HIV infection affects blood myeloid dendritic cells after successful therapy and despite nonprogressing clinical disease

We assessed the longitudinal changes in blood myeloid dendritic cell (mDC) and plasmacytoid dendritic cell (pDC) populations in subjects with primary human immunodeficiency virus (HIV) infection undergoing differ-ent rates of disease progression. The relative level and degree of maturation of all cell populations decreased significantly in untreated individuals with acute infection. Themost dramatic changeswere observed in the rapid progressor group, correlatingwith their rate of clinical progression. Levels ofmDCs remained lower than normal throughout follow-up for both rapid progressors who responded to antiretroviral therapy (ART) and untreated normal progressors. In contrast, mDC precursors were restored to normal levels during subsequent phases of infection in both rapid and normal progressors, and these levels were increased in long-term nonprogressors. pDC levels followed the pattern of CD4 T cell fluctuations. These findings provide evidence for an ongoing process affectingmDCs after successful ARTanddespite nonprogressing clinical disease followingHIV infection. During HIV infection, dendritic cells (DCs) at mucosal surfaces are among the first cell types to be exposed to the virus. As such, they facilitate presentation and/or transmission of HIV to CD4 T cells in the submucosal layer and draining lymphoid organs [1, 2]. HIV foot