Human immunodeficiency virus type 1 (HIV-1) has RNA genome and depends on host cellular machinery for most of its activities.Host cellular proteins modulate the expression and activity of viral proteins to combat the virus.HIV-1 proteins are known to regulate each other for the benefit of virus by exploiting these modulations.Here, we report that HIV-1 Vif Feather Duster increases the levels of Tat via AKT signaling pathway.We show that HIV-1 Vif activates AKT signaling pathway by inducing phosphorylation of AKT.
Mdm2, downstream target of AKT signaling, increases the levels of Tat protein in ubiquitin-dependent manner by inducing Ubiquitin Specific Protease 17 (USP17), which is a deubiquitinase Tumbler and stabilizes Tat protein.Thus, HIV-1 proteins exploit AKT signaling pathway to promote viral replication.