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HIV-1's high virulence might be an accident of evolution

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Cliff:
I agree with someone above.  It's great to find out these new discoveries, but they only seem to ask more questions and never really solve anything (at least not anything relevant to the here and now).

Plus I don't get the article...aren't all viruses, (and bacteria), well I guess all life itself, accidents of evolution?

MitchMiller:
What they mean by "accident" is that the loss of the gene is contrary to the survival of the virus.  If the host dies, the virus dies.  Therefore, it seems that evolution should have favored the less lethal form of the virus... that which survives in the host without overwhelming the host.... like herpes.  The host would have lived much longer and therefore been able to spread infection for a longer period of time.  However, it seems that somehow the strain of HIV that cross over to humans had lost the gene used to strike a balance with the human immune system so as not to overwhelm it, resulting in death of the host.  It opens up the possibility that humans can live with HIV if meds can recreate this delicate balancing act between the virus and the immune system... much as has been observed in macque monkeys.
The article does seem to pay credence to docs that are currently using immuno suppressive drugs on their HIV patients. 
I like to follow the basic science articles so I have a feeling what therapeutic vaccines seem to have the most support in the literature... because someday I hope to participate in a trial and you typically only get one chance with a vaccine trial.  Past participation in one usually disqualifies you for other future trials.

HIVworker:
I think when it comes to HIV, it doesn't matter to it what it ultimately does to the host, the fact that the infection is persistent enough to last years without immediate pathological consequence allows it to be transmitted prior to AIDS. This separates it from other pathogenic viruses like EBOLA that have clear acute infection when they make the jump into humans with immediate fatal consequences to the host. This allows HIV to spread quicker through the population. I also don't like the term 'accident' as it implies some process of logical thought - which the virus has none. It exists because it is and it is widespread because of the non-lethal effect of initial infection.

While it is an interesting idea to immediately suppress the immune system to lower the height of the flames, in chronically infected people it is not the answer in my opinion. However, the idea that somehow you can give the immune system something to stop the HIV-activating elements that it uses to fuel it's fire is certainly an interesting prospect. Both Nef and Vpu have been assigned many functions by research, only a few of which are likely to be correct. However, the reason SIV is not pathogenic and HIV is in certain hosts has been a question that many have tried to answer. This might represent finally the reason why and assign to reason to Nef and Vpu. While it is not of use right now, it will at least open the door for something new to think about and try. It would be fantastic to use one of HIV's brother's tricks against it to suppress the fire. At least it would be a new therapy that hasn't been tried and it might further slow HIV's burn through the immune system enough for it to recover and fight off OI's.....and stopping AIDS.

Finally, I do understand that science can be viewed to move slowly and not make discoveries of immediate impact. However, everything new about HIV is something more that we know. While it might not be possible to come up with a Nef or Vpu treatment in less than 5 years, it is possible to use information such as this to redirect the efforts of current treatments to make them more effective. Anything we learn from nature is good. Mother nature knows how to fend off SIV, we just have to learn how....and we might have just found out. We might not have to replicate the exact Nef-like activity, but at least know what is important to stop. For instance, stopping cells being so active against HIV. Anti-Nef treatment isn't the only thing to try....

R

whizzer:
Regarding immunosuppresive drugs and HIV.  I was combing through the NIH clinical trials website and there is study recruiting to look at using Enbrel (enteracept) as salvage therapy in those with multiple failed regimens.

Enbrel suppresses tumor necrosis factor.  HIV stimulates tumor necrosis factor to increase the number of active CD4s, or something like that.  I'm not remembering my TNF biology too well, but the two are somehow related.

Anyhow, this is being looked at.

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