ABSTRACT
The human immunodeficiency virus type 1 (HIV-1) is the etiologic agent of the acquired immunodeficiency syndrome. HIV-1 directly targets host defenses by infection of T-lymphocytes, macrophages, and dendritic cells of the immune system and replicates best when those cells are activated. Weiss and colleagues demonstrated in 1984 that monoclonal antibodies to CD4 blocked HIV-1 entry into cells suggesting that CD4 was a critical component of the viral receptor. This observation was directly confirmed following the cloning of the gene and demonstration in 1986 that it enabled the infection of CD4 transduced human cells. With the discovery of the chemokine receptor gene family as HIV-1 entry coreceptors, HIV-1 strains can also be classified by co-receptor utilization. Strictly non-syncytium-inducing viruses primarily utilize CC chemokine receptor 5 and are termed ‘R5 HIV-1’ while strictly SI viruses primarily utilize the chemokine receptor CXCR4 and are termed ‘X4 HIV-1.
