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I wanted to wish you a happy holidays. I also was hoping to submit another science pick of the week for your show.
Lets just say that I'm still looking for my jaw under my desk as I type this. This is perhaps the coolest science article that I have read this entire year.
Hi TWIV, TWIM, AND TWIP Persons of Note!
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Short (<15 min) talks that highlight the human side of research. iBioMagazine goes “behind-the-scenes” of scientific discoveries, provides advice for young scientists, and explores how research is practiced in the life sciences. New topics will be covered in each quarterly issue. Subscribe to be notified when a new iBioMagazine is released.
right up your alley - you'll enjoy these - and they are short enough to use in the classroom or a meeting!
(High school teacher and FOT (follower of TWIvmp)
I have read/heard before that HIV can sequester itself in various cells in the human body and hide there in an inactive state for years. The information I have seen and heard seems to suggest that the virus is activated by anything that stimulates the immune response (and hence causes an otherwise inactive cell to become active). What I am wondering is this - has anyone ever attempted to intentionally draw out the inactive virus by stimulating the immune system and then bombarded the active replicating virus with anti-viral therapy?
Kathy Collins replies:
The so-called "flushing out" strategy your listener is referring to is a popular idea amongst HIV researchers. It makes a lot of sense based on our understanding of HIV latency. The idea is to activate HIV gene transcription, and induce the production of HIV proteins that are toxic (either directly or via the immune response). Meanwhile, antiretrovirals are maintained to prevent any newly made viral particles from spreading to uninfected cells. (The antiretrovirals themselves do not harm the infected cells, they just inactivate the virus and prevent spread.)
Limited attempts have been made to accomplish this goal using cytokines that activate T cells or histone deacetylase inhibitors that stimulate transcription. To my knowledge, these attempts have not been encouraging so far. However, there is a lot of ongoing work in this area and there is a lot of hope that this strategy will work if we can maximze the efficiency of the approach and minimize the toxicity.
So, your listener is right that this is a good idea and hopefully one day it will work to help eradicate HIV and cure disease.
Hello TWiV crew,
First off, I want to thank you for the podcasts, TWiV, TWiP, and TWiM. They make the commute and the gym almost pleasant!
It is, however, humbling and a little painful to listen to at times, because I'm a 3rd year graduate student in immunology (I study the immune response to Toxoplasma gondii reactivation in the brain) and yet half the things you say go way over my head, with the laypeople who write in making more insightful comments than this will be. I often wonder how I made it into grad school in the first place! So forgive me if the following is a silly question.
So, we incubate all cells at 37 C. All of them. From fibroblasts to microglia. But winter has made it fairly clear that at least my fibroblasts are not all at 37 C, and microglia probably aren't, and many other cells probably aren't. Besides, I'd heard that the 98.6 F temperature was obtained using a faulty thermometer. I know that temperature can alter protein expression, and fevers are at least speculated to inhibit viral replication (is that right?). So has anyone looked at whether small temperature deviations (for example growing microglia or neurons at 37 C vs whatever their normal temperature is) has any effect on cell function, or on say viral replication? Are there parts of our bodies more susceptible to viral infections because of a temperature difference?
A quick Google Scholar search turned up nothing for me, so maybe it's not a valid question, but I'd like to hear it from folks wiser than I.
In TWiV #144, you and Dick bantered, saying that the NCIS actors sounded like they didn't understand what they were saying when using technical terms. You will be delighted to learn then that Pauley Perrette, the actress who plays the forensic scientist Abby, was an undergrad honor student in sociology, psychology and criminal science and had started her masters in Criminal Science at Georgia State. At some point she decided she wanted to act instead, so she left the program, went to New York, did the requisite starving actress bartending for a while, and finally won the role of Abby which was ironically doing the very things she was studying.
A good rule of thumb in our house: Never doubt Abby! :-)
Greetings from Virginia. I enjoy twiv very much. It was great to see a Miller spread in episode 162, but I am sorry to say that the electron micrograph is not of bacterial transcription. Those are eukaryotic 35S rRNA genes. I am not sure of the source organism. I have worked predominantly with bacteria and yeast. I will ask Ann and Yvonne who are the experts in spreads from higher eukaryotes. Old papers from Ann's and Oscar's labs have pictures of adeno and SV40 transcription if you are interested.
I look forward to each new twiv episode and enjoy revisiting older ones. Thank you for the entertainment and enlightenment.
P.S. My non-scientist husband wants you to know that he also really enjoys twiv.
The full text of this retraction hasn't been published, but from the excerpts posted on retraction watch, it looks like they probably only retracted their conclusion, not the rest of the paper.
Prof. Racaniello, you were quoted in retraction watch as saying "With the retraction of the Lombardi et al and Lo-Alter papers, this brings to an end any hope that there might be a retrovirus associated with CFS." You were also quoted in the Washington Post as saying “There’s no evidence at the moment that any virus is associated with chronic fatigue syndrome.”
I hope these were misquotes or taken out of context since you do say it is theoretically possible that ME has a retroviral cause, but it seems to me that they probably were not. Putting aside the evidence for retroviral association with ME, I thought you were aware that it is completely accepted by science that ME is strongly associated with a number of opportunistic viruses such as all or almost all herpes viruses, mycoplasma fermentans, echovirus, enteroviruses, parvovirus and virally-associated blood and lymph cancers.