Anti-idiotypic therapeutic strategies in HIV infection.

Abstract

The CD4 molecule has been shown to act as the major cellular receptor for the human immunodeficiency virus (HIV) (Dalgleish et al., 1984; Klatzmann et al., 1984; Maddon et al., 1986), and viral tropism for CD4+ cells is mediated by the interaction of the HIV major envelope glycoprotein gp120 with CD4; this has been shown to occur with high affinity in vitro (Smith et al., 1987). Monoclonal antibodies (MAbs) to CD4 can prevent the induction of syncytia by HIV in lymphocyte cultures in vitro (Dalgleish et al., 1984; Sattentau et al., 1986) and have also been shown to block the attachment of whole HIV particles or purified gp120 to CD4+ cells (McDougal et al., 1986; Lundin et al., 1987) These effects, which were central to the elucidation of CD4 as the virus receptor, have been presumed to be mediated either by steric hindrance or by direct competition for the gp120 binding site itself.