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TWiV 190 Letters

Cara writes:

Hello Vincent and Team TWIV,

I love Virology, and it is with much chagrin that I admit I have only recently started listening to TWIV. However I have tried to mend the error of my ways by: 1) proselytizing the benefits (keeping up-to-date with and learning new virology) and fun (the weather and witty banter) of listening to TWIV; and 2) now also sucking up to Team TWIV (check).

I enjoyed listening to the recent webcast with the five postdocs in Glasgow. At the end, you had mentioned that you would be interested in chatting with some postdocs at ASV in Madison. I will be attending ASV and would be excited to chat with you.

My adventures with viruses first started with serosurveillance of rotavirus strains circulating in sub-Saharan Africa. After moving to the US, I completed my Ph.D. degree with Dr. Rebecca Dutch at the University of Kentucky studying the unusual proteolytic processing of the Henipavirus fusion proteins. I am presently a postdoc with Dr. Peter Sarnow at Stanford, where my research has focused on the rather interesting interaction of Hepatitis C virus with miR-122 and cellular RNA granules. I am also thrilled to mention that, as of September I will be an Assistant Professor at the RNA Institute at SUNY Albany.

I look forward to the opportunity to meet you at ASV.

Regards from a Postdoc and Assistant Professor in Waiting,


Jim writes:

This is a 2-column version all on one page for easier scanning, though the print is smaller.I'm Dutch and start slow, but just keep slogging away.


Smithfield, VA

Sizun writes:

Howdy again Twiv-ters (Twitters, get it?),

Its me again, emailing from Singapore, where the weather is really hot and sunny at 32C.

It is great that the 8 month long H5N1 saga is drawing to a close, with the publication of the Fouchier paper in Science. Indeed, Science can only progress with publications, and I am always a big fan of open access (why should research that is done using public money be restricted from public access?). It is great that the Fouchier paper, along with the many commentaries, are freely available in the online Science magazine website.

I would like to draw your attention to one of the interesting accompanying analysis by Martin Enserink titled “Public at Last, H5N1 Study Offers Insight Into Virus's Possible Path to Pandemic” ( In paragraph 10, Martin clarifies a statement from Ron that called the ferret passage approach “really stupid”. Turns out, the Dutch word of “simple” (which I believe is simpel) is also used for “stupid”. I have only managed to verify this via the mighty google translate, but it would be great to have a native Dutch speaker verify this. However, it is interesting how this one statement was misinterpreted to show that Ron regretted doing the experiment, which I highly doubt he does, after watching the TWIV episode in Dublin. What he is doing is a time-tested way of adapting a pathogen to a new host, and is great basic science.

I would like to thank you and the gang for your great coverage, and clarification of the whole event, right from the start (when I was applying to grad school) till the end (where I will be embarking on grad school). It has been great to hear your analysis and opinions as the events unfold, and the breakdown of the Kawaoka paper when that came out. Now that all these great information is readily available on the internet on your website and in TWIV, I think it will serve as a great textbook example on the fears of new knowledge, and how a lack of information and knowledge on a subject can cause a great amount of unwarranted fear.

I would also like to suggest an interesting paper, also hot out of the oven, in PLoS Computational Biology, titled “Standing Genetic Variation and the Evolution of Drug Resistance in HIV” ( It is an interesting model that a population geneticist builds, using publically available clinical information on anti-HIV drugs, to suggest that pre-existing mutations in the HIV population may be the root cause of HAART treatment failures. Of course, there any many assumptions that have to be made to keep a model simple (the great old KISS theory), but the main one that was undertaken was that a single mutation was enough to confer resistance. How well would you think this assumption (and subsequently, the whole model) hold up in real life? As we have seen in the H5N1 papers, we need multiple mutations even in the relatively small sialic acid binding site to confer a change in specificity. Also, these single mutations would probably have to be close to or within the active site or drug target site of the target enzyme (say the protease, or RT) to be effectively conveyed resistance via a single amino acid change. Im not sure if the author accounted for this fact (that a single mutation in a specific region of the HIV genome, and not just a random part of the genome, accounts for resistance). If not, would the model still be as effective?

Sorry to bore you with this long email. You can wake Dickson up now (just kidding, I love your TED talk by the way). Once again, thank you all for everything that you have done so far in educating the world about viruses, and keep up the great work! I will continue looking forward to your next episode of TWIV!



Naureen writes:


My name is Naureen. I am an undergraduate first-year student at Columbia University. I am amazed by the TWiV site. I wanted to ask if there any internship opportunities or volunteer positions available for someone like me.

Thank you very much!

Mark writes:

Dear Dr. Racaniello and co.,

You say in TWiV #175, which spoke about microneedle injections of flu vaccine in mice, that there were no dendritic cells with flu found in the mice lymph nodes used, which begs the question of what happens to the dendritic cells that have been shown to leave from the skin tissue. Since the experiment to see whether these dendritic cells left the skin was performed in vitro, would there be any issue with getting these cells to lymph nodes in vivo from skin tissue? Also, where did they get the lymph nodes that were tested for flu-bound DCs? I would believe that lymph nodes closer to the injection site would be more likely to have the relevant cells, but then again the location shouldn’t make a large difference. Ultimately, I guess what this question comes down to is this: they didn’t find flu dendritic cells in the lymph nodes of these mice, so how do you explain their immunity? Is it likely an experimental aberration or a new mechanism that has gone undiscovered until now?Thanks,


From a student in my virology class:

Dear Twiv experts:

On a recent episode (174) you had discussed a question raised by a listener about the validity of informative flyers that are distributed to all blood donors. I was happy to see that Twiv was recently featured on the main iTunes page, and consequently garnered many more followers. However, despite the fact that Twiv is free, I was wondering what you would consider to be the most effective way to communicate basic facts about virology to those who might not have access to wireless, or those who might not regularly attempt to further educate themselves (think globally). Are flyers the best bet, or are you forever confident in the powers of the internet? I know that there are several international initiatives to increase awareness about HIV and other major public health issues, but do you foresee a future where education about viruses will be one of these top-tier concerns as well? I?d be interested in hearing your thoughts!


A recent twiv addict

Lance writes:

Hi Vincent,

I'm a bit behind I'm afraid but I've just been listening to TWiV 180 - and you were asking about the sylvatic cycle of dengue.

My understanding of this is in line with what Alan said - yes there is a sylvatic cycle of dengue, and there's probably a little bit of cross-talk going on in both directions but the overwhelming majority of dengue infection of humans occurs by transmission from other humans not from the Sylvatic cycle, so in current public health terms the sylvatic cycle isn't that important. It's importance is more in the potential for emergence of a future serotype of dengue in humans. I have attached a good review on the subject.

I also had a comment on TWiV 172, in which I thought you did a great job explaining a complex paper. You were talking about the potential for experiments in mice without any CD8+ T cells, if I remember correctly. The problem here is that if mice were KO for CD8+ T cells then they could then be sensitive to measles encephalitis. There are models where you can make mice that have transgenic T cell receptors so that all the T cells in the mouse are specific for one virus, or one antigen/epitope. I'm pretty sure these don't exist for measles (as this doesn't infect mice normally as you point out) but it might be possible to make them - in other words you have a mouse that has measles-specific CD8+ T cells, but as far as LCMV is concerned it has no CD8+ T cells (because they are all specific for measles). Then you would have measles-specific CD8 T cell immunity but no T cells as far as LCMV is concerned. If that abolished disease you could be fairly sure that LCMV-specific T cells were required for disease to develop. I don't know if there's a way to selectively paralyse the T cell response to only one virus.

By the way you met my boss, Tom Solomon, in Dublin recently and I hear he's going to do a TWiV with you later in the summer - that's great news!

Keep it up,


Alex writes:

Dear Vincent!

3 years ago I was writing my master's thesis on Rhinovirus, so I was a great fan of your show. Now I'm back, infected with HIV (so to say) and you're still here with your shows and lectures. Amazing! Many thanks!


Claire writes:

Dear Virology Experts,

My name is Claire, and I am a 3rd year PhD student at Colorado State University. I study a retrovirus called Walleye Dermal Sarcoma Virus (WDSV) in Dr. Sandra Quackenbush and Dr. Joel Rovnak’s lab. I dearly love listening to your program in the lab, and look forward to days where I’m by myself so I can listen to episodes I have missed. I call these TWiV marathon days.

To get to the point, I recently listened to episode 163 “What Rous Wrought” and really thought that you gave a great introduction to the beginning of viral oncology. However, there was one statement that didn’t rub me the right way. One of you mentioned that viral induced tumors are an accident of the viral infection, occurring out of chance due to the virus messing with the cellular machinery. You guys make this statement a fair amount on TWiV (episodes 162 and 174), and this statement is correct for many of the oncogenic viruses out there. However, this is not a completely true statement, and WDSV is one example of an exception.

WDSV causes seasonal dependent tumors in walleye fish. The seasonality of the tumors correlates with the reproductive cycle of the fish, and tumor formation and regression is required for spread of the virus from fish to fish. Let me explain, a naive fish is infected with the virus during spawning when virus is found at high concentrations in the water. The newly infected fish is disease free though the summer, however in the fall tumors (dermal sarcomas) form on the surface of the fish. These tumors grow and proliferate through the winter. During the time of tumor development and proliferation, there is no viral particle production and only two viral proteins are produced (RV-cyclin and the orf b protein). These protein are coded by open reading frames (orf’s), orf a and orf b, that are in addition to the gag,pol and env genes. Things start to get really interesting in the spring, when the expression profile of the virus changes and new viral particles are produced. At this time, the tumors start to regress and eventually fall off the fish. The shedding of the tumors releases the new viral particles into the water, and this is timed to occur at spawning. This is the only time of the year when massive amounts of walleye congregate together, allowing for efficient spread of the virus. At other times of the year, walleye are spread out around the lake in small schools. The life cycle of WDSV is clearly dependent on tumor formation and regression. Without the tumor, as well as the correct timing of tumor development and regression, WDSV would not be transmitted as effectively, if at all. After the whole ordeal, the fish that had the tumors the previous season will be fine for the rest of its life, and will never develop tumors again.

I’m sorry for the lengthy email, but it might be a good idea to get away from the “tumors are an accident” statement. Keep up with the wonderful work, and I hope that you are going to be doing a lunch episode at the ASV meeting in Madison this summer.



Stephen writes:

Hello twivuminati,

Listening to you guys talk about money spent on science reminded my of this image. I don't know how accurate it is but it's an interesting way of displaying the information.

Love the podcast and listen every week. I hope it continues for a long time. Thank you for taking the time to do it.

Kristoffer writes:

Hello twimerrinos!

Thank you all for a great family of podcasts that lasts! Here is a link, which I think, can help persons understand papers of the scientific kind, and to feed the knowledge gland!

Here just below the arctic circle, we still have snow, which blow(s). The thermometer says 33f, time to turn up the heater!

Enough with the rhymes, I'm almost committing lingvistical crimes, here's the link, oh! I need a hot drink!

Best regards

Neva writes:

Hi TWIV fellas,

Harnessing our virus friends:

"Imagine charging your phone as you walk, thanks to a paper-thin generator embedded in the sole of your shoe. This futuristic scenario is now a little closer to reality. Scientists from the U.S. Department of Energy’s Lawrence Berkeley National Laboratory (Berkeley Lab) have developed a way to generate power using harmless viruses that convert mechanical energy into electricity....."

Reminds me of the Star Trek conundrum of whether the proliferating nano creatures constituted a life form.

Fun with science,



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