Hepatitis C virus NS2 protein triggers endoplasmic reticulum stress and suppresses its own viral replication.

ABSTRACT:

Background & aims

We previously reported that the NS2 protein of hepatitis C virus (HCV) inhibits the expression of reporter genes driven by a variety of cellular and viral promoters. The aim of the study was to determine whether the broad transcriptional repression is caused by endoplasmic reticulum (ER) stress.

Methods

Phosphorylation of the translation initiation factor eIF2α and HCV replication was detected by Western and Northern blot, respectively. De novo protein synthesis was measured by metabolic labeling. Activation of ER stress responsive genes was determined by promoter reporter assay, as well as mRNA and protein measurement by real time PCR and Western blot.

Results

Transient or inducible NS2 protein expression increased eIF2α phosphorylation and reduced

SUBMITTER: von dem Bussche A 

PROVIDER: S-EPMC3077220 | biostudies-literature | 2010 Nov

REPOSITORIES: biostudies-literature