Autoimmune Hepatitis (AIH) is a chronic liver hepatitis of unclear etiology. Rarely AIH can be triggered by viral hepatitis, especially Hepatitis A virus(HAV), Hepatitis B, Hepatitis C and Hepatitis E virus(HEV). We present a case of AIH which developed in a patient with recent HAV infection. 45-year-old female from Mexico with past history of traumatic brain injury presented with progressive yellowish discoloration of eyes, headache and confusion. She had been diagnosed with acute Hepatitis A in Mexico 1 month prior to her presentation and had full recovery with supportive management. On presentation her vital signs were normal. She was confused, icteric, and had asterixis. Her ALT and AST were 2869 U/L and 1469 U/L respectively. Total bilirubin was 15.1 gm/dL, with a direct bilirubin of 6.2 gm/dL, INR 1.6 and Ammonia 55 μmol/L. Her initial MELD (Model for End-Stage Liver Disease) was 22. Work up for etiologies of chronic liver disease showed a ferritin of 1657 ng/mL and IgG 2580. Her ANA, anti-mitochondrial antibody (AMA), anti-smooth muscle antibody, P-ANCA, C- ANCA, Anti-LKM1 antibody were negative. Ceruloplasmin and Alpha-1 antitrypsin levels were normal. Anti HAV IgM, HEV IgG and IgM were positive, but HEV RNA was undetectable. Abdominal ultrasound and CT scan showed no significant abnormality. Transjugular liver biopsy was performed revealing a portosystemic gradient of 7mmHg and histologic consistent with autoimmune hepatitis (panlobular hepatitis with abundant portal and perivenular lymphoplasmacytic infiltrate). She was started on oral prednisone and azathioprine. Her liver enzymes and liver function improved. After 1-week MELD score improved to 16. She was discharged on a prednisone taper. At 6 months follow-up she had normal liver enzymes and synthetic function, and HEV IgM and IgG remained positive. HAV infection is common but development of post viral hepatitis AIH is unusual. We describe a patient with acute autoimmune hepatitis after HAV infection. HAV infection can rarely act as a trigger for autoimmune hepatitis by initiating a self-perpetuating immune-mediated liver inflammation and can present acutely after resolution of viral hepatitis. Although other viral hepatitis markers were positive(HEV) raising the concern for coinfection, she had no HEV viremia. It is crucial to differentiate between acute viral hepatitis and AIH since their treatment is different and recognize the potential for immune mimicry in acute immunologic flares.