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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 TRIM5alpha. 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. TRIM5alpha 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.