HIV and AIDS vaccine
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HIV and AIDS vaccine
Why is it so difficult to make HIV Vaccine?
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HIV and AIDS Vaccine: Is it HIV or an Immune System which causes an Onset of AIDS?

Highlights

HIV triggers pathogenesis leading to an onset of AIDS (Therefore, answer for the above question is yes, it is HIV)
Fast mutation rates of HIV cannot always explain the lack of AIDS, since an identical (or similar) HIV cannot cause an onset of AIDS in certain individuals (in this case, it is not HIV)
An individual with a homozygous mutation of CCR5 (CCR5D32 ) is not susceptible to AIDS even with a higher titer of HIV in an individual (no, it is not HIV)
When HST is infected and depleted by HIV, it will lead to an onset of AIDS. However, as long as HST is spared by a depletion mediated by HIV or reconstituted by HST with a homozygous mutant form (CCR5D32 ), there will be no AIDS (again, it is an immune system which plays a critical role of getting AIDS, especially of an availability of HST).
But it all starts from HIV infection (yes, it is HIV)

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HIV and AIDS Vaccine: CCR5 (R5)-tropic HIV Susceptible CD4 T cells (HST).

What is it?
R5-tropic HIV Susceptible CD4 T cells (HST).
CD4 T cells that are susceptible to an infection and depletion by R5-tropic HIV.

Why are they so important?
Because the lack of HST undoubtedly leads to AIDS and providing HST with a homozygous mutant form of CCR5 (CCR5delta32) cured an AIDS patient by reconstituting an immune system.
Moreover, individuals who have homozygous mutant form of HST (CCR5delta32) are resistant to getting AIDS even in the presence of high titers of R5-tropic HIV.

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HIV and AIDS Vaccine: Lacking HST leads to AIDS and providing HST cures AIDS.

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HIV and AIDS Vaccine: SAV001 (Canadian) HIV vaccine trials

What could be the foreseeable problem for this trial? Will it work this time?
If yes, what the differences are. Why will it be different from previous unsuccessful trials?
If not, why that will be the case?

Based on immunological findings, I predict the following negative outcome. During vaccination, *HST will expand as I outlined previously. Even with multiple failures, it never seems to ring the bell. It is even more so to whom his (her) background is infectious agents, such as HIV itself. Unfortunately, the expanded HST has not provided a convincing protection from ensuing real HIV infection in all cases up to now. Instead of protecting it, the expanded HST becomes preferable and ample targets for HIV for their maximum expansion. This should be the main concern for any HIV vaccine trials, whether it is based on live recombinant, attenuated or chemical and radiation inactivated (killed) recombinant HIV, as in SAV001. Unfortunately, it has never been brought up, or rather not being brought up. It is probably due to the lack of current immunological understanding on HST even among the top-notch immunologists. HIV is different from any other pathogens against which we were successful making successful vaccines.

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HIV and AIDS Vaccine: Why does the number of CD4 T cells decrease gradually in AIDS patients?

The number of CD4 T cells in HIV infected individuals decreases gradually, which takes place spanning a decade so, or even longer. Why will that be the case? How does it work? Are all CD4 T cells supposed to be killed after activation by HIV as generally considered currently? Are any CD4 T cells getting killed after activation by HIV? These questions can easily be asked by any seasoned immunologist, since we do not have any general information on this issue, other than CD4 T cells are killed after activation by HIV. Even though AIDS has been around almost three decades and we have known that HIV is a causative viral agent, this apparent phenomenon is not clearly explained and even not clearly understood to investigators of HIV pathogenesis. Here, the possible mechanism that can explain this apparent phenomenon will be discussed.

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