LIGATION OF CR-1 (C3B RECEPTOR, CD35) ON CD4(-LYMPHOCYTES ENHANCES VIRAL REPLICATION IN HIV-INFECTED CELLS() T)

The present study provides evidence for a role of the C3b receptor, CR 1 (CD35), in activation of HIV replication in CD4(+) T lymphocytes. Li gation of CRI with cross-linked anti-receptor MoAbs or with aggregated C3b enhanced transcription of viral genes and the release of p24 and RT activity from cultures of purified normal CD4(+) T lymphocytes that had been infected with HIV-1 in vitro. No effect was observed upon li gation of CR2 (CD21), a C3 receptor that is also expressed on human CD 4(+) T cells. Cross-linking of CR1 also enhanced HIV replication in pe ripheral blood CD4(+) lymphocytes isolated from HIV+ individuals. The enhancing effect of CR1 was not related to a mitogenic effect induced by stimulation of the receptor on T cells. The CR1 specificity of the enhancing effect was established by the observation that the addition of soluble recombinant CR1 to the cultures abolished the enhancement o f p24 release induced by anti-CR1 MoAbs. Our results suggest that HIV replication may be triggered in resting HIV-infected CD4(+) T lymphocy tes through interaction with C3b-bearing immune complexes or particles .