A 44-year-old woman with HIV/AIDS (CD4 lymphocyte count of 18/μL), parvovirus B19–induced anemia, and years of idiopathic elevated liver enzyme levels was admitted to the hospital with subacute progressive malaise and body aches. On initial evaluation, she was found to have worsening liver enzyme levels (aspartate aminotransferase 10 × upper limit of normal [ULN]; alanine aminotransferase 7 × ULN; alkaline phosphatase within normal limits). At that time, she underwent an extensive workup for liver disease, including viral and autoimmune hepatitis serologic testing, as well as magnetic resonance imaging and biopsy of the liver. Her hepatitis A and C antibodies were nonreactive, she had evidence of seroprotection from prior hepatitis B immunization, her autoimmune laboratory results were negative, the magnetic resonance imaging results did not demonstrate any abnormalities, and the biopsy results demonstrated nonspecific preserved hepatic architecture with periportal lymphocytic inflammation and mild fibrosis. She was discharged with a working diagnosis of hepatitis secondary to antiretroviral toxic effects exacerbated by parvovirus B infection and alcohol use, though she reported only occasional social alcohol intake.