Recent studies have yielded important findings on the pathogenesis of HIV
infection. HIV infection leads to immune dysfunction through CD4+ T-cell
depletion (immunodeficiency) and immune activation (immunosuppression).
In vivo imaging studies of nonhuman primates indicate that the total
body pool of CD4+ T cells may provide more accurate quantitation of
immune depletion in HIV infection than the peripheral blood CD4+ count.
Immune activation appears to be driven by both a homeostatic response
to CD4+ cell depletion and an inflammatory response to HIV infection. The
evidence is mounting that ongoing inflammation and coagulation account
for the increased risk of serious nonopportunistic events in patients with
HIV infection. Studies in long-term nonprogressors indicate that the HIVspecific
immune responses in these patients are distinguished by clonal
expansions of antigen-specific CD8+ T cells. Additional study of the precise
mechanisms that allow immunologic control of infection in these patients
may contribute to development of vaccines and immune-based therapies.
This article summarizes a presentation made by H. Clifford Lane, MD, at the
International AIDS Society–USA continuing medical education program held
in May 2009 in Chicago