CD4-independent binding of HIV-1 to the B lymphocyte receptor CR2 (CD21) in the presence of complement and antibody.

Published

Journal Article

Complement and antibody contribute to infection-enhancement and possible expanded cellular tropism of HIV-1 in vitro through a process requiring complement receptors. Until now, however, the ability of HIV-1 to bind complement receptors has not been documented or characterized. We investigated whether antibody and complement permitted HIV-1 to bind to the B lymphocyte receptor, CR2 (CD21), in an effort to learn more about infection-enhancement, and also because CR2 can mediate B cell proliferation and antigen localization in lymphoid organs in other systems. HIV-1 incubated with antibody and fresh human serum as a source of complement bound approximately 10-fold greater to cells expressing CR2 than to HIV-1-permissive cells lacking this receptor. A similar effect was observed using cells which expressed CR2 but no CD4. This binding was minimal in heat-inactivated and C3-deficient sera, and was significantly reduced by the anti-CR2 MoAb, OKB7, but not by the anti-CD4 MoAb, OKT4a. Thus, complement and antibody acted in concert to facilitate the binding of HIV-1 to CR2 independently of CD4. CD4-independent binding of HIV-1 to CR2 was not sufficient to produce infection in Raji-3 cells. Titres of antibodies mediating CR2 binding correlated with antibody titres as measured by immunofluorescence (P < 0.01) and infection-enhancement (P < 0.05) but were discordant with titres of neutralizing antibodies, a result consistent with the utilization of CR2 for enhanced infection of cells. The ability of complement and antibody to facilitate the binding of HIV-1 to CR2 in the absence of CD4 provides new insights into mechanisms of HIV-1-induced immunopathogenesis and infection-enhancement.

Full Text

Duke Authors

Cited Authors

  • Montefiori, DC; Zhou, J; Shaff, DI

Published Date

  • December 1992

Published In

Volume / Issue

  • 90 / 3

Start / End Page

  • 383 - 389

PubMed ID

  • 1360879

Pubmed Central ID

  • 1360879

International Standard Serial Number (ISSN)

  • 0009-9104

Digital Object Identifier (DOI)

  • 10.1111/j.1365-2249.1992.tb05855.x

Language

  • eng

Conference Location

  • England