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Hepatitis E virus (HEV) infection is a major cause of acute hepatitis and jaundice worldwide.1 HEV genotypes (gt) 1 and 2 are transmitted through the faecal-oral route and cause primarily waterborne epidemics, whereas the zoonotic gt 3 and 4 are transmitted via the consumption of undercooked or raw pork or game meat. Infection of immunocompromised patients with HEV gt 3 may result in chronic hepatitis E and the development of cirrhosis. Beyond liver disease, HEV can cause a number of extrahepatic manifestations, including neurological complications such as neuralgic amyotrophy and Guillain-Barré syndrome. Very similar to hepatitis A virus (HAV), HEV harbours a positive-strand RNA genome, and both are found as so-called quasi-enveloped virions in blood and as naked virions in bile and faeces.2
Although HEV is known to be enterically transmitted, there was limited evidence for infection of the gastrointestinal tract. In a study published in this journal, Marion et al addressed this question by the development of different cell culture systems, including primary human small intestinal epithelial cells, polarised primary enterocytes and intestinal tissue specimens obtained from small bowel resections.3 Using primary HEV gt 1 and 3 isolates from stool samples of patients with hepatitis E as well as virus derived from the gt 3 Kernow-C1 p6 clone, the …
Contributors NO, DM and JG wrote the manuscript.
Funding The authors acknowledge support by the Swiss National Science Foundation (grant number 31003A_179424) and the Gilead Sciences International Research Scholars Program in Liver Disease.
Competing interests None declared.
Patient consent for publication Not required.
Provenance and peer review Commissioned; internally peer reviewed.
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