HIV compromises the human body to defend against infection. Yet people who are infected with herpes are at less risk of developing AIDS.

How does this work?

This question comes from this paper, which is hard for me to follow since I am uneducated on this field. http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1716975/

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    $\begingroup$ Can you please clarify to which Herpes virus you are referring? There are a dozen or so that infect humans, each of which target either mucosal/epithelial tissue, B cells, T cells, lymphocytes or other leukocytes. $\endgroup$
    – user560
    Mar 11, 2012 at 2:29
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    $\begingroup$ I think HSV is sufficiently descriptive enough to characterize and generalize herpes. $\endgroup$
    – bobthejoe
    Mar 11, 2012 at 7:15
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    $\begingroup$ @bobthejoe I don't think it is. For example, HSV-1 and HSV-2 are massively different infections, and both are extremely common in humans. $\endgroup$
    – Fomite
    Mar 12, 2012 at 0:44
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    $\begingroup$ Also, can we have a citation on this claim? Most of what I've seen suggests that HSV-2 is a risk factor for the acquisition of HIV, and that is is the suppression of HSV using acyclovir that helps prevent HIV. $\endgroup$
    – Fomite
    Mar 12, 2012 at 0:46
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    $\begingroup$ ncbi.nlm.nih.gov/pmc/articles/PMC1716975 Here is one. Its hard for me to follow, no where near that educated on the matter. $\endgroup$ Mar 12, 2012 at 11:18

1 Answer 1


Alright, having read the citation linked, and doing a little poking of my own, here's my approach at an answer:

Some human herpes virus infections may compete with HIV infection. Essentially, some strains (not the ones you normally think of) infect CD4 cells - the same cells targeted by HIV. These strains down regulate transcription in CD4 cells, which in turn interferes with the HIV infection process. This pertains, it appears most notably, to HHV-7.

However the actual impact on HIV disease isn't clear. Strain competition triggers some fascinating evolutionary pressures, but HIV is notoriously prone to mutation, and competition for CD4 cells might not impact HIV infection on a clinical - rather than microbiological - scale.

Additionally, the two most commonly thought of forms of herpesvirus infection, HSV-1 and HSV-2 are associated with increased acquisition of HIV infection. The clearest reasons for this are genital lesions and inflammation at the site of HIV infection. There's also some interesting dynamics in play for active coinfection, such as the impact of acyclovir treatment for HSV impacting HIV, or HAART treatment for HIV impacting HSV.


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