Abstract
The HIV-1 Vpu protein is required for efficient viral release from human cells. For HIV-2, the envelope (Env) protein replaces the role of Vpu. Both Vpu and HIV-2 Env enhance virus release by counteracting an innate host-cell block within human cells that is absent in African green monkey (AGM) cells. Here we identify calcium-modulating cyclophilin ligand (CAML) as a Vpu-interacting host factor that restricts HIV-1 release. Expression of human CAML (encoded by CAMLG) in AGM cells conferred a strong restriction of virus release that was reversed by Vpu and HIV-2 Env, suggesting that CAML is the mechanistic link between these two viral regulators. Depletion of CAML in human cells eliminated the need for Vpu in enhancing HIV-1 and murine leukemia virus release. These results point to CAML as a Vpu-sensitive host restriction factor that inhibits HIV release from human cells. The ability of CAML to inhibit virus release should illuminate new therapeutic strategies against HIV.
Publication types
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Research Support, N.I.H., Extramural
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Research Support, Non-U.S. Gov't
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Retracted Publication
MeSH terms
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Adaptor Proteins, Signal Transducing / genetics
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Adaptor Proteins, Signal Transducing / metabolism*
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Animals
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COS Cells
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Cell Line
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Chlorocebus aethiops
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Electroporation
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Gene Deletion
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Green Fluorescent Proteins / metabolism
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HIV-1 / genetics
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HIV-1 / metabolism*
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HeLa Cells
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Human Immunodeficiency Virus Proteins / genetics
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Human Immunodeficiency Virus Proteins / metabolism*
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Human Immunodeficiency Virus Proteins / ultrastructure
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Humans
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Ligands
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Plasmids
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T-Lymphocytes / ultrastructure
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T-Lymphocytes / virology
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Transfection
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Viral Regulatory and Accessory Proteins / genetics
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Viral Regulatory and Accessory Proteins / metabolism*
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Viral Regulatory and Accessory Proteins / ultrastructure
Substances
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Adaptor Proteins, Signal Transducing
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CAMLG protein, human
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Human Immunodeficiency Virus Proteins
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Ligands
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Viral Regulatory and Accessory Proteins
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vpu protein, Human immunodeficiency virus 1
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Green Fluorescent Proteins