Molecular Basis for Cell Tropism of CXCR4-Dependent Human Immunodeficiency Virus Type 1 Isolates

摘要: Laboratory isolates of human immunodeficiency virus type 1 (HIV-1) that utilize CXCR4 as a coreceptor infect primary macrophages inefficiently even though these express low but detectable level cell surface CXCR4. In contrast, infection by CXCR4-tropic HIV-1 is readily detectable. Here, we provide evidence suggesting this difference in tropism results from higher requirement for laboratory isolates. Transfected COS7 cells high CD4 were infected significantly more efficiently two compared to the prototypic isolate IIIB. More importantly, overexpression either wild-type or signaling-defective on dramatically enhanced efficiency yet only modestly virus. Overexpression had, limited effect macrophage HIV-1, although was markedly enhanced. We therefore conclude exhibits efficient than do and can explain poor ability replicate macrophages. generally, propose tropisms displayed different strains culture largely be explained basis differential requirements and/or expression levels.