Inhibition of HBV Release by BST-2.
- Author:
Zhu HAN
;
Xiaofang YU
;
Wenyan ZHANG
- Publication Type:Journal Article
- MeSH:
Animals;
Antigens, CD;
genetics;
immunology;
GPI-Linked Proteins;
genetics;
immunology;
Hepatitis B;
genetics;
immunology;
virology;
Hepatitis B virus;
genetics;
physiology;
Host-Pathogen Interactions;
Humans;
Virus Release
- From:
Chinese Journal of Virology
2016;32(2):215-221
- CountryChina
- Language:Chinese
-
Abstract:
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.
