Han Zhu, Yu Xiaofang, Zhang Wenyan
Bing Du Xue Bao. 2016 Mar;32(2):215-21.
Bone marrow stromal antigen 2 (BST-2) is a kind of host restriction factor. Since it was discovered to be responsible for the defect in virion release of HIV-1 mutants lacking the accessory gene vpu in 2008, it was thought to mainly restrict the viruses by directly tethering viral particles at the plasma membrane. Recent reports suggest that BST-2 also can inhibit the the release of HBV particles, which are budding in the intracellular vesicles, expanding the antiviral spectrum of BST-2. Futhermore, the machanism that BST-2 used to restrict HBV release in multivesicular bodies (MVBs) is similar to that used to restrict HIV at the plasma membrane. However, HBV have evolved strategies to antagonize the antiviral action of BST-2. There are two different opinions about the antagonist. One is HBV inactivated BST-2 by HBx requiring a hepatocyte-specific environment. Another thought envelope protein HBs counteract the antiviral action of BST-2. In this review, we focus on the current advances in the anti-HBV activity of BST-2.
骨髓基质抗原2（BST-2）是一种宿主限制因子。自2008年被发现与缺乏辅助基因vpu的HIV-1突变体病毒体释放缺陷有关以来，人们认为它主要通过将病毒颗粒直接拴系在质膜上来限制病毒。最近的报告表明，BST-2还可以抑制在细胞内囊泡中出芽的乙肝病毒颗粒的释放，从而扩大了BST-2的抗病毒谱。此外，BST-2在多泡体（MVBs）中限制乙肝病毒释放的机制与在质膜上限制HIV的机制相似。然而，乙肝病毒已经进化出对抗BST-2抗病毒作用的策略。关于这种拮抗剂有两种不同的观点。一种是乙肝病毒通过需要肝细胞特异性环境的HBx使BST-2失活。另一种观点认为包膜蛋白HBs可抵消BST-2的抗病毒作用。在这篇综述中，我们重点关注BST-2抗乙肝病毒活性的当前进展。
