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- Title
The cytoplasmic body component TRIM5a restricts HIV-1 infection in Old World monkeys.
- Authors
Stremlau, Matthew; Owens, Christopher M.; Perron, Michel J.; Kiessling, Michael; Autissier, Patrick; Sodroski, Joseph
- Abstract
Host cell barriers to the early phase of immunodeficiency virus replication explain the current distribution of these viruses among human and non-human primate species. Human immunodeficiency virus type 1 (HIV-1), the cause of acquired immunodeficiency syndrome (AIDS) in humans, efficiently enters the cells of Old World monkeys but encounters a block before reverse transcription. This species-specific restriction acts on the incoming HIV-1 capsid and is mediated by a dominant repressive factor. Here we identify TRIM5a, a component of cytoplasmic bodies, as the blocking factor. HIV-1 infection is restricted more efficiently by rhesus monkey TRIM5a than by human TRIM5a. The simian immunodeficiency virus, which naturally infects Old World monkeys, is less susceptible to the TRIM5a-mediated block than is HIV-1, and this difference in susceptibility is due to the viral capsid. The early block to HIV-1 infection in monkey cells is relieved by interference with TRIM5a expression. Our studies identify TRIM5a as a species-specific mediator of innate cellular resistance to HIV-1 and reveal host cell components that modulate the uncoating of a retroviral capsid.
- Subjects
IMMUNODEFICIENCY; VIRAL replication; HIV; AIDS; LABORATORY monkeys; PRIMATES
- Publication
Nature, 2004, Vol 427, Issue 6977, p848
- ISSN
0028-0836
- Publication type
Letter
- DOI
10.1038/nature02343