Keratin 8 is involved in hepatitis B virus replication.

Hepatitis B virus (HBV) infection can result in fatal liver diseases, including cirrhosis or liver failure, and its replication and pathogenesis depend on the critical interplay between viral and host factors. This study investigated HBV replication-related host proteins and the effect of candidate proteins on HBV replication. Isobaric tags for relative and absolute quantitation (iTRAQ) were used to measure HBV replication-related proteins in HepG2 cells and HepG2.2.15 cells. KRT8 was up-regulated in HepG2.2.15 cells but not in HepG2 cells, and KRT8 was overexpressed in an HBV-infected patient's liver tissue. This result suggested that KRT8 is involved in HBV replication. To further clarify the relationship between KRT8 and HBV replication, KRT8 gene expression was inhibited by siRNA. The silencing of KRT8 mildly suppressed HBV replication. Moreover, overexpressed KRT8 significantly increased HBV replication, and the inhibition of HBV DNA did not suppress KRT8 expression. Thus, the host protein KRT8 is involved in the replication of HBV DNA, and it dramatically enhances HBV replication.