Specific recognition and accelerated uncoating of retroviral capsids by the TRIM5alpha restriction factor |
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Authors: | Stremlau Matthew Perron Michel Lee Mark Li Yuan Song Byeongwoon Javanbakht Hassan Diaz-Griffero Felipe Anderson Donovan J Sundquist Wesley I Sodroski Joseph |
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Affiliation: | Department of Cancer Immunology and AIDS, Dana-Farber Cancer Institute, Harvard Medical School Division of AIDS, Boston, MA 02115, USA. |
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Abstract: | The host restriction factor TRIM5alpha mediates species-specific, early blocks to retrovirus infection; susceptibility to these blocks is determined by viral capsid sequences. Here we demonstrate that TRIM5alpha variants from Old World monkeys specifically associate with the HIV type 1 (HIV-1) capsid and that this interaction depends on the TRIM5alpha B30.2 domain. Human and New World monkey TRIM5alpha proteins associated less efficiently with the HIV-1 capsid, accounting for the lack of restriction in cells of these species. After infection, the expression of a restricting TRIM5alpha in the target cells correlated with a decrease in the amount of particulate capsid in the cytosol. In some cases, this loss of particulate capsid was accompanied by a detectable increase in soluble capsid protein. Inhibiting the proteasome did not abrogate restriction. Thus, TRIM5alpha restricts retroviral infection by specifically recognizing the capsid and promoting its rapid, premature disassembly. |
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