Journal
NATURE MEDICINE
Volume 14, Issue 6, Pages 641-647Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/nm1778
Keywords
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Funding
- NCI NIH HHS [5R01CA112414, R01 CA112414-02, R01 CA112414] Funding Source: Medline
- NIAID NIH HHS [AI058828, P30 AI054999, R01 AI058828, P30 AI054999-03, R01 AI058828-05] Funding Source: Medline
- NATIONAL CANCER INSTITUTE [R01CA112414] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [R01AI058828, P30AI054999] Funding Source: NIH RePORTER
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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.
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