Ajinkya writes:
Dear Vincent,
I hope this email finds you well. I have been an avid listener of TWIV and enjoy your podcasts very much. I am also a recent graduate of Northwestern University, Chicago (graduated with a Master’s degree in Biotechnology), currently studying working as a Research Tech at the Gottwein Lab at Northwestern University’s Feinberg School of Medicine. I study KSHV and EBV Herpesviruses. Although I was excited to hear that about your contest to give away free copies of Principles of Virology, I was also sad about the fact that you wanted more Twitter followers in return. Well, I am not on Twitter (trying to curb my social media addiction) and so will not be able to follow you. But, I can tell you that the reason I listen to TWIV is to know more about the seemingly infinite types of viruses that I do not get time to read about, but more important than that, I listen so as to learn how to critically analyze and interpret data mentioned in a paper like you and Rich and Kathy and Dickson do.
I appreciate the time and effort all the TWIV hosts put into making episodes and I feel like I must tell you not to be disheartened about the lukewarm response you received for the contest. I am certain about the fact that there are many like me who are not on Twitter but appreciate your work nonetheless. That being said, I’d be delighted to get a copy of Principles of Virology and assure you that I would put it to good use ! (No Pressure !)
Thank you for your efforts and keep up the good work.
Sincerely,
Ajinkya
PS: It’s a cool 8 degrees Celsius here in Chicago with yet another Chicagoan winter on the horizon.
Steen writes:
Cpf1, priority, patents, credit, press releases
Candidate listener pick/snippet: a piece by Sarah Zhang in Wired. http://www.wired.com/2015/10/battle-genome-editing-gets-science-wrong/
New paper and review (behind paywalls):
Cell, Zetsche…Zhang – http://doi.org/10.1016/j.cell.2015.09.038
Nature, Makarova…Koonin – http://doi.org/10.1038/nrmicro3569
Anthony writes:
Dear Twiv panelists,
Where did this virus originate from?
http://news.sciencemag.org/biology/2015/09/new-human-virus-discovered-old-blood-samples
http://mbio.asm.org/content/6/5/e01466-15
Thanks so much,
Tony
Steve writes:
Here’s a fascinating article on origins of HAV that just appeared in PNAS Early Edition that you might consider for a future episode of TWiV.
http://www.pnas.org/content/early/2015/10/27/1516992112.abstract
Steve Bachenheimer
Dept. of Microbiology and Immunology
UNC Chapel Hill
Anthony writes:
Virus weather report
The APHIS document above discusses at some length wind as a possible factor in virus dispersal.
Asal writes:
Dear TWiV team,
I am a Molecular microbiology lab technologist and an avid TWiV listener.
When in 2010 I first discovered TWiV, I was so excited for being able to learn more virology by listening and not just by reading. Ever since, I have enjoyed learning both updated and basic virology through your highly informative podcasts. I started listening to TWiV while staining shell vial cultures in our BSL-3 lab at med fusion in Texas and now I have been mostly listening while driving in slow traffic. I would recommend listening to TWiV to everyone who is not only interested in viruses but also is interested to see how scientists share and exchange their opinions, ideas and knowledge with respect, and humor.
On TWiV episode Cat in the HAART, there were questions raised about screening male patients for Pap testing and HPV. It has been almost two years that we, at our Molecular ID lab, perform FDA-approved HPV DNA testing by Hamilton Roche cobas 4800 system on anal and pharyngeal Pap vial collections from the male population. The reverse HPV-Pap algorithm has also been recently approved by using the same platform. Here is the link:
http://www.roche.com/media/store/releases/med-cor-2014-04-25.htm
The assay tests for HPV16, HPV18, and other-high-risk HPVs (including 11 subtypes). We sometimes obtain triple positives on anal/rectal collections. Samples may be preserved and transported in both ThinPrep and SurePath vials.
I also had a question regarding the OPV And IPV used for eradication. I am wondering if any country has ever used them in combination in a way that IPV has been followed by OPV to reduce the risk of vaccine-related paralysis associated with OPV.
When I was in junior high school in Iran, the eradication program took place in my hometown, Tehran. In my vague memory I recall my parents took my youngest sister twice to the vaccination stations within a year or two, and I remember my father saying they gave the oral one this time, referring to the second round. At the time I did not know enough of the fascinating world of viruses, so I didn’t pay attention to the details of how it was carried out then. My parents do not recall it either.
In 2001, during my second year of undergraduate studies in microbiology, I took my virology course taught by Dr. Talat Mokhtari-Azad who had conducted the polio eradication plan in Iran. After reading Vincent’s interesting and concise article about OPV, IPV, and the history behind them, it became a question for me whether the eradication in my hometown was really ever conducted in a combination format. I have tried to get in contact with my former virology professor but have not received a reply from her yet.
Do you know of any eradication plan in any region that was administered using both OPV and IPV?
At the end, thank you for your wonderful show. Virologists are admirable scientists and the ones who spread the knowledge on viruses and microbes to the world will be remembered in the history, the history of social media and virology!
Keep up with the great show!
P.S.: Today, October 6th, is partly cloudy, 18° C here in Colleyville, Texas.
Kind regards,
Asal
Elinor writes:
Hello all,
I hope this can be considered a follow-up even though I’m a week late.
In your discussion on mucosal immunology you wondered why inactivated flu vaccines, given systemically, are protective since flu infections occur at a mucosal site. I think it’s in large part due to this:
Normally you think of IgA as the mucosal antibody, but in the lungs, there is actually a lot of IgG, which is transudated from the blood across the epithelium onto the mucosal surface. This happens in normal lungs but even more so if there’s inflammation. In the upper respiratory tract, on the other hand, there is plenty of IgA and not as much IgG. I don’t know what the situation is in the gut but perhaps IgG is not transudated in the same way there.
I also wanted to say that I was glad to hear you guys discuss feline immunodeficiency virus recently, as well as about Stephanie’s coronavirus research in pigs. I’m a VMD-PhD student, and it’s great to get more exposure for work on viruses that are relevant for both animal and human health.
John writes:
Dear Twiverati,
I hate writing in critically because you are all so wonderful, but I had a couple of critiques/questions/problems regarding some points of discussion in TWiV #361. The problem is, when everything is fine, writing in would waste your time!
Anyhow, there were a few nagging things about your ebola virus transmission discussion that I couldn’t get past. If someone else has written in about any of these, feel free to skip that point. Here they are:
1) Directionality of transmission from patient S–>P or P–>S. As far as I understood the paper you were discussing, P first experienced Ebola disease symptoms 7 days after her sexual encounter with S. You said it was possible that P transmitted to S, because the incubation window would accommodate those seven days. I recall Tom Friedan and many CDC representatives repeatedly saying that it’s impossible to transmit EBV during the incubation period. Has that been overturned? If it hasn’t, it is hard to see how transmission could have flowed any other way than S–>P, or (and I think this more likely), some other person who is totally unrelated gave it to P, and S’s one positive is just the contamination that Alan suggested.
2) “If [sexual transmission of ebola virus] were likely, it would be the next HIV.” No! If HIV had an infection cycle similar to EBOV, it wouldn’t even be the current HIV. The reason HIV is so efficient and dangerous is that it persists in patients as an asymptomatic infection for a period of years, which increases the chances of sexual transmission to multiple people. It was also a totally unknown agent to medical science for decades of its initial spread, during which it got into the transfusion blood supply as well, where it spreads much more readily than by sexual activity.
In order to be “the next HIV,” EBOV would have to persist in semen for years or it would have to be so common for it to be transmitted sexually that this route would have been obvious from epidemiological data. Right? And even then, it kills so readily and quickly that I doubt it would achieve HIV-levels of prevalence. I suppose a third option would be for there to be a high number of asymptomatic carriers of EBOV, but I don’t think there’s any evidence of that, either.
3) Lassa fever. Patient S repeatedly tested negative for ebola virus while he was ill with an unspecified hemorrhagic fever, which he survived. Also common in West Africa is Lassa fever, which infects hundreds of thousands of people annually and in 20% of them causes a hemorrhagic fever, though mortality is much lower than for EBOV. Was patient S tested for Lassa virus during his illness?
4) Rich’s comment about SSPE and paramyxoviruses. This is rather close to my PhD work, so of course I took a lot of interest in that comment. Interestingly, persistence of infection has also been observed in Nipah virus infections, with reappearance of symptoms months after their apparent resolution. Persistence of paramyxoviruses is thought to rely on a few things: the ability of the surface glycoproteins to fuse adjacent cells when expressed on the cell membrane (forming “syncytia”) and mutations in the matrix protein that prevent typical virion budding. It’s my understanding that EBOV has to enter an endosome in order to fuse, and it relies on the cholesterol transporter NPC1 to facilitate fusion within endosomes. It seems fairly unlikely to me, then, that cell-cell fusion can be facilitated by EBOV, and that seems to make a mechanism like the one seen in SSPE less likely, doesn’t it? That’s not to say that there isn’t another mechanism of EBOV persistence, or that EBOV doesn’t find some way to cause cell-cell fusion. I just think that the hypothesis of a parallel to paramyxoviruses is less likely than other explanations. Of course, I might just be wrong about EBOV dependence on endosomes for fusion.
Anyway, I hope these aren’t too nitpicky or combative. It was a great episode, which is why I ended up with so much to say. To end on a positive note, Vincent’s Rocky Horror Picture Show reference (see androids fighting), made me laugh out loud.
Yours,
Dr. Leighland Feinman (aka John Skylar)
PS: Oh, yeah, I defended my PhD since my appearance on TWiV. So there’s that! What’s next? Not sure, but excited to find out.
Judi writes:
Here’s a link to Doudna’s Ted Talk on CRISPR – perhaps a listener pick
http://www.ted.com/talks/jennifer_doudna_we_can_now_edit_our_dna_but_let_s_do_it_wisely
Ramon writes:
Pick of the week
