戊型肝炎病毒
病毒学
戊型肝炎
肝炎
病毒
医学
黄疸
基因型
生物
免疫学
胃肠病学
基因
生物化学
作者
Noémie Oechslin,Darius Moradpour,Jérôme Gouttenoire
出处
期刊:Gut
[BMJ]
日期:2020-01-08
卷期号:69 (5): 796-798
被引量:7
标识
DOI:10.1136/gutjnl-2019-320206
摘要
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-Barre 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 …
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