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TWiV 146 Letters

Jonathan writes:

First and foremost, this and the podcast of the virology course lectures available on iTunes is a gift to the public. I am applying to medical school and I appreciate the material on a topic I did not have time to take but have had a long standing interest. So- thank you! To the question: after listening to the first lecture I found a PLoS ONE article that states that a research team has drafted a double-stranded RNA (dsRNA) that, to the best of my understanding, binds to a viral RNA particle prior to being incorporated into the host's genetic material, and then exploits a apoptosis pathway in that infected cells, quenching the propagation of future virons in that instance. The article is entitled "Broad-Spectrum Antiviral Therapeutics" by Rider, et al. PLoS ONE 6(7): e22572. doi:10.1371/ Are there any comments about "survival of the fittest" with respect to virus in light of this?

Thank you,

Jonathan

University of South Florida

Dave writes:

Dear TWiVers,

It was great to have seen the live podcast at ASV! I am looking forward to seeing another one next year in Madison…

I was curious to hear what kind of reactions you had to the July 27 PLoS One paper (Rider TH, Zook CE, Boettcher TL, Wick ST, Pancoast JS, et al. (2011) Broad-Spectrum Antiviral Therapeutics. PLoS ONE 6(7): e22572. doi:10.1371/journal.pone.0022572). The news headlines that I saw were akin to "drug that could cure any viral infection." While trying (specifically) to target cells possessing viral double stranded RNAs seems like a reasonable approach, do you think this DRACO approach actually has the potential to be a broad-spectrum antiviral (ignoring, for now, any possible issues with drug delivery…)?

Thanks in advance for any thoughts…

Keep up the great work…

Cheers,

Dave

P.S. I wanted to share that this Spring, I had my undergraduate virology students use TWiV to learn about potential pieces of literature that they could then download and read as the basis for their in-class oral presentations. Overall, the students liked hearing a little context about the paper from TWiV before going through it themselves in detail to prep for their talks about the experiments/data. An added bonus of the exercise was that a number of them now are regular TWiV listeners!

David B. Kushner, Ph.D.

Associate Professor of Biology

Dickinson College

Carlisle, PA 17013

Jason writes:

Thanks for your show.

I'd love to hear a discussion about this remarkable paper in PLoS ONE:

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0022572

Broad-Spectrum Antiviral Therapeutics

Thanks,

Jason

Executive Director, PersonalGenomes.org

http://bit.ly/jasonbobe

Michael writes:

Here's the paper,

http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3144912/

In the media:

Time article - http://healthland.time.com/2011/08/11/mit-scientists-develop-a-drug-to-fight-any-viral-infection/ - "Scientists at MIT are developing a new drug that may fight viruses as effectively as antibiotics like penicillin dispatch bacteria."

Times of India article - http://timesofindia.indiatimes.com/life-style/health-fitness/health/Soon-a-revolutionary-pill-to-cure-HIV-flu/articleshow/9563867.cms - "Scientists are developing a new drug, which is showing great potential to revolutionize the world of medicine with its ability to cure everything from colds to HIV."

Alfred writes:

I was hoping the TWIV crew could weigh in on this PLoS paper describing a broad spectrum antiviral:

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0022572

Thank you.

Al

Alex writes:

Good afternoon Dr. Racaniello and fellow TWIV'ers;

Thanks for a great podcast series. I'm an electrical engineer will little background in the biological sciences. I really enjoy listening and learning. You provide a new world that I had no familiarity with, before.

I came across an interesting article about a possible broad spectrum anti-viral. You probably have received other emails about this.

Can you comment about this in a future podcast?

http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0022572

Thanks and keep up the great podcasts.

Best regards,

Alex

Reynard writes:

I'm sure you are getting requests for this already so I'll keep it short. I would love to hear a twiv panel comment on the recent success of DRACO. These are exciting times!

Thank you for your continued efforts,

Reynard

Shelby writes:

I'd love to hear your thoughts about chicken pox and if it is really beneficial in the long run to get the vaccine.

Shelby

Camby, IN

Juanjo writes:

Dear Professor Racaniello,

as a plant virologist working in a research institute in Spain, I have been waiting for a good occasion to communicate with you and the rest of co-host of TWiV. I started last February to listen to the shows during my daily commute trips (20 minutes train plus 15 walk thru the campus of the Autonomous University of Barcelona). I got hooked ("memetically" infected?) almost instantly, and since then I wait anxiously for every new chapter while hearing backwards in your archive. At a pace of 4-5 chapters a week, I am afraid I'll be soon running short of new materials. Please receive my deepest gratitude for this truly entertaining and educational initiative.

The motivation for this letter comes after your nice conversation with Professor Raul Andino (TWiV 138). Dr Andino was extremely didactic when explaining his recent work on RNAi suppression in insect viruses. He was also able to provide a comprehensive revision of the current knowledge on RNAi mechanisms, and how viruses deal with this. When commenting on the mode of action of plant virus suppressors of RNA silencing, he was right to say that most plant viruses have adopted a small-RNA sequestering strategy (Lakatos et al., 2006, EMBO J 25, 2768-80). Interestingly, a few exceptions are also known, and some plant viruses target the RISC complex as the Cricket paralysis virus does. In addition to polerovirus P0 and cucumovirus 2b proteins, shortly after the Nayak et al paper appeared and demonstrated the activity of CrPV-1A on Drosophila Argonaute 2 (Nayak et al. 2010, Nature Structural & Molecular Biology 17, 547-554), two independent studies with Turnip crinckle virus (Azevedo et al., 2010, Genes Dev 24, 904-15) and Sweet potato mild mottle virus (Giner et al., 2010, PLoS Pathogens 6, e1000996) showed an additional mode of action, based on antagonyzing host Argonaute. These two unrelated plant viruses have got RNAi suppression activity by mimicking cellular Argonaute-interacting proteins which contains WG/GW (Tryptophane-Glycine or Glycine-Tryptophane) conserved motifs. Indeed this new strategy adds up an example of the broad variety of modes of action of viral RNAi suppressors.

The final comments of Professor Andino and yourself about the importance, usefulness and basic interest of keeping up the good work with model organisms like Drosophila, Caenorhabditis (and I should add Arabidopsis in the case of plants) were also quite opportune.

Thanks again for TWiV.

Your faithful listener,

Juanjo Lopez-Moya

Centre for Research in Agricultural Genomics (CRAG) CSIC-IRTA-UAB

Campus UAB Bellaterra (Cerdanyola del Valles) 08193-Barcelona (Spain)

Valorie writes:

Virology fascinates me but alot of it goes right over my head. Can you recommend a basics or beginners book for people outside the medical field so I can start from the ground up? (Something that dumbs the complex ideas down for me like a "..for dummies" or "A Complete Idiots Guide To..." book would be ideal!)

Thanks alot!!

John writes:

Dear TWIVers:

I have a couple of questions related to TWIV138, where you discussed short-term adaptive immunity in insects based on RNA interference. As I understood it, double-stranded RNA injected into insects causes a kind of systemic immunity, based on getting cells all over the insect to produce siRNA that will mark the viral RNA for destruction inside the cell. (Is this more-or-less right?) If I understood right, your guest said that the immunity to the viruses from the siRNA lasted for a week or two, which I guess is a substantial part of a fly's lifespan.

The first question this raises in my mind: is it a common consequence of viral infections to have viral genetic material (DNA or RNA, depending) end up floating around outside cells? It seems like this would happen when cells burst open with newly-made virus particles, and could also happen just from random luck, with viral RNA or DNA slipping out of the cell when something else exits. And any kind of immune response that kills infected cells could also leave some leaking DNA or RNA. This seems like it would be true both in insects and in mammals. I also wonder whether, under normal circumstances, there's a lot of host DNA or RNA floating around between cells.

This made me wonder how the insect cells could distinguish self genetic material from nonself genetic material. The mechanism your guest described, if I got it straight, involved ds-RNA. Healthy animal cells shouldn't be producing ds-RNA, so maybe the answer is that insects only respond to ds-RNA. But this made me wonder if he or other researchers have tried single-stranded RNA viruses or any kind of DNA viruses, to see if similar immune mechanisms there. If they do, then I guess there must be some kind of mechanism to keep from having all the insect's cells make siRNA against some protein they need to survive.

Finally, I was curious how this ties into DNA vaccines in mammals. The fact that DNA vaccines work at all suggests that having viral genetic material floating around must be a useful signal that there's a viral infection that needs to be fought off. But I don't really feel like I understand the mechanisms there--it seems like some antigen presenting cell must be taking up random DNAs it finds by the side of the road and expressing its genes. (Is that right?) Would the same sort of thing work with viral RNA? I'd love a show where you talked about DNA vaccines.

Anyway, thanks again for your wonderful podcasts, which have really opened up a new world for me, and thanks for answering my amateur questions.

--John

Cliff writes:

Hey guys!

My name is Cliff and I am new to the whole podcast scene. I started out with a Nursing podcast, and found my way to yours via i-tunes. Now, I would like to begin by saying I am not a scientist, (like most everyone else that emails you), but I am enjoying learning about viruses. The first time I listened to you all, I actually laughed at my first scientific joke, and then I knew I could make it in the healthcare field. You are educators, and you have become good friends of mine while I work to maintain a woman's building in Ann Arbor. As you thanked Al in TWIV 132 for spending the afternoon with you, I would like to thank you for spending days with me this summer. You guys are like friends of an athlete that never leave his side until he loses his flair, except for me it's more like you won't leave my side until my mp3 player dies. I feel like I can be chatty with you. I can even be sarcastic with you.

Athlete talk is bringing me to my point. I wanted to email ya'll after listening to episode 133 where, I think it was Rich, asked Kathy if she spoke with Majic Johnson recently since he played ball where she works now (UofM) with HIV. Now, over at MSU where I participate in the Decathlon and am working on getting into the Nursing program, I noticed a big statue of Majic outside the Breslin. I guess MSU loves him even though he went to UofM. (There's the sarcasm). But not a big deal, I am starting to like all you guys even with the mistake.

Also thought I would share a virus reference I like with you. In the first Matrix movie, Mr. Smith speaks of how, "Humans aren't actually mammals. But there is another organism on the planet that are like Humans. VIRUSES. You multiply nonstop, use up the resources in an area, and then move to another. You are a virus of this planet" (Matrix, 1998-ish). I'm not a pessimist, I just thought you would enjoy that bit if you haven't seen it.

Now to make this worth your while I will ask a question... This may not be a good one, but I will ask anyhow. Since sickle cell anemia is a malformation of a blood cell, ( I learned from ya'll that it was in response to malaria and becoming resistant to it), I would guess there may be different receptors on it as well. Now for some people, sickle cell can be a big problem for them even if half of their blood cells are normal, so I am wondering if it would be possible to create a cure using a virus that would specifically attack sickle cells in the blood stream. But then again, Sickle cells would probably continue to be produced be the host since I am guessing it's in their DNA to produce them. I could probably google it to find the answer, but I would rather hear your thoughts on it. After all... you are my friends while at work.

I will come back again with some better questions as I start my Nursing courses and they arise. Until then,

Cheers,

Cliff

 

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