B cell-mediated infection of stimulated and unstimulated autologous T lymphocytes with HIV-1: role of complement

• Published in: Immunobiology (1979) Vol. 202; no. 3; pp. 293 - 305
• Main Authors: Doepper, S, Stoiber, H, Kacani, L, Sprinzl, G, Steindl, F, Prodinger, W M, Dierich, M P
• Format: Journal Article
• Language: English
• Published: Netherlands 01-09-2000
• Subjects: B-Lymphocytes - immunology; B-Lymphocytes - virology; Cells, Cultured; Coculture Techniques; Complement C1q - immunology; Complement C3 - immunology; Fc receptors; HIV Antibodies - immunology; HIV-1 - immunology; human immunodeficiency virus 1; Humans; Palatine Tonsil - cytology; T-Lymphocytes - immunology; T-Lymphocytes - virology; Tumor Cells, Cultured
• ISSN: 0171-2985
• DOI: 10.1016/S0171-2985(00)80035-2

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 receptor (FcR) - positive cells such as B cells, follicular dendritic cells or macrophages. In this study we demonstrate that the interaction between B cells and HIV has an impact on autologous primary T cell infection in vitro. We confirmed the presence of complement-fragments and virus-specific Ab on serum-treated HIV using a virus-capture assay. In experiments with CR2-specific Ab we showed that the virus/B cell interaction was mainly dependent on CR2. In infection experiments immobilisation of HIV on stimulated tonsil B cells greatly enhanced the infection of interleukin (IL)-2-activated autologous tonsil T cells. Surprisingly, enhancement of T 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-2. Taken 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 infection. These in vitro experiments mimic the in vivo situation in the lymphoid tissue and suggest an alternative mechanism for the infection of primary T cells.