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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 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 and stabilizes Tat protein. Thus, HIV-1 proteins exploit AKT signaling pathway to promote viral replication.

Human Immunodeficiency Virus Type 1 Vif Up-Regulates the Expression of Tat via AKT Signaling Pathway: Role of Ubiquitin Specific Protease 17