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      Phosphatidylserine on HIV envelope is a cofactor for infection of monocytic cells.

      The Journal of Immunology Author Choice
      Adjuvants, Immunologic, antagonists & inhibitors, biosynthesis, physiology, Binding Sites, immunology, Gene Products, env, HIV Infections, virology, HIV-1, pathogenicity, Humans, Jurkat Cells, Macrophages, metabolism, Membrane Fusion, Monocytes, Phosphatidylserines, Tumor Cells, Cultured, U937 Cells, Virion, Virus Replication

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          Abstract

          HIV-1 is an enveloped retrovirus that acquires its outer membrane as the virion exits the cell. Because of the association of apoptosis with the progression of AIDS, HIV-1-infected T cells or macrophages might be expected to express elevated levels of surface phosphatidylserine (PS), a hallmark of programmed cell death. Virions produced by these cells would also be predicted to have PS on the surface of their envelopes. In this study, data are presented that support this hypothesis and suggest that PS is required for macrophage infection. The PS-specific protein annexin V was used to enrich for virus particles and to inhibit HIV-1 replication in primary macrophages, but not T cells. HIV-1 replication was also significantly inhibited with vesicles consisting of PS, but not phosphatidylcholine. PS is specifically required for HIV-1 infection because viruses pseudotyped with vesicular stomatitis virus G and amphotropic murine leukemia virus envelopes were not inhibited by PS vesicles or annexin V. These data indicate that PS is an important cofactor for HIV-1 infection of macrophages.

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