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Among the numerous immunological abnormalities observed in chronically HIV-infected individuals, perturbations in memory CD4 T cells are thought to specifically contribute to disease pathogenesis. Among these, functional imbalance in the frequencies of T-regulatory (Tregs) and Interleukin-17/22 (IL-17/IL-22) producing T-helper cells (Th17/Th22) from mucosal sites, and T-follicular helper cells (Tfh) in lymph nodes, are thought to facilitate specific aspects of disease pathogenesis. However, while preferential infection of Tfh cells is widely believed to create an important viral reservoir in an immunologically privileged site in vivo, whether immunological perturbations among memory CD4 T cell populations are attributable to their relative infectivity by the virus in vivo is unclear. Here we studied peripheral blood and lymphoid tissues from antiretroviral (ARV)-treated and ARV-naïve Asian macaques, and isolated functionally-defined populations of memory CD4 T cells. We then assessed the degree to which these populations were infected by SIV in vivo to determine whether or not particular functionally-identified populations of memory CD4 T cells were preferentially infected by the virus. We found that SIV did not preferentially infect Th17 cells compared to T-helper 1 (Th1) cells, T-helper 2 (Th2) cells, or Tregs. Moreover, Th17 cells contributed proportionately to the total pool of infected cells. Taken together, our data suggest that while Tfh cells are more prone to harbor viral DNA, other functionally-polarized cells are equally infected by the virus in vivo, and that Th17 cells are not preferentially infected. [ABSTRACT FROM AUTHOR]