The probable existence of at least two distinct types of acute human hepatitis, their probable viral etiology, their different incubation periods, and their different primary modes of transmission were first suggested in the late 1930s.1 Type A (infectious) hepatitis appeared to behave in a relatively orthodox manner as a basically enteric infectious disease, but the behavior of type B (serum) hepatitis was shrouded in mystery. Limited human transmission studies in the early 1940s, while establishing its etiologic distinction from type A, led to epidemiologic dogma which went essentially unchallenged for more than 20 years. The concept of its exclusively parenteral mode of transmission was simple enough, but explanations of its origin and means for long-time survival provided fascinating challenges in epidemiology. Even though cross-challenge studies revealed no discernible immunologic relationship, it was suggested that type B virus represented an evolutionary offspring of type A, peculiarly adapted to