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Abstract
Human immunodeficiency virus (HIV)-1 infection causes progressive impairment of the
immune system in humans, characterized by depletion of CD4 T cells and loss of T cell
function. Increased markers of T cell activation and lymphoid hyperplasia suggest
that chronic T cell activation persists in immunocompromised hosts, and contributes
to the exhaustion of immune functions. Here we propose a revision of this hypothesis,
in which we suggest that chronic activation of innate immunity may negatively affect
adaptive T cell-mediated responses. We hypothesize that constant exposure of the effector
cells of innate immunity to HIV results in their chronic hyperactivation, with deleterious
effects on T cells. In particular, plasmacytoid dendritic cells (pDC) may be highly
susceptible to HIV-induced activation due to its interaction with the cellular receptor
CD4, expressed by pDC. Subsequent production of type I interferon and indoleamine
2,3-dioxygenase may exert suppressive and cytotoxic effects on T cells.