The HIV-1 capsid protein (CA) interacts with viral factors that support infection and host factors that restrict it. The host protein cyclophilin A (CypA) binds to CA and enhances the action of host restriction factors that block HIV-1 infection.
Christopher Aiken, Ph.D., and colleagues investigated how CypA potentiates the action of the restriction factor TRIM5alpha in African green monkey cells. They did not find evidence of a role for CypA in promoting binding of TRIM5alpha to the viral capsid or inhibiting reverse transcription of the viral genome.
Instead, the investigators observed a CypA-dependent reduction in the accumulation of nuclear HIV-1 DNA, suggesting that CypA promotes TRIM5alpha inhibition of HIV-1 nuclear import. They reported their findings in the journal PLOS ONE.
The authors propose that CypA uses a common mechanism involving interactions of the virus with nuclear pore components to potentiate restriction of HIV-1 infection by TRIM5alpha and other capsid-targeting inhibitors.
This research was supported by National Institutes of Health grant AI076121.
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