B Cell-Mediated Infection of Stimulated and Unstimulated Autologous T Lymphocytes with HIV-l: Role of Complement

Abstract

In vivo, human immunodeficiency virus type 1 (HIV-1) is opsonized with complement fragments and virus-specific antibodies (Ab)Thus, HIV is able to interact with complement receptor (CR) - and Fc recpeptor (FcR) - positive cells such as B cells, follicular dendritic cells or macrophagesIn this study we demonstrate that the interaction between B cells and HIV has an impact on autologous primary T cell infection in vitroWe confirmed the presence of complement-fragments and virus-specific Ab on serum-treated HIV using a virus-capture assayIn experiments with CR2-specific Ab we showed that the virus/B cell interaction was mainly dependent on CR2In infection experiments immobilisation of HIV on stimulated tonsil B cells greatly enhanced the infection of interleukin (IL)-2-activated autologous tonsil T cellsSurprisingly, enhancement ofT cell infection by B cell-HIV complexes was observed even in the absence of mitogenic stimuli such as PMA and was independent of the addition of exogenous IL-2Taken together, these results indicate that primary B cells are able to efficiently transmit opsonised HIV to autologous primary T cells and induce a massive enhancement of infectionThese in vitro experiments mimic the in vivo situation in the lymphoid tissue and suggest an alternative mechanism for the infection of primary T cells.