Immunoproteasome induction is suppressed in hepatitis C virus-infected cells in a protein kinase R-dependent manner.

Hepatitis C virus (HCV) alters the processing of antigenic peptides to evade the host's immune response. Eui-Cheol Shin at Korea Advanced Institute of Science and Technology in Daejeon and colleagues have shown that HCV suppresses the ability of the host's antiviral protein IFN-γ to induce protein complexes called immunoproteasomes. These complexes are key for breaking down viral proteins into smaller fragments that can trigger an immune response by specialized white blood cells. In HCV-infected cells, IFN-γ can stimulate the expression of genes encoding immunoproteasome subunits but the complexes fail to assemble. The authors show that the mechanism through which HCV prevents the assembly of IFN-γ induced immunoproteasomes involves protein kinase R, an enzyme that arrests protein synthesis. Further research will determine whether these findings can be applied to the design of novel antiviral drugs.