Journal
JOURNAL OF VIROLOGY
Volume 78, Issue 10, Pages 5423-5437Publisher
AMER SOC MICROBIOLOGY
DOI: 10.1128/JVI.78.10.5423-5437.2004
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Funding
- NHLBI NIH HHS [HL 57485, P50 HL054785] Funding Source: Medline
- NIAID NIH HHS [P30 AI028691, P30 AI 28691] Funding Source: Medline
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In cells of Old World and some New World monkeys, dominant factors restrict human immunodeficiency virus type 1 (HIV-1) infections after virus entry. The simian immunodeficiency virus SIVmac is less susceptible to these restrictions, a property that is determined largely by the viral capsid protein. For this study, we altered exposed amino acid residues on the surface of the HIV-1 capsid, changing them to the corresponding residues found on the SIVmac capsid. We identified two distinct pathways of escape from early, postentry restriction in monkey cells. One set of mutants that were altered near the base of the cyclophilin A-binding loop of the N-terminal capsid domain or in the interdomain linker exhibited a decreased ability to bind the restricting factor(s). Consistent with the location of this putative factor-binding site, cyclophilin A and the restricting factor(s) cooperated to achieve the postentry block. A second set of mutants that were altered in the ridge formed by helices 3 and 6 of the N-terminal capsid domain efficiently bound the restricting factor(s) but were resistant to the consequences of factor binding. These results imply that binding of the simian restricting factor(s) is not sufficient to mediate the postentry block to HIV-1 and that SIVmax capsids escape the block by decreases in both factor binding and susceptibility to the effects of the factor(s).
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