We have studied the binding of biotinylated HIV particles to various cell lines and peripheral blood mononuclear cells (PBMCs). Viruses were harvested from cultures of cell surface-biotinylated cells productively infected with HIV-IIIB. Labeled HIV particles bound to and infected CD4(+) cell lines and PBMCs. The interaction between gp120 and CD4 contributed in part to HIV binding to CD4(+) cells. However, HIV binding was for the most part independent of CD4 expression and sensitive to polyanion inhibition. Polyanion-sensitive interactions involved heparan sulfate in cell lines but not in primary T cells. Interestingly, HIV binding to primary cells was heterogeneous and targeted discrete subsets of CD4(+) and CD4(-) cells. The CD4(+) T cell subset that displayed high HIV-binding capacity contained mostly CD4(+)CD45RO(+) cells, whereas the subset showing undetectable HIV binding contained higher proportions of CD4(+)CD45RO(-) cells. Consistently, purified CD4(+)CD45RO(-) cells or purified CD4(+) T cells with low virus-binding capacity showed lower HIV entry and delayed HIV replication when compared with purified CD4(+)CD45RO(+) or purified CD4(+) T cells with high virus-binding capacity, respectively. Our data suggest that the binding of HIV to cell surface-expressed CD4 might be inefficient in a subset of CD4(+) T cells and that increased binding of HIV to activated and CD4(+)CD45RO(+) cells may contribute to the higher susceptibility of these cells to HIV infection.
No takes yet. Share an insight, caveat, or question.
Blanco et al. (2002) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: