UC San Diego

N6-methyladenosine (m⁶A) is the most prevalent modification of mammalian cellular RNAs. m⁶A methylation is linked to epigenetic regulation of several aspects of gene expression, including RNA stability, splicing, nuclear export, RNA folding, and translational activity. m⁶A modification is reversibly catalyzed by methyltransferases (m⁶A writers) and demethylases (m⁶A erasers), and the dynamics of m⁶A-modified RNA are regulated by m⁶A-binding proteins (m⁶A readers). Recently, several studies have shown that m⁶A 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 m⁶A modification in HBV/HCV replication and its contribution to liver disease pathogenesis. A better understanding of the functions of m⁶A 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.