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T-Cell Reinfection
Sep 19, 2004

Hello Doctors,

Thanks you for all your wonderfull information. It helps me to understand my situation. 1- Once the T-Cell is invaded by HIV virus and the DNA is implanted, does the same T-Cell get reinfect again and again? Does the HIV DNA gets planted in a specific location in T-Cell chromosone? 2- I know there a lot of mutation taking place with HIV virus in the body, but is there a 'Common Denaminator' between all the variation in the HIV viruses? 3- Is there a way to force the body to produce an antibody to this common denamitor if there is such a thing? 4- I understand that about 10 billion virus are produced daily in my body, what happens to these viruses? are they being distroyed somehow? 5- By taking HAART medication for a long period of time, are we not producing a super virus in the body? eventually the virus will mutate so many times and produce a version that is resistant to all drugs. 6- Lastly, how does the virus 'buds' out of T-Cell? Is there any research or new drugs in that catagory being developed?


Response from Dr. Pierone

There are very good questions and probably better answered by a virologist. But here goes.

CD4 cells must get re-infected with HIV, there would be no way for virus to undergo recombination to explain the observation for the heterogeneity of global viral subtypes. Given the explosive nature of HIV replications (billions of viruses per day), re-infection of individual cells is probably common. I don't know if HIV DNA gets implanted in the same location in the chromosome, I suspect there would be multiple sites of potential attachment.

In fact, there are common denominators among different subtypes and mutant strains of HIV. These highly preserved parts of the HIV genome are likely the elements that are essential for virus survival. These are also the target for immune-based therapies and vaccine development for prevention of HIV transmission. Naturally produced antibodies against HIV are not protective (we diagnosis HIV by measuring antibodies against it), so much of the vaccine work is focused on how to produce and enhance cell-based immunity.

Although 10 billion viruses are produced daily (damn bastards), they live for only a day and a half (serves them right). Long-term HAART may lead to development of virus that is resistant to all available HIV medications. Long-term HAART may also not lead to development of any resistance mutations. It depends on the adherence of the person taking HAART.

Lastly, exactly how virus buds I am not sure. But based on schematic representations of the virus life-cycle (simplified for clinicians like myself) I see that there are maturation inhibitors in the pipeline that occur at a step following protease cleavage.

Thanks for posting!

Re: Low viral load and pep
Fusion inhibitors and clinical trials.

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