commute.
Recently you gave away a Drobo after judging essays entered for the competition. As one who submitted an entry, I would at some point enjoy learning the desired essay response (if I missed the episode in which this was divulged, please share, but I only recall the announcement that there was a winner). Maybe I could learn from my mistakes since the lack of a Drobo on my desk is evidence I didn’t “get it right.”
Regards,
Dan
TWiV 88
Sharon writes:
Hello fellow virus lovers,
I first want to comment about Vincent’s pick of the week a few weeks back, the book “Polio” by David Oshinsky. I am currently studying poliovirus in Julie Pfeiffer’s lab (as you revealed many moons ago with a previous email I sent), and I received this book as a gift from my mother. David Oshinsky was in San Angelo, TX (my home town, and in the first sentence of the book) speaking about his book and receipt of the Pulitzer Prize and doing a signing. My mom attended the event and subsequently purchased a book for she and I. I love it! This is a wonderful historical perspective of the societal impact of poliovirus and impending vaccine “arms race” between Salk and Sabin that you don’t necessarily get from Pubmed. This book has been circulating in our lab for a while now and I recommend it to anyone.
I would like to recommend a pick of the week that I think hasn’t been suggested yet. It’s a PBS special called “Naturally Obsessed” (http://naturallyobsessed.com/). The film (~1 hour long) is a documentary that follows 3 graduate students in the pursuit of their PhDs and the divergent routes they take. We watched the video for a lab meeting, and all sympathized with the students in the video in regards to the rigor (and dissapointments of mountains of negative data) of graduate school. It does have a happy ending!
One more short mention. I have listened to every TWIV podcast and have heard you all ask several times if anyone is studying gastrointestinal (commensal) bacterial effects on viruses. No one to date has published on this subject, but keep an eye out.
As always, I love the podcast! Thank you for broadening my virology knowledge!
Best,
Sharon
Andrew writes:
Dear TWiV,
I’m an second year undergraduate in Genetics at the Queens University in Belfast, Northern Ireland. I’ve been listening to TWiV for about a year now and I find it fascinating! I had not been much interested in viruses until I discovered your podcast and took a introductory virology module this year, but now I’m considering the field of virology as a long term career.
What caught my eye the most within my Virology course is the idea of virus-mediated gene therapy, something that (and I could be wrong) I don’t remember you talking about on the show. My sister is affected by Type 2 Spinal Muscular Atrophy, a condition which is caused by the loss of the SMN1 (Survival Motor Neurone 1) gene and my question is,
How far away are we from being able to successfully carry out gene therapy for genes such as this?
My thoughts are: that one of the main problems would be the size, from my basic knowledge I know we have successfully put GFP (Green Jellyfish Protein) into a measles virus and had it express GFP in ferrets etc, but genes like the SMN1 gene are considerably bigger (28kbp as supposed to the 1kbp GFP) so, what are the current and theoretical limits of gene size we can integrate into viral genomes?
And finally, what would be stopping us from simply building our own viruses to deliver the genes? I’ve heard about the poliovirus which was built from scratch because the sequence was known and it was simply ordered as primers and put together to create a live virus, but with lots of different strains of different viruses being sequenced and publicly available, wouldn’t it be possible to engineer and build a fit to purpose virus? It seems locigal to me that you could take different sequences from wild viruses and create a viral genome of your own. A capsid protein from here, a reverse transcription enzyme from there, a replicase enzyme from somewhere else and so on. Could it be possible that we could greate a virus that would give a persistent infection of the appropriate tissues that shows little or no harmful cytopathic effect and delivers your missing gene?
I would love to hear you talk about this on the show, look forward to my TWiV fix every week,
Sincerely,
Andrew in Belfast, Northern Ireland
Brent writes:
Hi Guys, excellent podcast for IT business analyst with no virus knowledge. Just wondering about flu/cold transmission in the household. Would sharing toothpaste be a valid way to transmit easily. I figure it would ie person with cold , toothpaste tube to brush, mouth to brush, next person has toothpaste tube to brush, brush to mouth. or it this paranoia . or does tooth paste kill it? interesting
Would it be a high chance of catching the cold?
thanks
Brent
James writes:
Hello Twiv,
Thank you for putting together a great podcast. My question refers to the podcast “Gators go Viral,” in which you talk about viruses attacking cancer cells (jaw dropper). I was wondering and it might be a little early to talk about this but is there any chance of evolution/resistance in these cancer cells when you expose them to this virus treatment.
Thank you,
James
TWiV 87
James writes:
Dear TWIV,
I’ve really enjoyed hearing about the paths you and your guests took to enter the fields of virology and parasitology.
I was wondering if Dr. Dove could talk for a few minutes about how and why he decided to transition into science journalism. Does he have any advice for PhD students who are considering making the switch? And how bad is the job market considering all the cuts media companies are making as of late?
Many thanks,
James in Japan
Marcie writes:
Dear Vincent, Dick, and colleagues,
I love both your shows and would strongly encourage you to increase the frequency of TWIP if possible!
I was volunteering in my son’s second grade classroom this morning reading a book about the human body with a student who needs extra practice reading. This student has struggled to be engaged by things he reads but this morning he was full of questions and this is why I am writing to you. Two pages of this short book were about blood and germs and there was a photo of some red blood cells next to a photo of some “germs” that I assume were rod shaped bacteria. These photos spawned a lengthy session where the student asked many questions about germs including, do they move?, how do they move?, how do they get inside our bodies?, what shapes do they have?, and a host of others. I drew him some examples of different shapes (paramecium, amoeba, ebola), and told him that paramecia swam using little hair-like things (I could not think of the word cilia at the time) and amoeba moved by oozing little feet-like things forward and then oozing the rest of itself into that “foot-like” projection. We also discussed more passive forms of movement like being blown on the wind, or being forcefully pushed by air as in coughs or sneezes. The student really wanted to know whether any germs had hair-like projections that the could deploy to facilitate being carried by air/wind like dandelion seeds. I told him that I was not aware of any but that I knew some very smart scientists who knew a lot about microbes and I would ask. So, are there any microbes (or other parasitic things) that can deploy hair-like projections to help them to travel?
Are there any books with good photos of microbes that you could recommend for early-elementary kids? I am hoping for a book with a picture of a microbe that simply says something like, “Here is a picture of the bacteria X. X is helpful/harmful to animals because it does Y and Z. X moves by (flagellum) and is passed from person to person by (touch). More complicated explanations would also be fine as I could translate them into simpler words, but something he could read himself would be ideal.
Thank you for your help!
Marcie
Jason writes:
Hi Guys,
I thought you might like this article. You have to love the headline anyway. I have heard that malware/viruses could potentially be transmitted to pacemakers before, but it looks like Gasson has a proof of concept.
http://news.techworld.com/personal-tech/3224739/scientist-infected-with-computer-virus/?cmpid=TD1N1&no1x1&cmpid=sbslashdotrplant
Keep up the good work,
Kind regards,
Jason
TWiV 86
Stann writes:
I found your podcast through the Microbe World website. Thanks to Microbe World, I’ve been unable to sate my thirst for knowledge about the microscopic organisms that act as the foundation for our planet. So, I stumble across a podcast about viruses? Hells yeah. Until recently my RSS feeds have only been filled with skeptical podcasts, making me the residential expert on why homeopathy is bunkem, but now I get to amaze my roommates with fascinating info on viruses and their ilk.
When I first discovered your podcast, I jumped head first into the latest episode, and was kind of lost, and almost bored. Not one to give up so easily, I decided to take it slow and go through your previous episodes. Clearly this was the best strategy, because your first episode on West Nile was so jam packed with information on a virus that I knew almost nothing about. Ever since, I’ve been hooked. In a world where ignorance is praised and brainless celebrities reign over cable television, people like yourselves, whose only agenda is to educate, give me hope for the human race.
In summary, I love the show and wish you best of luck in the future. Of course, my best wishes are somewhat selfish, as I hope for more episodes every week. 
-Stann
Darnelle writes:
I am studying virology at Columbia University and would like to pose a question to the expert panel of virologist @ twiv. In the most recent lecture we were introduced to vaccines, and my question pertains to such.
It is my understanding that the same virus that causes the ‘chickenpox’ that we get when we are younger also causes the ‘Zoster rash’, yet two different vaccines are given to treat these diseases. Why is this the case? Are the degrees of the vaccines different, given that they are delivered to different age groups? Why doesn’t the immune response developed after chickenpox protect you against zoster rash?
Darnelle
Sheldon writes:
The likely culprit for the PCV contamination of the rotavirus vaccine
is trypsin. I came across this statement in a document that
described the manufacturing process for Rotateq.
“Rotateq manufacturing process
—————————————-
“The applicant has put adequate measures (EVCP for pre-master seeds,
gamma irradiation of bovine serum and porcine pancreatic trypsin) in
place to ensure absence of adventitious agents for the above materials
and the virus removal or inactivation steps have been validated.”
at page 10 of
http://www.ema.europa.eu/humandocs/PDFs/EPAR/Rotateq/066906en6.pdf
So did the gamma irradiation quote kill unqote the PCV viruses in the trypsin?
The document I referred to had trypsin irradiated before use in
production. Could the problem be that the trypsin used at the very
start of the process was not irradiated?
I really enjoy listening to your podcast.
Sheldon
Paddy writes:
Dear Professors
I have been a loyal listener since late 2008 and sent an e-mail at around TWIV #15 asking for clarification on the definition of “infectious” and “contagious”. At that time I had just enrolled in a virology course after work and now, after having completed several of the courses, I am now enrolled in the MSc Virology program – at 43 years and with a couple of kids I did a great deal of thinking about this but I am thoroughly enjoying it and am occasionally mesmerized by the beauty and complexity of viruses as well as awed by the devastation they can cause.
I enclose my last assignment (complete with the marker’s comments and spelling mistakes) which I dedicate to you guys – obviously it is relatively rudimentary as far as you guys are concerned but late nights of listening to TWIV definitely have helped me get through the courses so far.
One problem that I have encountered is that getting my hands on pertinent recent publications that explain concepts at a level that would be completely useful to me is, at this stage, quite hard. The publications in Pubmed etc. are very often a bit hard to decipher and very focused on specific issues. I understand why this is so but finding references for assignments is quite hard – but I am sure that it gets easier over time especially when listening to TWIV.
I have a question – what are the steps to uncover a virus that has not previously been identified ? I have enclosed a brief description of one such suspected virus known as RRV or rodent respiratory virus – I have thought about looking a bit closer at this because it has some relation to my current job. I have enclosed the tech sheet from this – as yet unknown virus. Insofar as the pulmonary lesions are concerned it would look (from the pathology) that it could seem to be something like the RSV (SS RNA from a subfamily of Paramyxoviridae) that human neonates can sometimes get.
I understand the principles of PCR and multiplex PCR but I can’t see how you identify something entirely new with them. Can you at some point discuss this and perhaps also how they have uncovered some in the past.
Best
Paddy
Joe writes:
While I was listening to your discussion of the antibodies we have to the Alpha 1,3 sugar group and how it could be used to target disease agents I had a thought. It struck me that it would seem to be very much easier to use this as the ultimate bio-weapon and target a key functional group in our bodies than to try to target HIV which is always mutating. As this is not my area, I hope I am wrong. It seems that one could target a surface feature on heart cells or lung cells or liver cells and cause the body to attack itself in a way similar to the “cytokine storm” discussed related to the 1918 flu. As I said, I hope there is a technical reason that makes this impractical. If not please do not read this on air as I don’t want any knuckleheads to get any ideas!
Love the shows.
Regards,
Joe
Alaina writes:
Hey guys,
I have a job assisting a medical professor in doing literature searches and compiling information for the new edition of a book he is writing. The other day he asked me to gather some information on the XMRV virus. Having listened to the episode of TWIV you did on XMRV a while back, I was able to converse knowledgeably with him about it right away. So, I guess I just wanted to say thanks for helping me impress my boss!
Virally yours,
Alaina
Welkin writes:
Dear Vince and Dick;
Congratulations on producing a brilliant series of podcasts. I have been
hearing about TWiV almost since you began podcasting, to the point where I
had come to believe I was a fan without having actually listened to a single
episode. I even deluded myself to the extent of recommending it to others.
With the recent purchase of an iPhone, I have made up for this fraud, and am
working my way back through all the episodes.
I especially enjoyed the episode on Reverse Transcriptase, and the
discussion on endogenous retroviruses – HERVs were the topic of my thesis
when I was a graduate student in John Coffin’s lab. Dick was amazed that we
(humans) haven’t gotten rid of all those “useless” retroelements from our
genomic DNA. In point of fact, we have jettisoned them by the bucketful
over the course of evolutionary time. The sheer abundance of these elements
is all the more amazing, then, once you realize that the ones we know about
are just a tiny fraction of the whole. These are the pernicious few that
made it through the evolutionary grinder and still cling tenaciously to our
genomes.
The most obvious evidence for loss comes in the form of solitary LTR’s, the
element left behind when recombination between the two identical ends of the
ERV loops out the intervening retroviral genes. Solo LTRs vastly outnumber
intact proviruses in our genomes, indicating that large chunks of them are
more frequently lost than not. There are other mechanisms of loss, and
probably a majority of integrations that land in germline DNA simply don’t
survive down the generations, so we don’t know about all the stuff that was
there once upon a time. It is staggering to realize that retroviral
epidemics like the current HIV epidemic have a constant presence throughout
evolution.
Keep up the great work, and if you get a chance, check out “Small Things
Considered”, Elio Schaechter’s blog on microbes and viruses (yours truly is
an associate blogger).
Thanks again for all the great listening
Welkin
TWiV 84
Matthew writes:
Hi Twiv,
Firstly, love the podcast, I listen to it on my way to work. Don’t change a thing!
I recently wrote to you asking about the possible link between a high-arginine diet and herpes simplex outbreaks in humans (does lysine prevent outbreaks?). While researching I found this study which to my untrained eye seems to be saying that HSV-1 DNA in the neuron nucleus is histone-bound and folded into chromatin when it is it latent. This suggests an epigenetic control pathway via HDAC inhibitors. Perhaps diet could play a role in the suppression of HSV-1, as diet is linked to epigenetic silencing of genes in animal DNA.
Please could you talk a little about the epigenetics of viruses ?
Cheers,
Matthew
Jesper writes:
Dear professors,
A while back you discussed the idea of applying mutations to computer viruses to see how they evolved. Someone wrote in and explained that it simply doesn’t work that way in machine code.
I am currently reading The Red Queen by Matt Riddley. Great book, I must say. On the discussion of sex as a means to out-evolve the threat from parasites he mentioned a computer program named Tierra.
Tierra is a virtual environment where programs compete for resources (mainly by copying themselves and thus their ‘species’ would occupy more of the environment). The author of Tierra threw in a small randomization in the copying algorithm, to simulate mutations. As in the biological world, most mutations were detrimental and caused program malfunctioning and thus death, but somewhat to his surprise, some mutations appeared that didn’t kill the host. First, they had no impact at all. Then suddenly “parasitic” programs came into being. These programs had no code for reproduction, but used the required instructions from other programs. Some of the initial mutated programs were immune to the parasites. And on it went.
I found a nice article on the project on http://www.infidels.org/library/modern/meta/getalife/coretierra.html (continues onhttp://www.infidels.org/library/modern/meta/getalife/epgp.html and http://www.infidels.org/library/modern/meta/getalife/resources.html).
All the best, and I thoroughly enjoy both twiv and twip. In terms of podcast competiveness for attention resources, you rock!
Keep up the good work!
–Jesper
Sweden
Jim writes:
Wanted to make sure you didn’t miss this.
Jim
New handheld HIV detector fits into your iPod case
By Bryan Nelson
The portable device takes less than 10 minutes to perform the test, and it could revolutionize how HIV is monitored in remote regions of Africa.
Bill writes:
Drs: I’m still hooked on TWIV. Are you still thinking about a TWIV episode focused on this cool emerging virus based cancer therapy?
The company is now about to enroll its first patient to a Phase 3 “registration” trial focused on head and neck cancers, but there are many studies being conducted in and around the principal discovery that reovirus exploits the RAS flaw that is common to 70% of all tumor cell lines….It is shaping up to be a huge story…time for you guys to get on it.
Best Regards,
Bill
Lenn sent:
EQUINE HERPESVIRUS – USA (02): (NEW JERSEY) SUSPECTED
*****************************************************
Date: Thu 1 Apr 2010
Source: APP.Com [edited]
A total of 6 New Jersey non-racing horse farms, including 5 in
Monmouth County, were under quarantine Thursday [1 Apr 2010] because
of a possible outbreak of a deadly equine virus.
Except for a farm in Millstone, the Monmouth County farms are all in
Howell according to the state Department of Agriculture, whose
Division of Animal Health announced the quarantine Thursday [1 Apr
2010]. The 5th farm is in Gloucester County, according to the
agriculture department.
The disease, called the [equine herpes], is not harmful to humans and
other animals, but it can spread quickly to horses and is often fatal
to them, according to the agriculture department.
“Quarantines are necessary to ensure that this serious disease does
not spread,” said state Secretary of Agriculture Douglas H Fisher.
“Our investigation is continuing as we work to protect the health and
safety of horses in New Jersey and other states.”
The agriculture department noted tests, so far, have not confirmed the
disease. But the quarantines went into effect after 2 horses showed
clinical signs of the disease and were euthanized and another with
similar signs died, according to the department.
One of the farms is connected in some way to all the other farms under
quarantine, Lynn Richmond, an agriculture department spokeswoman. The
quarantines were put in place over various days within the last week
or so, and are expected to remain in place for weeks, Richmond said.
[Byline: Joe Sapia]
–
Communicated by:
ProMED-mail
[Equine herpesvirus 1 (EHV-1) and EHV-4 comprise 2 antigenically
distinct groups of viruses previously referred to as subtypes 1 and 2
of EHV-1. Both viruses are ubiquitous in horse populations worldwide
and produce an acute febrile respiratory disease upon primary
infection, characterized by rhinopharyngitis and tracheobronchitis.
Outbreaks of respiratory disease occur annually among foals in areas
with concentrated horse populations. Most of these outbreaks in
weanlings are caused by strains of EHV-4. The age, seasonal, and
geographic distributions vary and are determined by immune status and
horse population. In individual horses, the outcome of exposure is
determined by viral strain, immune status, pregnancy status, and
possibly age. Infection of pregnant mares with EHV-4 rarely results in
abortion.
Outbreaks with specific strains of EHV-1 infection result in
neurologic disease. Clinical signs vary from mild incoordination and
posterior paresis to severe posterior paralysis with recumbency, loss
of bladder and tail function, and loss of sensation to the skin in the
perineal and inguinal areas. In exceptional cases, the paralysis may
progress to quadriplegia and death. Prognosis depends on severity of
signs and the period of recumbency. Neurologic disease associated with
EHV-1 is thought to occur more commonly in mares after abortion
storms, but it has been reported in barren mares, stallions, geldings,
and foals after an outbreak of EHV-1 respiratory infection.
For prevention and control of EHV-4- and EHV-1-related diseases,
management practices that reduce viral spread are recommended. New
horses (or those returning from other premises) should be isolated for
3-4 weeks before commingling with resident horses, especially pregnant
mares. Management-related stress-inducing circumstances should be
avoided to prevent recrudescence of latent virus. Pregnant mares
should be maintained in a group away from the weanlings, yearlings,
and horses out of training. In an outbreak of respiratory disease or
abortion, affected horses should be isolated and appropriate measures
taken for disinfection of contaminated premises. No horse should leave
the premises for 3 weeks after recovery of the last clinical case.
Parenterally administered modified live vaccines are licensed in some
countries but banned in others. An inactivated vaccine is the only
product currently recommended by the manufacturer as an aid in
prevention of EHV-1 abortion. Vaccine should be administered during
moths 3, 5, 7, and 9 of pregnancy. Humoral immunity induced by
vaccination against EHV-1 and EHV-4 generally persists for only 2-4
months. Antigenic variation within each virus type means that
available vaccines do not cover all strains to which horses can be
exposed. Vaccination should begin when foals are 3-4 months old and,
depending on the vaccine used, a 2nd dose given 4-8 weeks later.
Booster vaccinations may be indicated as often as every 3-6 months
through maturity. Vaccination programs against EHV-1 should include
all horses on the premises.
Gary writes:
The original version of the “I’m positive!” joke (TWIV 78), as I heard it, is an atomic physics joke:
Two atoms are talking and one says to the other, “I think I lost an electron.”
“Are you sure!?!”
“I’m positive!”
Thanks for the excellent podcasts!
Gary
TWiV 83
PJ writes:
TWiV gets weird
Well, not really weird, but allow me some criticism:
I just listened to the "Darwin gets weird" episode, which was again a real treat! Thinking about Prions as non-mendelian inheritance factors seems logical, albeit the question is: how much information is carried by them? Do they belong to the general assortment of "stuff" in the zygote (which, with it's chemical gradients, also carries some information like orientation iirc) or should they be considered a 3rd factor?
However, and this is why I used the "TWiV gets weird" headline: you've ventured into an area that I'm rather passionate about when you mentioned a possible TWiV iPhone app. This might sound a little strange, but:
The whole Apple i-Ecosystem is built in such a way that it keeps stuff in, that is, it's a closed system. A native iPhone app will only run on Apple's iPhone, iPod and iPad, so everybody wanting to use it would have to buy one of those products. That's quite the opposite of what I call open access. Luckily, there's an alternative that has been invented by Tim Berners-Lee a while ago, called "The Web". Data available on "The Web" is usually open access by definition (unless the information owner wants to monetize or protect it). Now, a native application has the advantage that it can store data locally on the device, and here's the good news: HTML5 on most browsers (WebKIT as used on the iPhone and Safari but also as part of Google's Android and Palm's WebOS and Google Chrome, Firefox should not be far behind) have everything you need to write applications using JavaScript and persistant storage methods (using a local database). Those applications are basically websites on steroids that can work off-line. They are, by their very nature, cross platform, you can distribute them without having to go through the iTunes Appstore or Google Android Store, use them both on mobile devices and on the desktop.
I have been an open source advocate for many years now, and the trend towards closed platforms away from "The Web"(or, euphemistically "walled gardens") seems worrying to me. Many people seem to be willing to trade "freedom of access" for "ease of use" - even though this trade off is not really one we need to make.
So, if you do do such an application, please don't feed it to a closed platform, it would be a pity to have the data just there.
Thanks for the show
pj
ps: just to throw in my hat: a weekly TWiP would be highly appreciated
Howie writes:
Dear Professors TWIV and TWIP,
Awesome podcasts! This is science education at its very best. I am a mathematician who has started to work on population modeling. I listen to both podcasts regularly, and have watched about half of your virology course lectures.
Two comments:
1) For bacteria transfered from one medium to another, there is an initial lag phase where the individual bacteria are synthesizing RNA, enzymes, and other molecules they need for growth, prior to their resumption of division. Then comes the exponential growth phase which is eventually limited by the exhaustion of available nutrients and accumulation of inhibitory metabolites or end products. Thus at first the bacterial population is not growing.
2) The mathematical epidemiology world seems to believe that pathogens evolve to increase their fitness measured by their R_0 (basic reproductive rate), thus to become more easily transmitted, make individuals sick longer, and to decrease virulence (host mortality). I sometimes get a little confused by your discussion of this.
Keep up the great work!
Howie
Kara writes:
As I was listening to the episode of Futures in Biotech that Vincent was a guest on, I had a question. There was a philosophy towards antivirals you discussed on the show. Generally, antivirals should be used very cautiously avoiding monotherapy. I completely agree with you in the case of HIV and HCV and viruses that cause infections like those. That is the only way to go in that case, but I don't know that it is as practical current drug development market for other infections.
My question is about tamiflu and the other influenza drugs with similar targets. Isn't the fact that influenza is a self-limiting illness the reason we do not attack it with multiple drugs like we do with HIV? In an influenza infection, our bodies can often clear the flu without drugs and we come out without any lasting ill effects. HIV and HCV cause chronic diseases that ultimately kill their hosts.
Thank you for taking the time to read this and I look forward to hearing your thoughts. Thank you for making such entertaining thought provoking educational podcasts for geeks like me to listen to!
Kara
Levi writes:
Hi Vince, Dick, Alan, and the the rest of the TWiV team!
This email got a bit longer than I expected, so if you use it on the show please feel free to cut to the important parts.
I'm a grad student at the University of Florida and I study HSV-1 latency. My advisor is Dr. David Bloom, and I am also lucky enough to work right next door to Dr. Rich Condit. He recommended TWiV during our spring virology journal club and it has often been a source of material for our discussions. I wanted to give a little something back by suggesting that you all have a look at a film preview for a recent documentary about HIV/AIDS. I'm still catching up on my TWiV episodes, so I hope this isn't a repeat of something you have seen already.
As an avid moviegoer, I frequently go to Apple Trailers (http://trailers.apple.com/) to watch movie previews. While viruses in films are often subject to extreme artistic license, I recently saw a trailer for a film called "House of Numbers" that may make a more serious error. It is a documentary about HIV and AIDS, and it supposedly includes interviews with many of the heavy-hitters in the field. Unfortunately, the preview for the film had a heavy overtone of AIDS denialism of the kind promoted by Peter Duesberg and others. I have not seen the entire film so I don't know if it really pushes this agenda, but I hope not. The attitude of AIDS denialism can only hinder our efforts to counter the AIDS pandemic.
As you have mentioned in previous episodes, there are controversies and conspiracy theories surrounding many diseases, viruses, and vaccines, perhaps none more than HIV and AIDS. Hopefully this film takes an honest, objective look at HIV research and is not just a piece of sensationalism intended to stir up controversy or enhance a filmmaker's career. I will try to get my hands on a copy of the film so I can judge for myself. Perhaps the TWiV team can do the same.
Here is a link to the trailer: http://trailers.apple.com/trailers/independent/houseofnumbers/ Here is a link to the film website: http://www.houseofnumbers.com/ Here is a link to the Wikipedia article about the film:http://en.wikipedia.org/wiki/House_of_Numbers
According to the Wikipedia article, it appears that my fears may be well grounded. You can judge for yourself. These controversies and conspiracy theories can only be fought with quality research and education of the public at large. Hopefully, virologists like myself and those of the TWiV team can be a part of the process of separating fact from fiction.
I'll close by saying that I look forward to meeting you during your visit to UF this summer. As always, thanks for a great podcast, and keep up the good work!
-- Levi
TWiV 82
Erik writes:
Yesterday I sent my Skype audio question again, and I think it worked this time. In my question I mentioned a particular youtube video. Here's the link if you want to see what I was referring to. It's only 5 minutes long. I'm not sure if what I was saying even made sense, so I guess if you see the video then you'll understand at least what I was trying to say.
Regards,
~Erik
Joseph writes:
Dear TWIV,
I am a graduate student in the computer science department of the University of New Orleans studying Bioinformatics. I only recently discovered that Biology is nothing like what was presented to me in high school and have found this an excellent service to fill those knowledge gaps I have naively created. I am emailing both a response and a request.
At some point you requested your listeners provide what other webcasts they listen to, so I created a list of them in three orders: favorite, density, and discovered; all from least to greatest. Hopefully this helps. I'm not much of a list person but I figured it would be more useful than just a list of what I listen to. For your reference, I generally listen while doing non-critical tasks at work, driving commutes to work and campus, and walking/biking commutes to campus.
FAVORITE:
1.Software Engineering Radio
2.Machine Structures (Berkeley)
3.This Week in Virology
4.omega tau
5.This Week in Parasitism
6.Structure and Interpretation of Computer Programs (Berkeley)
7.Futures in Biotech
8.NPR: Science Friday
9.Molecular and Cell Biology (Berkeley)
10.Dave's Psych Classes (Berkeley?)
11.Berkeley Speakers
12.Security Now!
13.This Week In Google
DENSITY:
1.omega tau
2.Software Engineering Radio
3.This Week in Virology
4.Machine Structures (Berkeley)
5.This Week in Parasitism
6.Structure and Interpretation of Computer Programs (Berkeley)
7.Futures in Biotech
8.NPR: Science Friday
9.Molecular and Cell Biology (Berkeley)
10.Berkeley Speakers
11.Dave's Psych Classes (Berkeley?)
12.Security Now!
13.This Week In Google
DISCOVERED:
1.Security Now!
2.Futures in Biotech
3.Software Engineering Radio
4.Dave's Psych Classes (Berkeley?)
5.NPR: Science Friday
6.Structure and Interpretation of Computer Programs (Berkeley)
7.omega tau
8.Machine Structures (Berkeley)
9.Molecular and Cell Biology (Berkeley)
10.This Week in Virology
11.This Week In Google
12.This Week in Parasitism
13.Berkeley Speakers
With that aside, I have a question/request. I'm new to the biology field and am working with a bioinformaticist this summer. Specifically, we are corrolaborating with some biologists who have some information (which they published as Human T-Cell Leukemia Virus Type 1 Integration Target Sites in the Human Genome: Comparison with Those of Other Retroviruses published in Journal of Virology June 2007) on preferred integration sites of HTLV-1 in a HeLa cell line. This is contrasted with other virus families' preferred integration sites. Specifically, our goal is to create a model from the HTLV-1 preferred integration sites, hopefully find other studies using HTLV-1 with different cell lines, and incorporate that information into a model which will predict integration sites of HTLV-1 in a T-cell line. Natuarlly, the ultimate goal is to have a general enough model so that, given a virus's phylogeny, we can predict its preferred integration sites. Do you know of any similar studies with HTLV-1 integration sites and, as a complete amateur, what material/tools would you recommend I review? I am currently familiarizing myself with the UCSC Genome Browser and tackling any vocabulary issues I have in the aforementioned paper.
Thanks, I love the show. Maybe shoot for more metaphors when explaining processes or comparing/contrasting things.
~Joseph
P.S. I encourage TWIP on a bi-weekly basis, but I have a lot of TWIV to catch up on, so no rush from me.
José writes:
Hi Dr. Vince, Dick, Alan and Rich
My name is José, I´m a PhD student in Mexico City and i´m
working with innate immunity against dengue virus infection.
First of all, thanks for the great job with the cast, before i became a
fan of TWIV, i knew your work with RNA detection and innate immunity and i
never thought that doctors of your level were so enthusiastic with the
academic part of science, making it so fun and interesting.
i have some comments and questions.
1. there´s any viruses that we know that are transmitted in sea water
(seaborn), since there are so many of them in the sea my guess is that
some of them are capable to infect human, do you think that some of these
viruses actually uses the sea water for spread. Might be very interesting
evaluates the stability of the particles since they are resistant to high
concentrations of salt.
2. There are many reports of exclusive detection of viral PAMPs by TLRs
and RLHs, appears to me like the mechanism of detection depends of the
cell type, the genotype of the virus and the genetic aport of the host,
not just by the PRR involved. Since almost all of these kind of receptors
activates the IRF´s and NFkB families of transcript factors, these
differences in the specific combination of elements in the detection part
can give to the activation of a specific kind of dimer in the case of NFkB
(c-Rel, Rel-b, p50, etc) and for IRF´s (IRF3,7,1, etc) given to an
activation of different sets of genes in each case, given by the
differences in the affinity for the promoter sequences and the quantity of
the transcription factor. So the response it´s more complicated that just
"activated the IRF family and NFkB pathway".
3. About the T cell specific retroviral therapy question in TWIV 71 one of
the obstacles is that the region were the specific epitope it´s loaded in
the MHC, is not lineal in sequence it´s formed by the spatial structure of
the MHC. So if a virus have to integrates the sequence that codifies to
the specific CTL or Th must do it in fragments that have to fit exactly in
the gaps of the MHC and have to leave the sequence in open reading frame…i
think that's very difficult.
[the original question in twiv 71: Is possible to use gene therapy to insert genes into the major histocompatibility complex that could encode protien expressed on T-cells for a certain virus? ]
take a look at these microscopy technique that allows visualize in the
range of 40nm!!!!! so cool.
Thank you for the great show and sorry by english it´s very precarious.
TWiV 81
Jesper writes:
Dear Professors,
Having upped my daily dose of podcasts I stumbled upon This Week In Science. The latest show (http://www.twis.org/audio/2010/03/09/438/) they mentioned something that probably comes within your sphere of interest, namely the finding that viruses are a possible triggering factor to gluten allergy. A brief report is available on http://www.eurekalert.org/pub_releases/2010-03/aof-vim030510.php.
“Virus infections may be contributing factor in onset of gluten intolerance
Recent research findings indicate a possible connection between virus infections, the immune system and the onset of gluten intolerance, also known as coeliac disease. A research project in the Academy of Finland’s Research Programme on Nutrition, Food and Health (ELVIRA) has brought new knowledge on the hereditary nature of gluten intolerance and identified genes that carry a higher risk of developing the condition. Research has shown that the genes in question are closely linked with the human immune system and the occurrence of inflammations, rather than being connected with the actual breakdown of gluten in the digestive tract.
“Some of the genes we have identified are linked with human immune defence against viruses. This may indicate that virus infections may be connected in some way with the onset of gluten intolerance,” says Academy Research Fellow Päivi Saavalainen, who has conducted research into the hereditary risk factors for gluten intolerance. [...]”
I presume this may open up a huge field of both treatments and preventions.
As for This Week in Science it’s a general science news pick kind of show with an attitude. Not as in depth/subject focused as twiv, and no doubt satisfying a different need, but anything helping the scientific project is worth trying! I think Vincent may appreciate their music selection, but that’s mere speculation.
All the best,
–Jesper, Sweden
[here is the paper: http://www.nature.com/ng/journal/v42/n4/abs/ng.543.html#/]
Jason writes:
I was listening to the most recent episode of TWIV (episode 72) and was delighted to hear you discuss RNA silencing and viruses. It happens to be what I’ve devoted the last 6 or so years of my life to so it’s a topic that I am fairly familiar with and I just wanted to shed a little light on some things. First a brief background on myself – I defended my dissertation at the end of last May, graduating from NC State University where I performed research on a fairly obscure plant virus, Red clover necrotic mosaic virus. My research surrounded the role of plant RNA silencing as a host defense mechanism, and of course how the virus might circumvent this defense. Towards the end of my research I knew I wanted to transition out of plants and into animal virology so I applied to a variety of labs and ended up getting a Post doc position at Duke with Bryan Cullen. It’s been an interesting transition, and I’ve absolutely loved listening to your podcasts which I think do a great job providing digestible information for everyone from the common layperson to PhD’s like myself. Anyway at one point in the past episode you made a comment that all vertebrate viruses are surely chopped up into siRNAs. Rich wasn’t so sure about that, and he is definitely correct. I won’t say that it is a completely settled subject, but at this point it does not appear that RNA silencing is a general feature of viral defense in vertebrates, although some exceptions may exist. Certainly there is interplay between small RNAs and viruses, but a generalized antiviral link is pretty tenuous at this point. You mentioned how it would be useful to do some deep sequencing on infected cells to see if you could detect virally-derived siRNAs. Our lab has done that for a number of herpesviruses, and, along with other labs, has found that herpesviruses actually encode their own miRNAs. In fact, EBV encodes 25 miRNAs, while KSHV, HSV-1, and HSV-2 all encode multiple miRNAs as well (I can’t recall the number off the top of my head). A much broader study was recently published by Andy Fire and colleagues in PLoS Pathogens which you might find interesting: http://www.plospathogens.org/article/info%3Adoi%2F10.1371%2Fjournal.ppat.1000764
Keep up the good work!
Ewout writes:
Dear TWIV-staff,
Thanks for answering my mumps question! Great fun (and honour) to be cycling back from work and suddenly hearing my email on the iPhone!
Me and my colleagues would like to read the CDC response mail, with the references named in the podcast.
Would you be so kind to forward it to me if possible?
Hope you are able to continue this great podcast for a long while, I will advise more colleagues to listen to you.
I sent him the email, and he replied:
Thanks! We (Nat Inst Publ Health and MHS) are planning to go deeper into the mumps issue, since vaccination related diseases (measles/mumps etc) are an ongoing issue because of areas with low vaccination coverage (due to protestant reformed religion). Genotype G suddenly seems to hit vaccinated (non religious) students. I also contacted Israel a few weeks ago, thanks to your former TWIV about their outbreak.
TWIV is more than just an interesting podcast. It enhances science.
Bree writes:
Hello again,
I just wanted to say thank you once more for taking the time to answer my question on your podcast. It’s very exciting for me and the other members of my class to be able to have our questions answered after listening to your podcasts!
And to answer the question you asked during the last podcast – I have mixed feelings about podcasts as a learning tool. For someone like me, who only has a very basic grasp on the principles of virology, understanding everything that is being discussed by people who are very advanced in the field can be difficult. However, when I do understand the subject matter (and hopefully I will after completing this course!), I find that it’s relatively easy to follow and understand what is being said; I also find that listening to what someone other than my professor has to say about the topic being discussed is not only refreshing, but provides me with more than one viewpoint from which to understand and look at certain topics and new material.
Again, I greatly appreciate all of you taking the time to read and answer my question, and I look forward to hearing more questions answered on future podcasts!
Thank you.
Jim writes:
The Canadian Broadcasting Corp podcasts are my only connection with Canadian activities. Too bad we don’t hear more about our neighbors. I’d not heard about the Summit Awards until this podcast fromt http://www.cbc.ca/podcasting/pastpodcasts.html#ref14 . Not much about viruses, but listeners to TWIV might still be interested from the standpoint of career development and jobs. Here’s a summary of the 46 min program: Science at the Summit
“Two leading Canadian medical researchers – Benjamin Neel, and John
Wallace – discuss what it takes to rise through the ranks and
ultimately arrive at the lofty pinnacle where true scientific
advancements are made. Both received the $5 million 2009 Premier’s
Summit Awards. John Dirks, President of the Gairdner Foundation,
moderates the discussion, recorded at the MaRS innovation centre in
Toronto.”
In case I’ve not said so, all the TWIV podcasts have excellent sound quality and levels.
I’ve heard several references to online videos of lectures from places like MIT at http://www.academicearth.org/ . After viewing a dozen or so on chemistry, math, biology, computer science and physics I must say how much more enjoyable the TWIV podcasts are. Lectures do not appear to have changed from the last I attended 25 yrs ago. I expected to see more. In several there wasn’t even any chalkboard work, just a lecturer talking. Just a comment…..
[the podcast can be found at http://www.podcastdirectory.com/podshows/5624750]
Mike writes:
I just started listening to the show (after downloading every episode) and I’m really enjoying it. I have no science background, but I’m a geek and enjoy listening to Futures in Biotech so as soon as I heard about TwiV and TwiP I knew I’d have to check the shows out.
A worthy find, indeed! I shall be recommending it to other science minded friends. Keep up the great work!
Richard writes:
Thanks for posing the question, it has proved interesting to research, and think about. (referring to the flu/bacteria question).
I have a pick for you, this is a webpage that provides information for experimenting with phage at home. It gives info and experiments that require little or no equipment to be purchased. http://www.disknet.com/indiana_biolab/p.htm
Thanks again for the interesting and informative podcast.
Regards
Richard
Thomas writes:
Hello,
Love the podcast. Wish everyone was an enthusiastic about what they do as you guys are. I have some questions and clarification:
1. On TWIV 65 a pick of the week was Rebecca Skloot’s book “The Immortal Life of Henrietta Lacks”. The HeLa cells are infected with HPV18, but I cannot find any discussion about what makes these cells immortal. Certainly “experienced” virologists such as yourself can help in my quest for an answer to this question.
2. There are 2 current rotavirus vaccines (and one previous). Here is a history and a question (you can omit the history if it gets too long):
ROTASHIELD-FDA approved in 1998-a lyophilized tetravalent rhesus-human reassortant rotavirus. It is postulated that because it is rhesus and not bovine based, that the closer genetic similarity allowed it to replicate in the intestine and lead to intussussception.
ROTATEQ-a pentavalent human-bovine reassortant rotavirus vaccine. It has been wonderful for us primary care pediatricians-reduced RV related gastroenteritis hospitalizations by over 98%. The intussusception correlation has not been reported, but this vaccine is given to infants less than 6 months old and if you are 12 weeks old, you are too old to start it. These restrictions were put in place because intussusception after RotaShield correlated with increasing age of first vaccine and increasing age when getting any dose. Hard to imagine that at 12 weeks of age you are “too old” for a vaccine (no jokes about the experienced virologists in this podcasts at this point), but that is what we have to tell parents.
ROTARIX-just today the CDC reported that there is porcine circovirus type 1 (PCV1) present in RotaRix and has withdrawn it from the market. This is NOT swine in origin, just seen in pigs. They do not know if there is intact virus present or just DNA segments or whether this causes human disease, from what I can tell. They also do not report how this virus was detected. Can you dig into this and enlighten the masses? Let the second coming of swine flu begin in the media (they get things wrong a good part of the time) so that we can work at undoing their mistakes.
Here is a good tag line for those who want answers now that we don’t know: SLOW PROGRESS IS BETTER THAN NO PROGRESS.
Have a great day.
Joel writes:
Hi Vincent, Dickson, Alan, and Rich,
TWIV episode 72 was great. I had a few quick comments.
1) The original high profile paper describing CRISPR as an adaptive-type immune response in bacteria was from a research group at a dairy company. Apparently there are some common bacteriophage that are the scourge of cheese and/or yogurt production. I found it interesting that these phage are such a problem that the company funded basic research like this. (http://www.ncbi.nlm.nih.gov/pubmed/17379808)
2) While it is well documented that plants and insects use RNAi (siRNA-mediated) as a defense mechanism against viruses, RNAi (either miRNA- or siRNA-mediated) as a defense against viruses in animals with more complex immune systems has been contentious. An interesting exception is in germ cells. A novel class of small RNAs called Piwi-interacting RNAs (piRNAs) are highly expressed in germ cells and are thought to defend these cells against the replication and re-integration of endogenous retroviruses. Stringent defense against the replication of endogenous retroviruses is important to prevent ever-expanding genomic “junk” from being passed on to future generations.
3) If you are interested in discussing archaeal viruses, I would recommend having Dr. Mark Young from Montana State University as a guest on your show. His group has been spending years finding viruses in what amounts to boiling acid in the hot springs of Yellowstone park. (http://mbprogram.montana.edu/faculty.asp?per_id=101&in_id=12)
I received my Ph.D. studying rotaviruses and have moved on to a postdoc studying Leishmania, so I enjoy both TWIV and TWIP. Keep up the good work.
-Joel
PS Dickson, any chance you’ll be at the Woods Hole Immonoparasitology meeting in a month?
Henrik writes:
I really enjoy your show and am slowly starting to get the hang of basic virology. I like the way you revisit topics
from different angles. It helps to hear things again in a different way, so it doesn’t become boring.
And don’t forget the 101 stuff. Even if I’d rather learn about the sophisticated topics, the devil is usually in the detail, so understanding the basics is vital for really following your trains of thought.
I just watched a nice talk on fora.tv about an expedition to New Guinea.
You may find it interesting as they did a lot of virus sampling in the birds there.
http://fora.tv/2010/03/17/Expedition_Papua_New_Guinea_with_Jack_Dumbacher#fullprogram
http://www.calacademy.org/blogs/jdumbacher/
Keep up the great work!
Cheers,
Henrik
Dan writes:
Your recent episodes have again discussed aspects of H1N1 and influenza. Given advances in gene sequencing (deep techniques or
whatever) it seems that if these techniques became economical, swine populations (or birds) could be monitored for new influenza strains
on a regular basis. Once a new, say “novel” infection is discovered in the swine (before the virus becomes zoonoic, did I say that right?)
or transmitted to humans, an inactive vaccine could quickly be made from the swine virus through say for instance plant or insect
techniques (common by that time) that could be administered to humans along with the annual flu shot. I don’t think the vaccine
would be harmful to humans (inactive vaccine), but it could be an intelligent “shot in the dark” to head off a potential nasty pandemic
(via “cross reactivity”, did I state this right?). Is this idea science fiction, or does it have potential? Until a true “vaccine for all flu types” becomes reality, it seems this could actually be a way to protect our growing population from a devastating infection with high virulence.
Remember, when you end your podcast with “another twiv is viral”, I am the one who was just infected.
Yours sincerely,
Dan, the meteorologist in Colorado.
Ps: give my 3′s to Alan, he will understand
Anthony writes:
Dear heroes,
Iterations of flattery and humility. A question: does an individual who is infected with HSV-1 and who chronically develops lesions become newly infected with each outbreak? I.e. if retroviruses insert their DNA copy with impunity, would not each outbreak produce new virus to peruse the body and infect other cells? or even the same cell twice? It is my understanding that HSV-1 infects neurons in the face/neck. Do viruses, newly produced during an outbreak infect other nearby neurons? Do they insert many copies into the same infection-susceptible cell? My guess is no, because this would eventually be horribly detrimental to the host. If my guess is inaccurate, how many outbreaks must one go through before a secondary infection induces cancer or apoptosis in these rarely regenerated neurons?
Another question: How can a lowly research technician get money to study a brilliant idea he or she had? Then, how can said technician get the IP if his or her brilliant idea works?
Godspeed,
Anthony
Sophie writes:
Hi Vincent and cohost(s).
I have a question about HIV/AIDS. You always say that virus have a tendency to get less virulent, because it lets the host transmit it to more people. Could the reason for the prolonged life of HIV patients be due to the virus is adapting to us, or is it just the antivirals?
Furthermore could it be possible to find the mechanism that control whether it is HIV or AIDS you have (I’m thinking of something like the bacteriophage Lamda, with Cro and cI)? Or is it simply, when a high enough number of T-h cells are infected you will get AIDS?
Still love your podcast.
Sophie
Ken writes:
While discussing the evolution of H1N1 2009 pandemic influenza virus, Alan dropped the line, “Be a virus, see the world.” Which is, of course, a Far Side caption.
When teaching introductory microbiology courses, I used to disclose to the students, at the beginning of the virology lectures, that I understood they had, coming into the course, very little knowledge of virus biology. I understood this because one can get a sense of what Americans learn in high school and introductory college biology courses by scanning The Far Side. A high proportion of Gary Larson’s humor played on shared popular knowledge of biology. And the fact is (I know this because my beloved partner bought me the complete collection) that, in fifteen years of daily panels, there are exactly two that make any reference to viruses, and neither addresses virus biology.
I no longer do that bit, because my current students don’t know who Gary Larson is. And more of my students will already know something about the biology of viruses because they’re growing up around people who listen to TWIV.
Duncan writes:
This is the second time that I have emailed you and I have no desire to be considered a stalker, but I thought that I should let you know about the impact that TWIV and TWIP is having on at least one of your listeners.
Last time I emailed you I told you that I was planning on leaving my IT job to attend university and study for a degree in medical laboratory science. That was probably a year ago and I still haven’t left my job. Why I hear you say.
Well, I’m writing to tell you that it is pretty much your fault. You see originally I wasn’t even considering getting into research and that is why I was looking at the lab science degree. After a year or so of listening to your wonderfully podcasts, I discovered that my passion for microbiology runs much deeper than I had previously thought. After much thought I decided that if I was going to follow my dreams, I should follow them all the way and I am now going to be studying for a bachelor of biomedical science majoring in genetics and molecular pathology.
I’m not entirely sure what I will do after I’ve completed my degree but I have an open mind and deep fascination in viruses, parasites, bacteria, genetics, disease and what makes life tick at the cellular level. I may go on the do a PhD, I might even decide that after all that time at university I’m satisfied with my level of knowledge and go back to IT, but I very much doubt it. Whatever happens, I thought that you would like to know that you guys played, and are still playing, a major part in helping me to achieve my dreams with your inspirational shows. Thank you very much and keep on doing what you’re doing.
Cheers
Duncan
New Zealand
Belle writes:
I am appalled at the lack of sanitation in manicure salons. Even those salons that claim to disinfect and sterilize seem to cut corners. Has any study been made to determine viral transmission in these establishments? Many women have cuticles cut and pushed back, basically a surgical procedure done under non-sterile conditions. In addition to the well know viruses, other retroviruses including XMRV, might possibly be transmitted. There have been clusters of diseases in many neighborhoods of different illnesses. It would be tantalizing to explore the unsanitary conditions of these salons as sources of infections.
Years ago, it was said that upper-middle class women had higher incidences of breast cancer. I am not sure of the status of this statistic. Has anyone ever questioned these women about their attendance at manicure salons? beauty salons?
If you want to satisfy your curiousity of how unsanitary these establishments are, simply visit one and observe. Instruments are either not sterilized, sterilized inadequately, or reused from person to person. One establishement had their instruments in some kind of sandy material which they heated to 135 degrees F (they were proud to show this to me). Others have instruments soaking in liquids. Nail shavings are left on paper towels from person to person.
I am sorry if this email seems eccentric, but it is very disturbing to see the mess that goes on in most manicure salons. I do have some substantial medical knowledge. In addition, my nails look very ungroomed .
Sincerely,
Belle
Matthew writes:
I just discovered TWIV and have been devouring episodes. The one on the 7 types of virus genome was the best one yet. I will have many more questions to come but for now I have a somewhat practical question as I’m currently recovering from a recurrence of herpes simplex in my cornea. It’s interesting to think that I’m actually looking through herpes simplex viruses as I type this! It’s ok – I have acyclovir on the case.
What I’d like to know is: is there any truth in the idea that eating foods rich in arginine can trigger a recurrence of herpes ? The idea is that eating more lysine-rich foods can prevent recurrences by blocking absorption of arginine.
Thanks for doing the TWIV podcast. I love the episodes with you and Dick talking in technical detail. I think that viruses are beautiful, enigmatic things. Surely they hold clues to some of the profound mysteries of cellular life.
Cheers,
Matthew
Laura writes:
Dear Vince, Dick, Alan and Rich,
Thank you so much for the wonderful podcasts as both TWIV and TWIP are my favorites. They frequently make me laugh out loud getting me strange looks on public transport and at the gym. I teach High School Biology in Hong Kong and am currently doing a distance learning MSc. in Infectious Disease so all your info. is invaluable. I am writing to recommend a pick of the week which is Arno Karlen’s “Plague’s progress” which is both informative and a very easy-to-read stroll through the history of disease.
If any of you are ever over in Hong Kong and are at a lose to what to do send me an email and I will happily show you around to say thank you.
Regards,
Laura
James writes:
Hello all,
I was flicking through my RSS feeds when I came across this story about the New Zealand Blood Service moving to stop people with CFS from donating blood. This seems to be a precautionary measure until the science becomes settled as it is remarked in the story that the science is shaky at the moment.
http://www.stuff.co.nz/national/health/3607226/Chronic-fatigue-donors-face-rejection
And a quick question. If H1N1 Swine Origin is found to displace the H3N2 seasonal strain would you expect the WHO to switch their suggestion to a bivalent vaccine and thus instantly increase the amount of seasonal Flu vaccine that could be produced by a third? Just an interesting public health logistics though I had.
Kind Regards,
James
New Zealand
Stephen writes:
I was listening to your story about researchers who bought an assortment of groceries in Marseilles for testing. I wonder if they bought any Koala brand tea. This is important because “The Koala tea of Marseilles is not strained”
- Stephen
TWiV 80
Ricardo writes:
Again and again, You do it over and over. Your podcast is everything about teaching. I’m expecting every monday morning for the download to finish so I can have my “pleasure drive” to Ponte de Lima (a secondary campus from UFP). Episode 72 was really good, the CRISPR and the iRNA sequencing was very interesting. But, another thing made me wish my entire group of students could listen to you four. During the last episode I found myself thinking “… look how this guys learn…”. You are all grate teachers but you are also grate learners. During your 90″ talk we get questions, chains of events, summaries, research (google) it’s almost like a fight for knowledge.
Sorry for my English and congratulations.
Just an interesting software I herd about “Tableau Public”. http://www.tableausoftware.com/public/.
Ricardo
Etienne writes:
Hello Vincent Racaniello and TWIV panelists,
I was listening to twiv 72 and it was mentioned that archea only live in extreme environments ( hot vents, salt lakes, and extremely low ph for example). Tho it is true that they are well known to be the dominate life in those environments, it has been shown that they can be found in much more mundane settings. They even seem to play a major role in the production of nitrites and nitrates from ammonia in top soil.
For examples, here are 2 articles about DNA sequencing revealing the presences of archea genes in top soil. I tough that you might find them interesting.
Archaea predominate among ammonia-oxidizing prokaryotes in soils: http://scholar.google.ca/scholar?hl=en&as_sdt=2000&q=archaea+bacteria+in+soil
Molecular phylogeny of Archaea from soil
Etienne
Cedric writes:
Hello TWIV gang, I’m currently listening to TWIV #72 and just heard the discussion of viral infections in Archaea. One of the questions that came up was how viruses could survive the extreme conditions that archaea inhabit. I agree with Alan’s assertion that if archaea can make proteins that survive such extremes, viruses can too, but it is also worth pointing out that archaea do not only live in extreme environments. They tend to thrive in nutrient-poor ecosystems and at extremes of pH, temperature and other environmental parameters, but they are also found alongside bacteria and eukaryotes in soil and other mundane habitats. Like bacteria, archaea can also live inside other organisms, including humans, and as you know this is an excellent environment for horizontal gene transfer, including virus-mediated transduction. The section of the Wikipedia entry on archaeal habitats is well-referenced and talks a bit about their ecology: http://en.wikipedia.org/wiki/Archaea#Habitats.
I love the show and always enjoy the discussions. Keep up the good work!
–
Cedric
Angie writes:
Hello fellow Virologists,
Just wanted to drop you a line to say I LOVE, LOVE, LOVE your podcast! I just discovered it last month and I can’t get enough of it. I am a former Virologist (I worked on Herpes and Parvovirus), who is now a forensic scientist. Although I love my new job, I miss reading and discussing the newest papers/research on Viruses. This podcast fills that void. The way you discuss papers and answer email questions is great. It reminds me of journal clubs or informal discussions at lunch or conferences.
Thanks and Keep the podcasts coming. They are infectious!
TWiV 79
Ben writes:
I really enjoyed your podcast about reverse transcription. I was wondering what makes retroviruses like HIV impossible for our bodies fight off. Are there any retroviruses that can be eliminated from the body?
Paula writes:
I was browsing on the “Chronic Wasting Disease” website when I read that prions not only occur in the brain and spinal cord according to the TWiV #67 program, but also in the saliva, blood, muscle, urine, and antler velvet of symptomatic animals with the late-stage disease. So being that this prion has been found in all mammals including humans (again from the website), we do have the potential to become infected by prion exposure if we handle or consume the meat of an infected deer?
Sarah writes:
What is an enterovirus?
Heather writes:
Dear Dr. Racaniello,
I’m responding to your question regarding the usefullness of podcasts as a learning tool. The traditional classroom provides a forum to discuss and explore new concepts which gives depth to the learning experience. But I feel the podcast has several advantages as well which makes them worthwhile. Students can get exposure from a larger pool of experts who bring their unique background and expertise. Material can be instantly repeated if a section is missed or not understood. The podcast can be interrupted if the student wants to check out links related to the topic, look up terms or whatever may increase their understanding and interest. They can then return to the podcast at their convenience. Finally, there is the possibility of the two-way exchange of ideas, such as this email. Although this feature is not inherent in a podcast per se, it can provide the tools to open the door. I wouldn’t be sending you this email if it weren’t for your kind invitation. So Thank you.
Michelle writes:
I wanted to say “Thank you” for answering my question about viral resistance to antiviral drugs. I have studied microbiology, but virology is a new field for me. I have learned about bacterial resistance and the development of new drugs that combat resistance, so I was interested in knowing about this for viruses too. (As a side note, I learned from my veterinarian that the same thing is happening with certain parasites and drugs used to kill them.)
To answer your question…I think that podcasts are an effective way to learn. I have only listened to twiv, but I enjoy listening. The one thing I would caution is that if podcasts are used specifically for student education, that the presenters would have to be careful to stay on topic because it may be easier to stray when not in a classroom setting.
Ken writes:
I‘m reluctant to be seen as chastising such a distinguished group of scholars, but I know that you are committed to basic virology education.
Toward the end of the episode, y’all handled a question about what distinguishes the most complex viruses from the simplest bacteria.
Listening to the discussion, I was dismayed that I did not hear what I regard to be the critical word.
That word is Eclipse.
David writes:
I believe in TWIV #70 where someone asked the question, is there a virus that alters human behavior to facilitate transmission. Would rabies qualify?
I recall years ago speculation that rabies was the basis for the vampire legend. If I remember correctly, rabid people would try to bite other people, spreading the infection. If that is true, and if rabies can be spread by biting, then rabies could be considered a virus that spreads through altering its host behavior.
http://en.wikipedia.org/wiki/Vampire#Rabies
Gómez-Alonso, Juan (September 1998). “Rabies: a possible explanation for the vampire legend”. Neurology 51 (3): 856–9. ISSN 0028-3878. PMID 9748039.
Vincent writes:
Drs. Racaniello, Despommier, Dove, et. al.,
TWiV 78
Michael writes:
Hi guys really like the show even though some of it (not much) goes over my head. I also listen to twip and hope there will be a matching number of episodes to rival twiv. My name is Michael and I was talking to my dad the other day and he mentioned that he took parisitology from Dr. Brown (Stoolie) when he was at Columbia. Small world. I was also interested in checking out some classes at UCLA, I live in LA, and wanted to know if you had any recommendations as far as instructors or classes.
A couple of things I was wondering how your iphone app is coming along. I know lots of programmers and artists and would like to produce one of your ideas.
Secondly you guys mention all the time about the dearth of research being done. How would you like to start your own non profit? And is there a website that tracks current field studies or lists proposed studies? I have a great plan for a virtual corp. that could direct and help synergize field research. You guys would get to do the fun part i.e. plan the protocols and general aim of the project, and approve the personnel, take all the public credit. I would do what I do best which is organization and logistics. I think Field Studies International sounds good.
Well enough of your time for now thanks for the great podcasts.
Michael
Mary writes:
As much as you guys are adamant against engaging in political discussion, I know you also feel strongly about exposing the truths behind alternative medicine, anti-vaccination campaigns, and so much other medical and scientific disinformation espoused by quacks all over the world… so maybe this is something you might feel like passing onto listeners? I’m not sure if really counts as “politics”, anyway.
As you may know, science writer Simon Singh is being sued essentially for bringing debate on alternative medicine into the public forum, and the millionaire- and corporate-backed British libel laws, among the most repressive in the world, are allowing this to happen to responsible journalists, writers, anyone—even outside Britain, thanks to the thriving “libel tourism” the laws have given rise to. There is a movement sponsored by journalists and others, including scientists, to reform these laws, and it includes a petition, for which they are inviting signatures from around the world, because even those of us outside the UK are at risk for litigation.<
http://www.libelreform.org/sign
Just food for thought. (Please excuse me if this is wildly inappropriate.)
In a separate (or maybe conceptually related?) vein of thought, here is a good essay from the Journal of Cell Science a year or so ago (attached) on the importance of admitting and even embracing our own stupidity as scientists.
Thanks for the great shows!
Mary
Cedric writes:
Dear This-Week’s-TWiV-Crew,
I heard in a lecture from Prof. Steven L. Goldman of Lehigh University that atmospheric/wind currents can pick up dirt, bacteria, and viruses and transport them across entire oceans. I was wondering if this can or could have been a means of viral spread. Can a virus survive in the upper atmosphere, or would radiation render it inert? Is this a phenomenon that can be of significance in today’s world of human-created interconnectivity?
Many thanks for your podcast. I am a high school student working part time as an intern at a national lab and I love to listen to TWiV and TWiP while doing the menial chores.
Salubrious Salutations,
Cedric
John writes:
Listening to your show reminds me of the excitement I felt as a child reading Paul DeKruif’s “Microbe Hunters.” As a physician living in North Carolina, you are making me nostalgic for my days as a resident and intern at Columbia. Your show reminds me of what a great institution it was and is.
Benhard writes:
Dear TWiVers and TWiPers,
Since I’ve discovered TWiV (and TWiP), I’m addicted to virology (and parasitism), well, at least during my commute to work and back home. It took me quite some time to catch up but it was definitely worth it!
Although I’m working as a software designer for medicinal chemists in a pharmaceutical company, I’ve always been interested in the big picture of biology. Listening to TWiV (and TWiP as well) gives me a glimpse into how biologists work and think, which helps me communicate with them. There are many other podcasts which I’ve since also subscribed to but TWiV and TWiP are special in how well they match what I would be interested in from the respective fields and how entertaining the subject is presented.
The second reason I write is to suggest a Pick of the Week:
Last year, I learned about ‘Sustainable Energy – without the hot air’ (http://www.withouthotair.com/) by David MacKay. I knew his previous book ‘Information Theory, Inference, and Learning Algorithms’ as a treasure trove, but it’s probably too heavy reading for general consumption. Sustainable Energy, however, is fairly easy reading, full of facts and figures, surprising calculations, provides a big picture, and shows how the world might be able to escape it’s current agony. It provides a sober view on (British and world-wide) energy consumption and production with real figures and personalized measures. It could arguably be the most important book on the topic written to date. So, have a look and decide for yourself.
Keep up the good work (including the jokes)
Bernd
Dave writes:
Hi DrsVAD,
When GRID computing is promoted, the usual suspects mentioned are Seti@Home and Folding@Home. At least of equal merit and more germane to TWIV should be:
www.worldcommunitygrid.org (WGG)
I found the following factors (listed on the WCG website) more compelling than Folding@home:
“World Community Grid harvests the unused computing capacity of volunteer PCs around the world, creating a secure virtual supercomputer available at no charge to scientists engaged in not-for-profit humanitarian research.”
“The World Community Grid team helps scientists prepare research projects for grid computing, process results and reconfigure work for further computation. In return, research partners must commit to open publication of their results”.
Highlighted below are three research projects with a virology connection:
Current WCG Research:
| Help Cure Muscular Dystrophy – Phase 2 |
| Help Fight Childhood Cancer |
| Nutritious Rice for the World |
| Help Conquer Cancer |
| Human Proteome Folding – Phase 2 |
| FightAIDS@Home |
| Influenza Antiviral Drug Search |
| Discovering Dengue Drugs – Together |
| Help Cure Muscular Dystrophy |
| Genome Comparison |
| Help Defeat Cancer |
| Human Proteome Folding |
It would be good if you could give WCG an honorable mention along with Seti and Folding.
I am an Information Technology (IT) professional with no formal training in any of the sciences, but I really wanted to make a contribution to scientific research. My charitable cause is WCG.
Since 2004, I have donated 88 CPU years to WCG projects. This is equivalent to turning on a PC in the year 1922 and having it run 24 x 7 x 365 uninterrupted to present day, computing work units for the Current WCG Research Projects previously mentioned.
As you’re probably doing your goszinto’s right now, this involves 10 multi-core PC’s (9 quads and a dual for a total of 38 CPU cores) running pretty much at 100% load. Yes, my power bill does take a hit.
As for the TWIV and TWIP podcasts, thank you immensely DrsVAD for devoting your time and effort on the podcasts and especially for enthusiastically sharing your knowledge on virology and parasitism. I was hooked from episode 1 on both podcasts.
I suspect I’m not your average listener type since I don’t work in any scientific field and I’m circa Vincent’s age. My career ship has sailed, but in my next incarnation I hope I come back as a microbiologist or virologist. After finishing Volume 1 of Principles of Virology, it became obvious to me that to obtain a competent knowledge of viruses, I needed to take a deep plunge into biochemistry, cell / molecular biology and immunology. I’m just coming up for air, but what a fascinating journey. Science fiction pales in comparison to reality. Ready for Volume 2 of PoV.
For me, I love that you don’t dumb down the podcasts too much. There is delectability in the details. For example, when you were talking about a membrane lipid, you use the actual terminology phosphatidylinositol. This is helpful so I can do further investigation and also very useful to hear how terms are pronounced. Having no contact with scientific types, I have to guess at how some terms are pronounced. This can be problematic since often online audio dictionaries will not have technical terms. Now if we could just get Marc Pelletier (FIB podcast) to quit calling them [ am I no ] acids, life would be good.
My hope is that you continue to enjoy doing the podcasts as much as we, your audience, enjoy listening to them.
Keep it viral!
Dave
TWiV 77
Wladimir writes:
In regard to your question as to cases of known alteration of host behavior by virus that increases the rate of contact among hosts (Twiv 70), the most dramatic example is given by rabies. This extraordinary virus can convert a neurologically and behaviorally complex organism like a dog (or a person) into a vehicle that is behaviorally dedicated to increase the transmission of the virus. This seems to be done mainly by a sophisticated process of selective infection of particular neural structures that makes the host more aggressive and cause it to salivate more (increasing the load of viruses to be transmitted in the bite of the so-converted furious animal). I am copying to you below a fragment of the paper by Dr. Benjamin Hart “Behavioral adaptations to pathogens and parasites – 5 strategies” published Neuroscience and Biobehavioral Reviews in 1990, in case you want to provide to listeners further details of the elegantly macabre transmission tricks of the rabies virus.
all the best,
Wladimir
Effects of rabies virus on mammals. This is probably the most well-known example of a virus altering animal behavior. The virus infects domestic dogs and other canids and can turn a calm and placid animal into a wandering and vicious animal that attacks almost any target in sight. The rabies virus cannot survive except in living organisms, yet it is virtually always lethal in man, canids and many other hosts. In these instances, to be propagated the virus must be transferred to another animal before the host dies. In the furious or vicious form of rabies the virus usually enters a wound through a bite by an infected animal. The virus, which is in the attacker’s saliva, enters the open wound created by the bite, moves into exposed peripheral nerves and then travels up inside peripheral nerves to the brain. The virus then multiplies in several areas of the brain of the new host, but particularly in limbic system structures such as the amygdala, hippocampus and pyriform lobes. The limbic system is known to control emotional behavior, including aggressive and feeding behavior and damage or experimental electrical stimulation of this area can lead to rage and undirected, unprovoked attacks. The greater localization and multiplication of the virus in the limbic system compared with the neocortex is apparently what causes abnormal behavior, including wandering aimlessly and attacking and biting anything encountered. While the virus is multiplying in the brain, it is also descending back down peripheral nerves including those innervating the salivary glands. The virus enters the salivary gland tissue and saliva. The nerves supplying the laryngeal and pharyngeal muscles are often affected as well and the ensuing paralysis of these muscles makes swallowing difficult. This causes pooling of saliva, and when the infected animal bites a new victim the pooled saliva is a reservoir of virus to be injected into the new victim. When transmission of the rabies virus does not depend upon abnormal viciousness for transmission, such as in vampire bats where the animals naturally bite each other rather frequently, or where the virus may be transmitted by the airborne route, abnormal viciousness for transmission from neurological alteration does not occur. In vampire bats the rabies virus reportedly does not necessarily produce acute death and may not be fatal.
from HART, B. L. (1990). Behavioral adaptations to pathogens and parasites – 5 strategies, Neuroscience and Biobehavioral Reviews 14(3): 273-294
Jessica writes:
Regarding the question you received in TWIV #70 about why a person might get a cancer-causing virus, such as HPV, but not actually develop cancer, I thought I might add a bit to your discussion. It is generally believed that 5-7 events are required for a cell to become cancerous. There are many checks and balances present in our cells designed to prevent the formation of wacky cells, and generally when a cell starts displaying bad behavior, such as uncontrolled growth, it will go through apoptosis. In the case of HPV infection, the presence of the virally-encoded oncogenes contribute to cancer formation by counteracting these checks and balances. However, infection alone is not sufficient for cervical cancer formation, and many cofactors have been demonstrated to contribute, such as age, smoking, parity (the number of times a woman gives birth), and other genital infections. Without such cofactors, the virus can lay dormant in the cells, causing no apparent disease. Additionally, as you mentioned, a large portion of HPV infections are initially cleared by the immune system.
Why do I know all this? Well, I did my graduate work on papillomaviruses–not the cancer part per se, but I listened to enough seminars on it to pick up this much at least. I have since moved on to work on flaviviruses, including (gasp!) West Nile virus. I am an avid listener of your show, it helps me through my daily public transit commute. Thanks and keep them coming.
Jessica
PS I also love TWIP, can I put my vote in for higher frequency here?
Sophie writes:
Still love your show, but I have a question about the discussion about viruses and their status: Why is it so important wether they are alive or not? I don’t think many people really know when something can be called alive and would it actually make a difference if it was alive? As far as I know it would not make a difference (it’s not like bacteria has rights), so why is everybody so interested in this question, when people cannot even agree on a definition of life?
Thanks for all the information.
-Sophie
Christine writes:
I was listening to podcast #69 today and was interested in the comments about mmr vaccine and it’s effectiveness wearing off over time. I am in Australia and being 35 I got 2 doses of mmr as an infant and a rubella vaccination at 13. At 25 when I had my first child my immunity to rubella was considered “equivocal” or something like that and so after her birth I was again given a dose of mmr. Before getting pregnant with my second I was tested again and was “eqivocal” again and given another vaccination (less than 2 years since my last). When I came to have my third child, same thing with a gap of three years. My best understanding is that although I have some immunity it is not sufficient for protection from this disease. My doctor was concerned about me returning to teaching high school while preg. Luckily I was probably not exposed in my first preg and was kept too busy in later pregs to fit in work and kid(s).
I wonder how many other people there are like me out there contributing to outbreaks.
Christine
Avid twiv and twip listener.
Kurt writes:
I’m surprised at how few comments there are on iTunes. I’ve been listening for a long time, and figured huge numbers of others listen too. I gave you a nice review, but don’t know how to twitter. I hope your next contest has rules suitable for a technophobe. I came to you from iTunes, and never got around to looking at your website. The contest got me there, and I really like some of the links. Good work.
Your podcast is pitched over my head, but like any technical topic, just hearing the words lead to some level of understanding. The jokes need some work. I sometimes feel punished. Overall fun to listen to.
I appreciate what you are trying to do with distance learning. I listen to podcasts as I drive around Florida selling paint. I enjoy science, and lately have been listening to Physiology lectures by Gerald R. Cizadlo, Ph.D. Department of Biology The College of St. Scholastica. Take a look at http://faculty.css.edu/gcizadlo/ his lectures are on podcasts, and he puts his blackboard notes up on his website. That’s what I’d hoped for in your Virology 101 classes, since they are too dense for idle listening. I expect you will get to putting up lecture notes sometime. I like the pretty pictures of viruses.
Thanks for your good work. If I knew some arcane question I’d ask it, but, well, I don’t.
Kurt
Gary writes:
Just in case you haven’t seen this yet: here is an article describing measurement of the driving energy released as individual bacteriophages inject genetic material into bacterial hosts — I.e., the kinetic energy driving the process has now been quantified!!
http://pda.physorg.com/_news184588836.html
All the best,
Gary
PS: Again thanks for all your instruction. Your enthusiasm for, and love of virology is – without question – infectious.
Subbaro writes:
It was a good program on Reverse transcription of retro viruses. At least in a simplified way most of the aspects of it were explained. I would like to add that in addition to Cauliflower Mosaic Virus (CaMV), a plant Pararetrovirus of caulimoviridae, there are 20 different plant viruses belonging to BADNAVIRUS (Bacilliform virus with a dsDNA genome) group which show (para)retrovirus characters. Half of them are fully characterized now.
The following: Banana streak virus (BSV); Cacao Swollen Shoot Virus (CSSV); Citrus yellow mosaic virus (CYMV); Pineapple bacilliform virus (PBV); Rice tungro bacilliform virus (RTBV); Sugarcane bacilliform virus (ScBV) are economically very important viruses, especially RTBV which is associated with tungro disease of rice causing loss of millions of dollars. RTBV along with RTSV (Rice tungro spherical virus) a picorna virus produces lethal symptoms
Thanks
Subbarao
Jaturong writes:
I am a Thai doctor who is now doing Ph.D. study in Molecular Virology and Microbiology program at Baylor College of Medicine, Houston, TX. I know the show year ago from my fellow graduate student who sent out an e-mail to recommending TWiV to all students in our department and since then, I have become a big fan of the show. I am working on a mouse model system using mouse gammaherpesvirus to study the role of promyelocytic leukemia nuclear bodies (PML NBs) as host intrinsic immunity in acute infection and viral latency and the mechanism that the gammaherpesvirus uses to counteract these nuclear bodies.
Everything relates to viruses is always interesting to me, so I love every topic that has been discussed on the show. The show also encourages me to keep on working on my experiments even on days that things in the lab seem not to turn out as I expected. I also use the questions asked in the show to test my knowledge about virology by comparing mine with yours and the show’s guesses and I realized that there are many things I am supposed to know but I do not know. I do not have specific virology question right now but just wonder how do you manage your time to keep update of all virus-related articles and news, teach in classes, projects in lab, recording TWiV and response to those e-mails? After I graduate, I will be having my own lab and teaching virology in the medical school in Thailand as well.
Thank you for having a fantastic show for us and please keep it up. I really appreciate your input to educate people about viruses and am always looking forward to the next episode of TWiV.
Regards,
Jaturong
TWiV 71
Jennie writes:
I wonder whether we have entered a new chapter in the book of human knowledge sharing. I’m often working physically when I listen to my favorite science podcasters (TWIV, TWIP and Mark Crislip)…. so your entertaining program is intertwined with raking leaves, loading wood, washing dishes (but NOT vacuuming). I hope that learning and moving can be merged in this decade through a more thoughtful use of tech.
I love the unveiling of your subjects over the course of time…the interaction of the two of you is very important in peeling the layers…both of you ask each other good questions and your model is VERY important – neither of you is afraid of appearing ignorant by either asking questions or not knowing an answer.
Other aspects that you are modeling: the power of synergistic professional/personal friendship and the sublimation of professional rivalry that can humanize science and extend knowledge boundaries.
For years as an RN I’ve taught health care to people with a high school education (maybe not HS sometimes)…the wedge (or funnel?) of narrative is by far the best way of getting the information into their skulls. Stories, pictures and practice actually.
Your stories are the best!
Take good care of yourselves: walk where you want to go this year, eat more vegetables, have fun in the physical world and….GO GET EM IN 2010!
Your listener
Jennie
TWiV 70
Tom writes:
I just finished listening to the Original Antigenic Sin episode where you were talking about Wolbachia’s protective effect against virus infection in Drosophila. I was delighted that you were speculating about the effect in bees because Wolbachia has been one of my favorite subjects for years.
Some key things to know is that:
1. Beekeepers have used (overused) tetracycline routinely since I think the 1950s against a bacterial disease of the brood called American Foulbrood. This usage has almost certainly cleared any Wolbachia infections in domestic bees, if they once had it. Interestingly, we now have developed bees that are resistant to that disease, which make antibiotics unnecessary, though unfortunately they are still widely applied.
2. Wolbachia has been found to be very common in African bees (but only in Africa) in at least two subspecies. One of these races, Apis mellifera capensis, has the unusual trait of worker bees producing diploid (female) offspring parthenogeneticaly, possibly due to an effect of Wolbachia. Our European workers can only produce haploid offspring, which are always male.
3. Another well studied Wolbachia effect is something called cytoplasmic incompatibility. This can result in sperm produced by infected males killing eggs of uninfected females. Infected females on the other hand produce viable offspring using either infected or uninfected sperm. This gives infected females a huge reproductive advantage. Wolbachia is very selfish, and since it is passed on only maternally, in the cytoplasm the egg, it uses the genetically dead end male to kill off the competition.
My own pet hypothesis is that this could explain how descendants from 26 African honeybee queens released in Brazil in 1956 were able to make a nearly complete genetic sweep all the way to the southern US. Supporting evidence for this hypothesis is still lacking, since Wolbachia has yet to be found in this hemisphere, we are actively looking though. If found, it could be very useful not only for the possible protection from virus, but also for driving good genes into the population.
A person who we are working with to find Wolbachia in bees is David Schneider at Stanford. Here’s a quote from his article in Science last year,
“One might guess that an insect would be safe from having its microbiota altered. Honeybees are an exception, however, because we’ve been dosing commercial colonies of bees with antibiotics for decades. Before the rise of colony collapse disorder, one of the most important honeybee diseases was American foulbrood, caused by the bacterium Bacillus larvae. To deal with this threat, many beekeepers prophylactically treat their hives with tetracycline derivatives—the same antibiotics used to cure flies of Wolbachia. If these treatments cured queen bees, then all hives descending from these queens would also be Wolbachia free, because the microbe is transmitted maternally. A Wolbachia-virus sensitivity experiment may have already been performed on honeybees nationwide and may change the way bees interact with previously characterized pathogens.”
I find you and Dick brilliant in the way you come up with great ideas on the fly. It’s a pleasure to listen to such intelligent people bounce ideas around. Thanks for such interesting program.
Sincerely,
Tom
TWiV 60
Eric asked for “advice on how to bridge the gap between clinical medicine, public health, and virology research.” I asked Scott Hammer MD for his thoughts on this question. Here is Dr. Hammer’s response:
Hi Vincent:
Thanks for forwarding this comment. In response, I’d inform your interested listener that the career opportunities in Infectious Diseases are broad and include – fundamental laboratory research, clinical/translational research, clinician/teacher role at an academic center, epidemiology and public health (both domestic and international), private practice, and industry. A substantial proportion of Infectious Disease Fellows are pursuing Masters degrees in Epidemiology at their colocated Schools of Public Health so that they have formal training in both ID and epi/biostats/study design/global health, etc. For more information, I’d refer him to the following websites: the Infectious Diseases Society of America (www.idsociety.org), the American Society for Microbiology (www.asm.org) and the Association of Schools of Public Health (www.asph.org). In addition, he could surf the websites of some of the individual fellowship programs (Columbia, Partners (MGH and Brigham in Boston), Johns Hopkins, the University of Washington in Seattle, and the University of California San Francisco.
Hope this is helpful.
Best regards,
Scott
TWiV 59
Nick writes:
I’m a bit behind in my Twiv listening, but I’d like to comment on something you said in Twiv 47. You have reminded us several times in the past that “viruses are not alive” and you embellished on this during Twiv 47 by saying that if they are not alive, they can’t be killed. Actually, viruses can be killed, by treatment with formaldehyde or chlorox, boiling, or irradiation with x-rays or UV light. These are commonly-applied treatments that “kill” viruses. Were they alive before having been killed? Perhaps that is just a semantic question, but it seems to me that you cannot kill something that is not alive!
I think there may be some confusion in our minds about what a virus is. We most often think of viruses as being the virus particle, or virion, which carries the viral genome, wrapped in a protein and sometimes a lipid coat, from one cell to the next. This looks inert and not living. But this is a bit like saying that an oak tree is an acorn, or a sunflower is a sunflower seed. Viruses actually exist not only in the form of virus particles, but also in their intracellular forms, during which they carry out the many intricate and complex activities that lead to their reproduction. Sure enough, they need lots of things that cells provide, including energy, the machinery that makes proteins, and basic building blocks such as amino acids and nucleotides. But if you mean that “being alive” implies coding for those proteins and RNAs needed to synthesize proteins, produce energy, and make amino acids and nucleotides, this becomes a bit of a techical argument.
What about other “obligate intracellular parasites” such as chlyamydia and rickettsia? They can only reproduce inside cells, in part because they cannot synthesize certain amino acids and nucleotides. These organisms do make their own ribosomes and protein-synthesizing machinery, and reproduce by cell growth and division once inside an appropriate host cell. But are chlamydia elementary bodies (the infectious form that transports the chlymadia genome from cell to cell) alive? Are acorns and grains of wheat alive? The answer is yes, because they can reproduce under the right conditions; within certain cells, for chlamydia, and under certain conditions of humidity and temperature, for acorns and grains of wheat.
I argue that viruses are just as alive, simply that they have less of the equipment of life and depend more strongly on the host cell to provide this equipment. The recent sequencing of the genome of a monster virus, mimivirus, as well as the genomes of a number of other big viruses, brings viruses even closer to cellular life. Some of these viruses have more DNA and more genes than the simplest forms of cellular life. Mimivirus has genes for amino acid and nucleotide metabolism and for some parts of the protein-synthesizing machinery (but not ribosomes or energy production).
At any rate, I’m not comfortable with the notion that viruses are not alive. They are certainly part of the “biosphere” of living things. They share with other organisms the basic mechanisms of replication and expression of their genomes. They can reproduce themselves (with a little help from host cells), control many cellular processes, and undergo mutation and Darwinian evolution. Viruses have sex: they can recombine or reassort their genes. They can even have sex with cells, in both directions: viruses can insert their genomes into the cell’s genome, and they can pick up genes from host cells and integrate those genes into the viral genome.
Viruses may have originated from cells, or alternatively could have played a role in the origin of life, before cells as we know them existed. RNA viruses and viroids may even be evolutionary relics of the RNA world, which is thought to have preceeded the present world in which all known cellular organisms have DNA genomes. DNA viruses could have played a role in the transformation of cells from RNA to DNA genomes, by having introduced DNA genomes into RNA-based cells. For a fascinating argument in favor of this theory, see “Three RNA cells for ribosomal lineages and three DNA viruses to replicate their genomes: A hypothesis for the origin of cellular domains” by Patrick Forterre [PNAS March 7, 2006 vol. 103 no. 10, 3669-3674].
If you can kill it, it must have been alive!
I just listened to Twiv 48: your further discussion of this topic was interesting but sort of stalled. I got the impression that Rich agrees with me!
TWiV 57
TWiV 56
Joe writes:
TWIVERS,
Guys, what a great podcast. I am a chemical engineer with a MS in Environmental Management. I have been doing EH&S work in industrial settings for about 20 years after some years in R&D and manufacturing positions. I have always had a strong curiosity for all branches of science (physics, astronomy, electronics and biochemistry), as well as math and history. Emergency response and risk communication functions have always been part of my job over the years. Virology was relatively new to me when I found your podcast. I had spent quite a bit of time learning the state of the science related to avian flu and SARS so that I could gauge the level of preparedness my company should have for responding to a pandemic. I eventually concluded that we needed a plan and should be ready but that the H5N1 virus had some ways to go before it became a general threat to humans. That research had left me with an interest to learn more of the broader field of virology. When H1N1 hit this year in Mexico, I found your topical podcasts very helpful.
I have been rapidly catching up on your episodes as I drive (about 1 episode per weekday) and will be sad when I am forced to slow down to real time speeds. I don’t suppose you all have considered doing “Today in Virology” so that I will have a new episode each day!!!
To the point:
I strongly agree with your assessments of the limited value of face masks with respect to providing protection from airborne flu infections. Actual user practices leave many infection pathways open. Beyond just not getting a good seal, how do you train users to remove the mask without contaminating their hands and face. If you reuse the mask which would be necessary in an emergency, how do you keep the inside clean. When do you wear it and when do you take it off? I train people to wear respiratory protection in accordance with the OSHA requirements for fit testing, medical surveillance, industrial hygiene testing, etc. It will not be easy to translate those practices to an untrained inexperienced population.
I agree with Dick that the whole “hot and humid stops the spread of flu” dogma seems inconsistent with the facts. How do we know that flu does not show up in human stool? Do we have actual data? In Asia, could the transmission mechanism be airborne particulate avian feces? Could the reason the pandemic strains violate the seasonal rules be a function of increased intestinal transmission or conversely that their envelopes are more robust in withstanding environmental stresses? The great thing about science is that the more we learn the more questions we generate.
With respect to the study on flu transmission and absolute humidity, If I heard you correctly when you quoted the summary hypothesis of the paper, the authors proposed that the aerosol droplets float longer when dry. This set off my engineering “I doubt it” alarm! So I spent some time reviewing the basics of psychrometry and humidification. I have a new theory on why low absolute humidity correlates with transmission. I think the critical parameter is actually droplet temperature. Droplet temperature will be controlled by the Wet Bulb Temperature for any set of conditions. Wet bulb temp is the temperature of a wetted surface that is experiencing steady state evaporation into the local air conditions. The lower the Relative humidity, the faster the evaporation and more heat lost resulting in a cooler surface. Think swamp cooler in Phoenix vs. New Orleans. Let me give some data to elucidate:
(All data interpolated from Figure 12-2 of Perry’s Chemical Engineering Handbook 5th edition)
Take a volume of air with an absolute humidity of 30 grains of H2O per pound of dry air. (7000 grains = 1 pound) Sorry for the units, but I think in Fahrenheit!
@ 35 F = 100% Relative Humidity (RH) and the Wet Bulb Temp. (WBT) = 35 F (i.e., No cooling by evaporation)
@50 F = 55% RH WBT = 43 F
@80 F = 20% RH WBT = 55 F
As long as the absolute Humidity is low, the particle temperature will stay low until it dries out. In higher humidity, there will be little evaporative cooling and so a higher droplet temperature will be reached more quickly. My amateur virologist guess would be that the lipid coating has an upper temperature limit beyond which it loses strength and/or integrity. At higher temperatures and higher humidity the particle temperature gets too high for the virus to survive shear stresses related to contact with surfaces. In engineering terms it doesn’t bounce well if it is too hot! This would also be consistent with avian transmission routes via cold water bodies. I would expect drying rates at higher temperatures with low RH to be much faster and once the particles dry, their temperature would equilibrate to the bulk air temperature. This would be consistent with the data showing reduced transmission at higher temperatures. Do we have any data that would indicate if dried viruses are still infectious? The physics of these small particles is not straightforward. Also, none of this addresses how the properties of spit differ from pure water. If there is someone out there with the experience and the computer power, this could be an interesting research topic. Please include me in the Et. Al. part when you publish.
A couple of recommendations:
A great website for non biochemists wishing to understand the basics of DNA and RNA is DNAi.org. Great history, clear explanations and the coolest videos of translation and replication I have ever seen! When you watch an animated ribosome at work it makes you proud to be a DNA based life form!
A book for Dick: “The Great Mortality” by John Kelly; “An intimate history of the Black Death, the most devastating plague of all time” I found this when researching H5N1 and was struck by how it captures the social and environmental influences on the development of the plague and then the impacts of the plague on societies and their reactions. It puts some of the current responses to swine flu in perspective.
Future Topics:
Why all the differences in nucleic acid structures within viruses? What are the pros and cons of ssDNA vs. dsDNA vs. ssRNA+ vs. ssRNA- vs. dsRNA?
How does an encapsulated virus survive in the digestive system? My vote is for Hydrogen Bonding (the universal answer for all chemistry exams!)
Dick’s list of top ten vectors throughout history.
How and why retro viruses change our DNA. What’s in it for them? (yes I know I think they are alive!)
How about a session on rhino viruses since we can all relate to their impacts. Why so many, are the different strains new each year or just new to me, etc.?
PS. Doesn’t the Zoster vaccine qualify as one you take after infection like rabies?
Love the show and the latent humor
Joe
TWiV 55
Kevin writes:
Dear TWIVvers,
I was listening to TWIV episode #50, concerning the recent article from Ila Singh’s group about the prostate cancer – XMRV connection, on the same day the NY Times reported a study from Judy Mikowitz et al., finding an association between XMRV and chronic fatigue/immune dysfunction syndrome, aka CFIDS. The CFIDS story has been getting even more attention, due in part to the eagerness of patients and advocacy groups to contradict the common stereotype of CFIDS as a psychosomatic illness – what some people used to call the “yuppie flu”. I have no doubt that CFIDS is a “real” physical illness, and that it involves some kind of chronic infectious process; but as a computational biologist and professional skeptic, I suspect that the relationship between XMRV and disease is *much* more complicated than the people reading these stories are likely to believe.
Although the Singh and Mikowitz groups found strong evidence that prostate tumor cells and peripheral blood cells from CFIDS patients were more likely to harbor XMRV than controls, it’s still premature to assert that XMRV causes cancer or CFIDS. It’s equally probable that patients with both diseases have an immune deficiency, due to genetic or environmental factors or an infection with some *other* agent, that allows the virus to proliferate. Even if XMRV can be said to “cause” one or both of these diseases, the question remains: what is it that allows the virus to establish a foothold in some people but not others? This is of course something we understand poorly, for almost all viral pathogens, including your beloved poliovirus.
So I was intrigued when your guest Jason mentioned a mutation in RNAse L that he said was present in a large fraction of the prostate tumors, that could make the cells more susceptible to viral infection. I went online that night to look up the Singh and Mikowitz papers, and find out if the RNAse L mutation was found in the CFIDS patient’s cells also. It wasn’t – but as it turned out, Ila Singh’s group didn’t find the RNAse L association either. This was a larger, better controlled study than the 2006 paper from Joe DeRisi’s lab that did find the association, but I still have to wonder how the two groups came up with such diametrically opposite results. Any comments on this?
Also, I suspect I wasn’t the only listener who was confused by Jason’s statement that the mutation was found in the tumors, and thought this meant either that the virus was causing the mutation, or that the mutation was specific to the tumor cells. Since most listeners aren’t going to run home and read the original papers, perhaps you could clarify: the mutation we’re talking about is a variant of the RNAse L gene that some prostate cancer patients are born with and is a possible susceptibility locus – not something that’s specific to malignant tumor cells.
To end on a more positive note – I’ve been listening to TWIV for a few months now and have recommended it to many of my friends and colleagues. It makes my 45-minute commute to Livermore seem to go by in no time at all. I have lots of ideas for podcast topics – for one, it would be great if you did an episode focusing on viral strategies for evading our immune response. I would also love to hear your ideas about iPhone apps for virology research; I feel it’s really important to have ways to visualize and manipulate biological data that are both intuitive and beautiful. Thanks for all your hard work on the podcast.
Ben writes:
Hi,
I am not a scientist, researcher, or health professional, just a closet science-nerd who loves your show. I just had a few questions about viruses that I can’t seem to find answers for that I was hoping you could answer.
Are there virus-receptors on cells themselves? If so, why would a cell evolve a receptor to something harmful? How did viruses evolve in general if they kill off their hosts, that certainly couldn’t be a beneficial trait right?
How are viruses so infectious and damaging when they are merely an envelope of genes? Since they aren’t alive like bacteria I can’t imagine why they would exist just to kill things. The same goes with prions. There can’t seriously be an “infectious protein” can there? Proteins are just amino acids folds.
Hope you can answer some of these either by email or on your show. Thanks a bunch!
TWiV 48
Rodney writes:
Hello, I have been an avid listener of TWiV over the last 9 months or so and have very much enjoyed the podcast. It is always great to hear a broad, informed discussion on virology, and your recent podcast on viral classification was of particular interest to me. As a Viral Genome Curator at the National Center for Biotechnology Information (NCBI), I am currently working with the International Committee on Taxonomy of Viruses (ICTV) and several virology research communities in an attempt to address longstanding and emerging issues of viral classification. Your podcast provided a concise primer to this topic, but I thought it worth mentioning a few additional issues.
First off, all viruses are classified by nulceic acid, dsDNA, ssDNA, dsRNA, ect…, both by NCBI and ICTV. Although these divisions are given no rank, they provide functionally relevant handles with which to globally group viruses. Second, the way in which viruses are classified is somewhat variable. You might be surprised to know that despite developments in genomics, many viruses are still classified by morphology, using electron microscopy. This is particularly true of bacteriophages, and NCBI and ICTV are working hard together to develop more portable, computer based methodologies. However, it is worth noting that even when computational tools such as Blast and PASC are used to classify viruses, the line of demarcation that separate different “organisms” vary widely amongst different viral families. This variability may actually be a good thing as it allows different research communities to tailor taxonomy, making it more relevant to a specific group of viruses.
Perhaps the more pressing issues in virus classification arise as the traditional, isolate, passage, and physically characterize approach to viral discovery is altered by modern molecular techniques. In the past, viruses have been characterized by a number of criteria including host and disease. Yet, the proliferation of environmental sampling, emerging direct sequencing methodologies, and a greater appreciation of the broad host range of some viruses, creates a number of classification problems. For example, how does one know if a novel candidate genome gathered from a sewer or a biopsy is actually a virus? And for that matter, how does one know that the sequence at hand is a full-length, fully functional viral genome? The relevance of these questions grows every day as databases are filled with an increasing number of novel “genomes” obtained through these methodologies.
Of course, these direct sequencing projects do have a number of advantages. There is no need to passage the prospective viruses over host cells, so there is no laboratory adaptation to a particular cell line. Such open ended approaches also recover multiple isolates from a single sample, allowing one to track naturally occurring genetic diversity, and it is likely that the proliferation of new techniques, combined with good old fashion bench work, will fundamentally change our view of viral evolution and adaptation.
Take care and keep up the good work,
Rodney
Elliot writes:
The International Committee on the Taxonomy of Viruses (ICTV) web site at www.ICTVonline.org provides access to a database of the current taxonomic classification of viruses as well as the definitions and guidelines used by the ICTV to make the classification. The taxonomic ranks used to classify viruses are the Order, Family, Subfamily, Genus, and Species. (There are 5 orders currently recognized: the Caudovirales, Herpesvirales, Mononegavirales, Nidovirales, and Picornavirales.) All viruses are classified into species (including plant viruses), and investigators who study every recognized virus family are represented on the study groups that participate in the classification process (including plant virologists).
A viral species as defined by the ICTV is:
“… a polythetic class of viruses that constitute a replicating lineage and occupy a particular ecological niche”. A “polythetic class” is one whose members have several properties in common, although they do not necessarily all share a single common defining property. In other words, the members of a virus species are defined collectively by a consensus group of properties. Virus species thus differ from the higher viral taxa, which are “universal” classes and as such are defined by properties that are necessary for membership.”
Note that Poliovirus is no longer a species! It has been renamed Human enterovirus C.
As for how “different” a virus isolate needs to be to create a new species, this varies according to the virus family and varies especially according to the genome composition (DNA viruses vary much less than RNA viruses). Each ICTV Study Group provides species demarcation criteria specific for each virus family that define the criteria for establishment of a new species for that family.
Thanks for providing the opportunity for clarification. Love the program!
TWiV 47
Jesper writes:
Dear fellows of Twiv,
It is my understanding that us humans live in peace and symbiosis with some bacteria. Is there any such arrangement with any virus?
Another way to phrase the question; if all viruses were to be removed from the world, would we be better off?
A follow-up question, even more abstracted from the lab bench; if all viruses were gone, is it reasonable to believe that new ones would come into existence? How fast? From where? In one of the twiv episodes someone said “Any suffciently complex system has parasites”, so I assume given time something is bound to fill the niche of viruses.
All the best,
Jesper
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I am a neuroscientist but have a side interest in germs. I really enjoy your podcasts. Rodney has a lot of opinions that I have been subjected to over the years. I think he would make an interesting guest.
I just finished listening to episode 51 and have a follow up for you on Virogenetics. They were taken over by Sanofi. The technology on which the vaccine was developed goes back to 1995 for the ALVAC-HIV patent. There are 3 people on this patent. Paoletti, who Rich mentioned, Jim Tartaglia who now works for Sanofi and Bill Cox. Bill was the immunologist and he quit science to fly packages between Albany and Newark.
My understanding, through Bill, is that since the vaccine was designed to work against 2 strains the lack of higher efficacy may be due to other strains. This is quite possible in a place that is known to be a destination for sex tourists. It will be interesting to know which strains the infected people in the vaccinated group were infected with. They must have collected these data and it is not that difficult serotype or genotype, is it? Is the problem that the patients are infected with multiple strains? I feel like the scientists involved in this trial are holding something back. Perhaps they are waiting for a big meeting to have a press release but that is more of a big pharma maneuver.
TWIV 47
Still catching up! Not rushing through. Savoring each episode. Sorry if this has already been addressed.
Dick, congrats on your op ed on vertical farming. Keep in mind that the most overall efficient system would be a permaculture (simplified eco-) system so there would really need to be lots of wee beasties running around to balance the resource cycling.
As for the magic no-virus switch:
1) Human illness would almost certainly increase almost immediately upon throwing the switch. I can't imagine that bacteriophages are not an essential component of human health. It will be interesting, however, to find out if the human immune system coordinates with some bacteriophages.
2) Viruses would come back fairly quickly (at least some of them) unless the switch also eliminates retroviruses hidden away in various genomes around the world.
3) I believe that viruses would probably re-evolve eventually as I believe that they are related to microbial gene transfer systems. I suspect that the reason that we haven't seen novel viruses evolve lately may be related to A) there are a limited number of core viral types (the equivalent to the theoretical minimal genome for microbial life) and B) the niches that they could fill are already occupied. Hence, a novel virus might resemble a pre-existing virus sufficiently to confuse its origin and there is little pressure for one to evolve from current gene transfer systems.
Keep up the good work.
Hello. I listen regularily to your Podcast, and I've come across a video about FluMist and a conspiracy theory in general. Would you mind watching and commenting it from a scientific point of view (leaving all that conspiracy stuff out).
http://www.youtube.com/watch?v=oOi5o61toRs
Kind regards,
Daniel
Hello. I listen regularily to your Podcast, and I've come across a video about FluMist and a conspiracy theory in general. Would you mind watching and commenting it from a scientific point of view (leaving all that conspiracy stuff out).
http://www.youtube.com/watch?v=oOi5o61toRs
Kind regards,
Daniel
I was just listening to your podcast on plaque and you mentioned how much fun it would be to make time lapse movies.
You can make your own movies.
I too wanted to make time-lapse movies and ran across an electronic shutter control that works on regular digital cameras. Reading from their list, their product is compatible with canon, nikon, pentax, samsung, olympus, panasonic, sigma, leica, minolta, sony, fujifilm and kodak.
With one of these timer/shutter controls all you need to do is scrounge an adapter for your camera lens to fit on the microscope and you're in business. What's really great about it is that it's extremely easy. Even a virologist can do it.
After you've taken several thousand photos (in JPG format) over a period of several days (you program the interval between shots) you use a shareware program (JPGAvi) to convert them into an AVI format movie. The website for the timer is http://studiohut.com/category/28188972201/1/Tim... and the website for the JPG to AVI converter software I use is http://www.ndrw.co.uk/free/jpgvideo/index.html
For about $60 (including shipping) you can make your very own time-lapse movies. If you have any problems you must know some 12 year old kid who can help you get up and running. Maybe Dick can do it.
If you have a decent camera and can take acceptable quality pictures with it you'll be able to produce a professional quality time-lapse movie on your very first try. I'll say it again – it's easy.
I enjoy your show.
Regards,
BW
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