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Published 4 August 2003. doi:10.1083/jcb.200307062
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© The Rockefeller University Press, 0021-9525/2003/8/371 $5.00
The Journal of Cell Biology, Volume 162, Number 3, 371-375

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 After Hrs with HIV

Ali Amara1 and Dan R. Littman1,2

1 Molecular Pathogenesis Program, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016
2 Howard Hughes Medical Institute, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016

Address correspondence to Dan R. Littman, Skirball Institute of Biomolecular Medicine, New York University School of Medicine, New York, NY 10016. Tel.: (212) 263-7579. Fax: (212) 263-1498. email: littman{at}saturn.med.nyu.edu

To efficiently bud off from infected cells, HIV and other enveloped viruses hijack the host cellular machinery that is normally involved in vacuolar protein sorting and multivesicular body (MVB) biogenesis. The HIV Gag protein mimics hepatocyte growth factor–regulated tyrosine kinase substrate (Hrs), a modular adaptor protein that links membrane cargo recognition to its degradation after delivery to MVBs. In contrast to T cells, where HIV budding occurs at the plasma membrane, virus buds into vacuoles of macrophages, a process that may facilitate its spread within the infected host.

Abbreviations used in this paper: DC, dendritic cell; ESCRT, endosomal sorting complex required for transport; Hrs, hepatocyte growth factor–regulated tyrosine kinase substrate; MVB, multivesicular body; PI(3)P, phosphatidylinositol 3'-phosphate; UEV, ubiquitin E2 variant sequence; UIM, ubiquitin interaction motif; Vps, vacuolar protein sorting.


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