B cells of HIV-1-infected patients bind virions through CD21-complement interactions and transmit infectious virus to activated T cells

The impact of HIV-associated immunopathogenesis on B cells has been largely associated with indirect consequences of viral replication. This study dem onstrates that HIV interacts directly with B cells in both lymphoid tissues and peripheral blood. B cells isolated from lymph node and peripheral bloo d mononuclear cells (PBMCs) of 4 and 23 chronically infected patients, resp ectively, demonstrated similar capacities to pass virus to activated HIV-ne gative PBMCs when compared with CD4(+) cells from the same patients. Howeve r, in contrast to T cells, virus associated with B cells was surface bound, as shown by its sensitivity to pronase and the staining pattern revealed b y in situ amplification of HIV-1 RNA. Cell sorting and ligand displacing ap proaches established that CD21 was the HIV-binding receptor on B cells, and that this association was mediated through complement-opsonized virus. The se B cells were also found to express significantly lower levels of CD21 co mpared with HIV-negative individuals, suggesting a direct perturbing effect of HIV on B cells. These findings suggest that B cells, although they them selves are not readily infected by HIV, are similar to follicular dendritic cells in their capacity to serve as extracellular reservoirs for HIV-1. Fu rthermore, B cells possess the added capability of circulating in periphera l blood and migrating through tissues where they can potentially interact w ith and pass virus to T cells.