Figure 1. HIV-induced alterations of human B-cell subpopulations.

As immature CD19⁺CD20⁺ B cells exit the bone marrow, a small fraction can be identified in the peripheral blood by the expression of CD10 in the absence of CD27. The frequency of these immature transitional B cells, which can be further divided into CD21^low and CD21^hi subsets, is increased in the peripheral blood of HIV-infected individuals, probably as a result of the increased serum levels of interleukin-7 (IL-7) that are associated with HIV-induced CD4⁺ T-cell lymphopenia (a). Chronic HIV viraemia is associated with the expansion of several B-cell subpopulations, including activated mature B cells that have downregulated their expression of CD21 and express CD27, short-lived Ki-67⁺ plasmablasts that have downregulated their expression of CD20 and CD21 and express high levels of CD27, and tissue-like memory B cells that have downregulated their expression of CD21, do not express CD27 and have several features of virus-induced exhaustion (listed in FIG. 3) (b). HIV infection is associated with a loss of resting memory B cells (defined by the expression of CD21 and CD27) that is not reversed by antiretroviral therapy (c).