Abstract
It has been 15 years since HIV-1 tropism was recognized as a prognostic marker for CD4 T cell depletion and progression to AIDS [1]. The original studies were performed by testing HIV-1 strains for syncytia induction in MT-2 cell culture. These cell-based assays had a sensitivity of detection of 5% and predicted disease progression. They were, however, slow and labor-intensive and thus did not lend themselves to clinical use. The discovery of HIV-1 coreceptors in 1996 demonstrated that syncytia formation in MT-2 cells was usually induced by HIV-1 strains that used the CXCR4 (i.e., X4) coreceptor (hereafter, “X4 strains”) [2]. Early studies of coreceptor use (i.e., tropism) confirmed that HIV-1 strains that used X4 were as-
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