What is the mechanism by which HIV infection cause an initial drop in CD8+ cells

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theWUbear

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(Disclaimer: This question is not related to any schoolwork or research, just curious)

I was surfing the web and I came across a patient q and a where the physician explained rise/decline of CD4+ and CD8+ cells through time with HIV infection.

below is from http://www.thebody.com/Forums/AIDS/Labs/Archive/History/Q142217.html

The total CD8 cell count actually goes down immediately following infection (as does the CD4 cell count) for about 2-3 weeks - then over the course of the next month (i.e. roughly the second month of infection), the CD8 cell count increases (as does the CD4 count) to values higher than are typically seen in HIV negative individuals. During this period, the changes in the CD4/CD8 ratio are quite typical for HIV​

I understand that HIV gp120 binds CD4 on T Helper cells. I can see how you have an initial increase in helper and cytotoxic T cells as the body senses an infection and mounts a response, and then I can see how cytotoxic T cells would remain high (latent infection) while CD4 count would decline because your CD4+ cells are getting shredded by HIV. However, I can't understand why there would be an initial decrease in the amount of cytotoxic T cell/NK Cell during the first two weeks of infection.

Anyone know this?
 
change of heart.
 
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Haven't read it, let me know if this answers your question...

https://docs.google.com/viewer?url=...articles/PMC295794/pdf/jcinvest00026-0119.pdf

EDIT:

Quick skim:
The early disappearance of the naive CD8 cells is particularly surprising, since most discussions of T cell loss in HIV infection have centered around the specific infectability of CD4-bearing cells. However, since Bonyhadi and colleagues (17) have shown that the thymocytes expressing both CD8 and CD4 are infectable by HIV and will die when infected, the loss of naive CD8 T cells could well be due to the depletion of these double positive precursors. Alternatively, loss of thymopoietic capability could be due to a general destruction of the thymus or a progressive loss of the bone marrow's capacity to produce thymocyte progenitors. Hypotheses based on general failure of thymopoiesis are attractive since they could also explain the preferential loss of naive CD4 T cells

so basically, you lose part of the naive population initially, but as you mount an immune response you regain CD8 cell counts that are specific to fighting the infection.
Ok, back to studying...
 
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(Disclaimer: This question is not related to any schoolwork or research, just curious)

I was surfing the web and I came across a patient q and a where the physician explained rise/decline of CD4+ and CD8+ cells through time with HIV infection.

below is from http://www.thebody.com/Forums/AIDS/Labs/Archive/History/Q142217.html
The total CD8 cell count actually goes down immediately following infection (as does the CD4 cell count) for about 2-3 weeks - then over the course of the next month (i.e. roughly the second month of infection), the CD8 cell count increases (as does the CD4 count) to values higher than are typically seen in HIV negative individuals. During this period, the changes in the CD4/CD8 ratio are quite typical for HIV
I understand that HIV gp120 binds CD4 on T Helper cells. I can see how you have an initial increase in helper and cytotoxic T cells as the body senses an infection and mounts a response, and then I can see how cytotoxic T cells would remain high (latent infection) while CD4 count would decline because your CD4+ cells are getting shredded by HIV. However, I can't understand why there would be an initial decrease in the amount of cytotoxic T cell/NK Cell during the first two weeks of infection.

Anyone know this?
my memory of my HIV and immunology courses isn't 100%, but I think the reason CD8 cells decline initially is that the CD4 cells that activate them are being destroyed. It takes several days or more before the adaptive immune response kicks in and more T-cells proliferate.
 
Well done SDN....

Thank you Dr McSexy and rHinO1
 
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