Abstract
N6-methyladenosine (m(6)A) is the most prevalent modification of mammalian cellular RNAs. m(6)A methylation is linked to epigenetic regulation of several aspects of gene expression, including RNA stability, splicing, nuclear export, RNA folding, and translational activity. m(6)A modification is reversibly catalyzed by methyltransferases (m(6)A writers) and demethylases (m(6)A erasers), and the dynamics of m(6)A-modified RNA are regulated by m(6)A-binding proteins (m(6)A readers). Recently, several studies have shown that m(6)A methylation sites have been identified in hepatitis B virus (HBV) transcripts and the hepatitis C virus (HCV) RNA genome. Here, we review the role of m(6)A modification in HBV/HCV replication and its contribution to liver disease pathogenesis. A better understanding of the functions of m(6)A methylation in the life cycles of HBV and HCV is required to establish the role of these modifications in liver diseases associated with these viral infections.