Restriction of retroviral replication by APOBEC3G/F and TRIM5 alpha

Hendrik Huthoff, Greg J. Towers

Research output: Contribution to journalLiterature reviewpeer-review

79 Citations (Scopus)

Abstract

Pathogenic viral infections have exerted selection pressure on their hosts to evolve cellular antiviral inhibitors referred to as restriction factors. Examples of such molecules are APOBEC3G, APOBEC3F and TRIM5 alpha. APOBEC3G and APOBEC3F are cytidine deaminases that are able to strongly inhibit retroviral replication by at least two mechanisms. They are counteracted by the lentiviral Vif protein. TRIM5a binds to sensitive, incoming retroviruses via its C-terminal PRY/SPRY domain and rapidly recruits them to the proteasome before significant viral DNA synthesis can occur. Both of these proteins robustly block retroviral replication in a species-specific way. It remains an open but important question as to whether innate restriction factors such as these can be harnessed to inhibit HIV-1 replication in humans.
Original languageEnglish
Pages (from-to)612 - 619
Number of pages8
JournalTrends in Microbiology
Volume16
Issue number12
DOIs
Publication statusPublished - Dec 2008

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