Viral hepatitis
Hepatitis B (HBV) and C (HCV) chronically infect > 300 million people globally and represent leading virologic causes of end-stage liver disease and hepatocellular carcinoma. Hepatitis A and E are typically characterized by acute hepatitis and mostly follow a self-limiting course. As a result, research into viral persistence, pathogenesis, host immune responses, therapeutic discovery targets, and pathways to hepatocarcinogenesis has focused mainly on HBV and HCV. Functional genomics approaches have significantly advanced our understanding of viral hepatitis pathogenesis and immune-mediated therapeutic responses. Genome-wide association studies in HCV led to the significant discovery of polymorphisms in the Interferon lambda 3 (IFN-Λ3) locus that predicted virologic responses to interferon-based therapy. Further studies defined the functional variant as IFN-Λ4, but the rapid progress in antiviral therapeutics for HCV has now resulted in less clinical relevance for this IFN-response predictor. Genomic studies will continue to focus on HBV therapeutic development and hepatocellular cancer.