The Post-translational modifications of HIV proteins

人类细胞通过内在限制因子如BST 2的作用来防御逆转录病毒感染。BST 2限制子代病毒体从感染细胞中释放，而HIV-1蛋白Vpu拮抗这种限制。虽然Vpu的活性受磷酸化的调节，但是磷酸化依赖的Vpu功能的精确调节机制仍然是不清楚的。我们在这里报告，SCYL 2促进BST 2依赖性限制病毒释放诱导Vpu的去磷酸化。调节HIV蛋白翻译后修饰的分子机制可能是HIV/AIDS的替代治疗靶点。

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.