During a 1974 foodborne outbreak of viral hepatitis type A among Navy recruits, we evaluated clinical and laboratory features prospectively in 130affected persons. The ratio of anicteric to icteric persons identified during the outbreak was 1:3.5 but illness was relatively mild in this population of young adults. Infrequently reported in association with type A hepatitis, rash and arthralgias (but not arthritis) were reported by 14 and 10% of affected persons, respectively. Fourteen weeks after onset of acute illness, 8.5% of patients had persistently elevated aminotransferase activities and underwent percutaneous liver biopsy. Morphologic features included piecemeal necrosis, but clinical, biochemical, and histological evidence of disease resolved within five months to one year after the outbreak. Fecal shedding of hepatitis A virus began during the preicteric stage, did not persist beyond the second day of jaundice (even in patients with protracted illness), and was not detected in anicteric patients. Feces and serum obtained during the late incubation period, but not urine, were infectious in chimpanzees. Antibody to hepatitis A virus developed during convalescence, and serum anticomplementary activity was noted during acute illness. Failure of T-lymphocytes to bind sheep erythrocytes and form rosettes was observed, was found to be modulated in several cases by an intrinsic lymphocyte defect and in others by the presence in serum of an extrinsic immunoregulatory serum lipoprotein, “rosette inhibitory factor,” which persisted in patients with slow resolution.