In Chap. 8 , the critical studies by the army and at the Willowbrook school revealed the existence of two types of suspected viral hepatitis that were designated type A and type B. Even without isolating the agents themselves, much information was obtained about the clinical features of both diseases. It was quickly determined that type B was typically associated with exposure to blood or bodily fluids while type A was transmitted more casually through household contacts and by ingestion of contaminated food or water. This pattern of transmission observed for the type A disease was consistent with a virus shed in the feces, a conjecture that would eventually prove correct. However, even with these distinct routes of transmission, the clinical presentations of type A or type B infections are very similar. Both types of infection produced an assortment of manifestations from frank jaundice to less specific indicators such as fever, anorexia, vomiting, diarrhea, fatigue, abdominal pain, and elevation of certain liver enzyme levels. The range of frequency and severity of these symptoms sufficiently overlaps between type A and type B such that the types cannot be distinguished based on patient presentation alone. Nonetheless, experiments at Willowbrook and in other “volunteer” settings did define some differences between these two diseases. For example, the two diseases differ in their incubation periods with type A having a shorter duration from infection to clinical disease. Type A incubation is between two to four weeks while type B has an incubation period of two to five months. Additionally, although both type A and type B infections tended to be mild or asymptomatic in young children, type A never became chronic while type B in children often resulted in permanent, lifelong infections. These different characteristics were consistent and repeatable when infections were passed from volunteer to volunteer. Based on these early studies, the medical and research communities concluded that there were two distinct types of disease presumably caused by different viruses. But even with this clear clinical distinction established in the 1950s, the inability to readily propagate either virus outside of humans handicapped the research into these viruses throughout most of the 1960s. While the discovery of the Australia antigen was the breakthrough that keyed the identification of the hepatitis B virus in 1970, the presumptive hepatitis A virus remained elusive.

Hepatitis A Virus: Feces, Food, and Fomites

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发表日期：

2025年

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Van G. Wilson

摘要

In Chap. 8 , the critical studies by the army and at the Willowbrook school revealed the existence of two types of suspected viral hepatitis that were designated type A and type B. Even without isolating the agents themselves, much information was obtained about the clinical features of both diseases. It was quickly determined that type B was typically associated with exposure to blood or bodily fluids while type A was transmitted more casually through household contacts and by ingestion of contaminated food or water. This pattern of transmission observed for the type A disease was consistent with a virus shed in the feces, a conjecture that would eventually prove correct. However, even with these distinct routes of transmission, the clinical presentations of type A or type B infections are very similar. Both types of infection produced an assortment of manifestations from frank jaundice to less specific indicators such as fever, anorexia, vomiting, diarrhea, fatigue, abdominal pain, and elevation of certain liver enzyme levels. The range of frequency and severity of these symptoms sufficiently overlaps between type A and type B such that the types cannot be distinguished based on patient presentation alone. Nonetheless, experiments at Willowbrook and in other “volunteer” settings did define some differences between these two diseases. For example, the two diseases differ in their incubation periods with type A having a shorter duration from infection to clinical disease. Type A incubation is between two to four weeks while type B has an incubation period of two to five months. Additionally, although both type A and type B infections tended to be mild or asymptomatic in young children, type A never became chronic while type B in children often resulted in permanent, lifelong infections. These different characteristics were consistent and repeatable when infections were passed from volunteer to volunteer. Based on these early studies, the medical and research communities concluded that there were two distinct types of disease presumably caused by different viruses. But even with this clear clinical distinction established in the 1950s, the inability to readily propagate either virus outside of humans handicapped the research into these viruses throughout most of the 1960s. While the discovery of the Australia antigen was the breakthrough that keyed the identification of the hepatitis B virus in 1970, the presumptive hepatitis A virus remained elusive.