Coreceptor usage of human immunodeficiency virus type 2 primary isolates and biological clones is broad and does not correlate with their syncytium-inducing capacities
Entry of human immunodeficiency virus type 1 (HIV-1) into target cells is
mediated by binding of the surface envelope glycoprotein to the CD4
molecule. Interaction of the resulting CD4-glycoprotein complex with
alpha- or beta-chemokine receptors, depending on the biological phenotype
of the virus, then initiates the fusion process. Here, we show that
primary HIV-2 isolates and biological clones, in contrast to those of
HIV-1, may use a broad range of coreceptors, including CCR-1, CCR-3,
CCR-5, and CXCR-4. The syncytium-inducing capacity of these viruses did
not correlate with the ability to infect via CXCR-4 or any other
coreceptor. One cell-free passage of the intermediate isolates in
mitogen-stimulated, CD8+ cell-depleted peripheral blood mononuclear cells
resulted in the outgrowth of variants with CCR-5 only, whereas the
coreceptor usage of late and early isolates did not change. Since HIV-2 is
less pathogenic in vivo than HIV-1, these data suggest that HIV
pathogenicity in vivo is not directly related to the spectrum of
coreceptors used in in vitro systems
