Hepatitis A and E

Experimental work in humans led to the clinical recognition that viruses were etiologic agents of hepatitis A (infectious hepatitis) and hepatitis B (serum hepatitis). Later, the existence of two distinct hepatitis viruses was demonstrated: hepatitis A virus (HAV) and hepatitis B virus (HBV). HAV was first characterized in 1973 when scientists detected the virus in stools from human volunteers who were infected with HAV. The ensuing development of sensitive and specific serologic assays for the diagnosis of HAV infection and the isolation of HAV in cell culture were important advances that permitted the understanding of the epidemiology of HAV infection and, ultimately, control of the disease. With the accurate diagnosis of hepatitis A and hepatitis B, it became apparent that at least two non-A, non-B infectious agents existed. One was similar to hepatitis B, mainly transmitted parenterally, and another was similar to hepatitis A, transmitted by the fecal-oral route. In the 1980s, two seminal discoveries correctly identified the first one as hepatitis C and the second one became known as hepatitis E. Since then, hepatitis E virus (HEV) has been recognized as the agent responsible for enterically transmitted non-A, non-B hepatitis. Research to understand the epidemiology, viral characteristics, and immunity against this viral agent was propelled by the work of Balayan et al. and subsequently by cloning the virus, which allowed the development of diagnostic assays, better understanding of its epidemiology, and the development of vaccine candidates.