Adaptation of hepatitis C virus to mouse CD81 permits infection of mouse cells in the absence of human entry factors.

ABSTRACT: Hepatitis C virus (HCV) naturally infects only humans and chimpanzees. The determinants responsible for this narrow species tropism are not well defined. Virus cell entry involves human scavenger receptor class B type I (SR-BI), CD81, claudin-1 and occludin. Among these, at least CD81 and occludin are utilized in a highly species-specific fashion, thus contributing to the narrow host range of HCV. We adapted HCV to mouse CD81 and identified three envelope glycoprotein mutations which together enhance infection of cells with mouse or other rodent receptors approximately 100-fold. These mutations enhanced interaction with human CD81 and increased exposure of the binding site for CD81 on the surface of virus particles. These changes were accompanied by augmented susceptibility of adapted HCV

SUBMITTER: Bitzegeio J 

PROVIDER: S-EPMC2895659 | biostudies-literature | 2010 Jul

REPOSITORIES: biostudies-literature