Abstract
HIV-E, emerging from persistently infected HeLa-T4 cells, replicates better in fibroblasts and epithelial cells with respect to the parental, T cell-derived HIV-T. The two viruses share the same env V3 loop, but differ in cellular molecules incorporated on the envelope. Even when similar amounts of virus attachment occurred, HIV-E replicated better than HIV-T in cells from solid tissues, and the response to exogenous Tat was more efficient. This might be related to the long terminal repeat (LTR), because HIV-E has a TAR duplication, and a mutation in the Sp1-II binding site. Epithelial cells deserve further study, because they may be important in vivo for variant selection and latency.
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