Variability in the P6gag domains of HIV-1 involved in viral budding


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Abstract

The genetic variability within PT/SAP, LYP and LXXLF HIV-1 P6gag motifs, required for the binding to Tsg101 and AIP1 cellular host proteins during viral budding, was examined in 122 HIV-infected subjects. PT/SAP duplications were statistically more frequent in B versus non-B subtypes. Substitutions at LYP were fourfold less frequent in antiretroviral-experienced only in clade B. P6gag variability across HIV-1 subtypes and after antiretroviral exposure may influence interactions with host cells involved in viral budding.

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