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

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.

Specific targeting of hepatitis C virus core protein by an intracellular single-chain antibody of human origin.

The hepatitis C virus (HCV) core protein is essential for viral genome encapsidation and plays an important role in steatosis, immune evasion, and hepatocellular carcinoma. It may thus represent a promising therapeutic target to interfere with the HCV life-cycle and related pathogenesis. In this study, we used phage display to generate single-chain variable domain antibody fragments (scFv) to the core protein from bone marrow plasma cells of patients with chronic hepatitis C.