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TRIM5 acts as more than a retroviral restriction factor
Journal article   Open access   Peer reviewed

TRIM5 acts as more than a retroviral restriction factor

Suresh de Silva and Li Wu
Viruses, Vol.3(7), pp.1204-1209
07/2011
DOI: 10.3390/v3071204
PMCID: PMC3159411
PMID: 21866272
url
https://doi.org/10.3390/v3071204View
Published (Version of record) Open Access

Abstract

The retrovirus restriction factor TRIM5α blocks post-entry infection of retroviruses in a species-specific manner. As a cellular E3 ubiquitin ligase, TRIM5α binds to the retroviral capsid lattice in the cytoplasm of an infected cell and accelerates the uncoating process of retroviral capsid, thus providing a potent restriction to HIV-1 and other retrovirus infections. The precise mechanism by which this restriction is imposed remains under scrutiny, and evidence is lacking to link the E3 ubiquitin ligase activity of TRIM5α to its ability to restrict retrovirus infection. In a recent study, Pertel and colleagues have uncovered the link between the two, providing compelling evidence to suggest that following the interaction with the retroviral capsid, TRIM5 triggers an antiviral innate immune response by functioning as a pattern recognition receptor. This unique function of TRIM5 is dependent on its association with the E2 ubiquitin-conjugating enzyme complex UBC13-UEV1A and subsequent activation of the TAK1 kinase complex and downstream genes involved in innate immune responses. These findings have defined a novel function for TRIM5 as a pattern recognition receptor in innate immune recognition and provided valuable mechanistic insight into its role as a retroviral restriction factor. Here we discuss the significance of these new findings in understanding TRIM5-mediated HIV restriction.
HIV Infections - immunology Immunity, Innate - immunology HIV-1 - immunology HIV Infections - virology Humans Carrier Proteins - immunology

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