The cytoplasmic body component TRIM5α restricts HIV-1 infection in Old World monkeys

Matthew Stremlau, Christopher M. Owens, Michel J. Perron, Michael Kiessling, Patrick Autissier and Joseph Sodroski ()
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Matthew Stremlau: Harvard Medical School
Christopher M. Owens: Harvard Medical School
Michel J. Perron: Harvard Medical School
Michael Kiessling: Harvard Medical School
Patrick Autissier: Harvard Medical School
Joseph Sodroski: Harvard Medical School

Nature, 2004, vol. 427, issue 6977, 848-853

Abstract: 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 species1,2,3,4. 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 transcription2,3,4. This species-specific restriction acts on the incoming HIV-1 capsid5,6,7 and is mediated by a dominant repressive factor7,8,9. Here we identify TRIM5α, a component of cytoplasmic bodies, as the blocking factor. HIV-1 infection is restricted more efficiently by rhesus monkey TRIM5α than by human TRIM5α. The simian immunodeficiency virus, which naturally infects Old World monkeys10, is less susceptible to the TRIM5α-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 TRIM5α expression. Our studies identify TRIM5α 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.

Date: 2004
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DOI: 10.1038/nature02343

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