The Post-translational modifications of HIV proteins

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Human cells defend against retroviral infection through the actions of intrinsic restriction factors such as BST2.BST2 restricts the release of progeny virions from infected cells, while the HIV-1 protein Vpu antagonizes this restriction. Although the activity of Vpu is regulated by the phosphorylation, the precise regulatory mechanism for the phosphorylation-dependent Vpu function remains elusive. We here report that SCYL2 facilitates BST2-dependent restriction of viral release by inducing dephosphorylation of Vpu. The molecular machinery regulating the post-translational modifications of HIV proteins may be an alternative therapeutic target for HIV/AIDS.