Abstract
In owl monkeys, a retrotransposition event replaced the gene encoding the retroviral restriction factor TRIM5α with one encoding TRIMCyp, a fusion between the RING, B-box 2 and coiled-coil domains of TRIM5 and cyclophilin A. TRIMCyp restricts human immunodeficiency virus (HIV-1) infection by a mechanism dependent on the interaction of the cyclophilin A moiety and the HIV-1 capsid protein. Here, we show that infection by retroviruses other than HIV-1 can be restricted by TRIMCyp, providing an explanation for the evolutionary retention of the TRIMCyp gene in owl monkey lineages. The TRIMCyp-mediated block to HIV-1 infection occurs before the earliest step of reverse transcription. TRIMCyp-mediated restriction involves at least two functions: (1) capsid binding, which occurs most efficiently for trimeric TRIMCyp proteins that retain the coiled-coil and cyclophilin A domains, and (2) an effector function that depends upon the B-box 2 domain.
Original language | English (US) |
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Pages (from-to) | 404-419 |
Number of pages | 16 |
Journal | Virology |
Volume | 351 |
Issue number | 2 |
DOIs | |
State | Published - Aug 1 2006 |
Externally published | Yes |
Keywords
- Capsid
- Cyclophilin
- HIV
- Restriction factors
- Retrovirus
- Reverse transcription
- Tropism
- Uncoating
ASJC Scopus subject areas
- Virology