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Letters

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!

 

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