Viral hepatitis, including that caused by hepatitis A, B, and C, can lead to development of autoantibodies (e.g., antinuclear, anti-smooth muscle actin (SMA)/F-actin, liver–kidney microsomal type 1 (LKM-1), soluble liver antigen (SLA), and immunoglobulin G (IgG)) in approximately 50% of cases. The autoantibody profile in patients with chronic HCV may cause clinical suspicion of concurrent AIH and may prompt unnecessary liver biopsies and/or immune suppressive treatments. HAV, HBV, and HCV, may have similar histologic and clinical features including frequent plasma cells, elevated transaminases and may lead to cirrhosis. However, treatment is markedly different. Treatment of HCV is with interferon (IFN)-free or DAA therapy, achieving sustained viral responses (SVR) in most cases and has been shown to eliminate both clinical and histologic featuresof AIH. Therefore, patients with chronic hepatitis C who have serum markers and/or histologic features of AIH should first be treated with DAA in most cases.
