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The Molecular Biology of Hepatitis E Virus

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Hepatitis Viruses

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Abstract

There are two characterized forms of fecal-orally transmitted viral hepatitis: A and E (hepatitis A virus [HAV] and hepatitis E virus [HEV] respectively). The first confirmed epidemic of hepatitis E was in New Delhi, India in 1955 (1) and although the epidemiological features (e.g., fecal-oral transmission) suggested HAV as the etiologic agent, by 1980 there was clear evidence that a unique form of fecal-orally transmitted hepatitis was responsible for much of the epidemic hepatitis formerly ascribed to HAV. Indeed, HAV was excluded as the cause of the New Delhi epidemic by retrospective analysis of archived samples for evidence of HAV infection (2). The original observation of a common mode of transmission for hepatitis A and E is now eclipsed by our knowledge of the distinct epidemiology and molecular biology of HAV and HEV. Since the initial molecular cloning reported in 1990 (3) much has been learned about this virus. The unique features and our current understanding of HEV will be reviewed while highlighting issues requiring further investigation.

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  1. Infectious Diseases and Tumor Biology, Schering-Plough Research Institute, 2015 Galloping Hill Road, Kenilworth, NJ, 07033, USA

    Gregory R. Reyes

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  1. Gregory R. Reyes
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  1. University of Southern California, USA

    J.-H. James Ou

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© 2002 Springer Science+Business Media New York

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Reyes, G.R. (2002). The Molecular Biology of Hepatitis E Virus. In: Ou, JH.J. (eds) Hepatitis Viruses. Springer, Boston, MA. https://doi.org/10.1007/978-1-4615-0881-6_6

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  • DOI: https://doi.org/10.1007/978-1-4615-0881-6_6

  • Publisher Name: Springer, Boston, MA

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