Interesting article:
http://www.jimmunol.org/cgi/content/full/173/4/2211

They note:
"Two of the most important persistent infections afflicting mankind
that also lack effective vaccines are HIV and hepatitis C virus (HCV).
Effective immunity can be achieved, at least temporarily, against both
agents by an antiviral CD8+ T cell response (23, 24). Ultimately, this
fails, especially in HIV infection (24). Whether induction, and
subsequent domination by a Treg response, is one explanation for the
failure to control HIV requires investigation. Evidence from studies
on HCV indicates that the expansion of CD4+CD25+ Treg may account for
the suppression of effector CD8+ T cell immunity observed ex vivo in
those with persistent viremia (25). In HIV, the issue of Treg in
immunity was recently analyzed indirectly by Nixon and coworkers (26).
They indicated a possible role for CD4+CD25+ T cells by showing that
depletion from peripheral blood cells enhanced in vitro HIV T
cell-specific responsiveness. The results of another group indicated
that HIV-infected dendritic cells may induce Treg in vitro (27). The
role of Treg in HIV pathogenesis requires further study."

There's also an interesting one in a recent edition of Science that
discusses the effects of a poly-G repeat that seems to activate a
toll-like receptor 8 which in turn downregulates the immune
suppressive activities of Treg cells. Early results in mice suggest a
reduction in tumor growth.

Would this be or are there other therapeutic implications for humans
with HIV?

        George M. Carter