NS4B self-interaction through conserved C-terminal elements is required for the establishment of functional hepatitis C virus replication complexes.

ABSTRACT: Hepatitis C virus (HCV) is an important human pathogen, persistently infecting more than 170 million individuals worldwide. Studies of the HCV life cycle have become possible with the development of cell culture systems supporting the replication of viral RNA and the production of infectious virus. However, the exact functions of individual proteins, especially of nonstructural protein 4B (NS4B), remain poorly understood. NS4B triggers the formation of specific, vesicular membrane rearrangements, referred to as membranous webs, which have been reported to represent sites of HCV RNA replication. However, the mechanism of vesicle induction is not known. In this study, a panel of 15 mutants carrying substitutions in the highly conserved NS4B C-terminal domain was generated. Five mutations had

SUBMITTER: Paul D 

PROVIDER: S-EPMC3126587 | biostudies-literature | 2011 Jul

REPOSITORIES: biostudies-literature