Orosz L, Sárvári KP, Dernovics Á, Rosztóczy A, Megyeri K. Pathogenesis and clinical features of severe hepatitis E virus infection. World J Virol 2024; 13(2): 91580 [DOI: 10.5501/wjv.v13.i2.91580]
Corresponding Author of This Article
Klára Megyeri, MD, PhD, Associate Professor, Department of Medical Microbiology, University of Szeged, Dóm tér 10, Szeged 6720, Csongrád-Csanád, Hungary. megyeri.klara@med.u-szeged.hu
Research Domain of This Article
Gastroenterology & Hepatology
Article-Type of This Article
Review
Open-Access Policy of This Article
This article is an open-access article which was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution Non Commercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: http://creativecommons.org/licenses/by-nc/4.0/
World J Virol. Jun 25, 2024; 13(2): 91580 Published online Jun 25, 2024. doi: 10.5501/wjv.v13.i2.91580
Pathogenesis and clinical features of severe hepatitis E virus infection
László Orosz, Károly Péter Sárvári, Áron Dernovics, András Rosztóczy, Klára Megyeri
László Orosz, Károly Péter Sárvári, Áron Dernovics, Klára Megyeri, Department of Medical Microbiology, University of Szeged, Szeged 6720, Csongrád-Csanád, Hungary
András Rosztóczy, Department of Internal Medicine, Division of Gastroenterology, University of Szeged, Szeged 6725, Csongrád-Csanád, Hungary
Author contributions: Orosz L, Sárvári KP, Dernovics Á, Rosztóczy A, and Megyeri K collected the data and wrote the paper.
Conflict-of-interest statement: Authors declare no conflict of interests for this article.
Open-Access: This article is an open-access article that was selected by an in-house editor and fully peer-reviewed by external reviewers. It is distributed in accordance with the Creative Commons Attribution NonCommercial (CC BY-NC 4.0) license, which permits others to distribute, remix, adapt, build upon this work non-commercially, and license their derivative works on different terms, provided the original work is properly cited and the use is non-commercial. See: https://creativecommons.org/Licenses/by-nc/4.0/
Corresponding author: Klára Megyeri, MD, PhD, Associate Professor, Department of Medical Microbiology, University of Szeged, Dóm tér 10, Szeged 6720, Csongrád-Csanád, Hungary. megyeri.klara@med.u-szeged.hu
Received: December 31, 2023 Revised: February 8, 2024 Accepted: April 15, 2024 Published online: June 25, 2024 Processing time: 176 Days and 1.6 Hours
Abstract
The hepatitis E virus (HEV), a member of the Hepeviridae family, is a small, non-enveloped icosahedral virus divided into eight distinct genotypes (HEV-1 to HEV-8). Only genotypes 1 to 4 are known to cause diseases in humans. Genotypes 1 and 2 commonly spread via fecal-oral transmission, often through the consumption of contaminated water. Genotypes 3 and 4 are known to infect pigs, deer, and wild boars, often transferring to humans through inadequately cooked meat. Acute hepatitis caused by HEV in healthy individuals is mostly asymptomatic or associated with minor symptoms, such as jaundice. However, in immunosuppressed individuals, the disease can progress to chronic hepatitis and even escalate to cirrhosis. For pregnant women, an HEV infection can cause fulminant liver failure, with a potential mortality rate of 25%. Mortality rates also rise amongst cirrhotic patients when they contract an acute HEV infection, which can even trigger acute-on-chronic liver failure if layered onto pre-existing chronic liver disease. As the prevalence of HEV infection continues to rise worldwide, highlighting the particular risks associated with severe HEV infection is of major medical interest. This text offers a brief summary of the characteristics of hepatitis developed by patient groups at an elevated risk of severe HEV infection.
Core Tip: Hepatitis E virus (HEV) typically causes a self-limiting infection, but it can establish a persistent infection progressing into chronic hepatitis, cirrhosis or acute liver failure, particularly in individuals with compromised immune systems and preexisting liver diseases. In recent decades, the prevalence of hepatitis E has increased dramatically, and this trend continues unabated. Thus, a better understanding of the pathogenesis of hepatitis E and the development of more effective prevention and treatment strategies have become an urgent medical problem. We herein discuss the major features of HEV, the conditions predisposing to severe hepatitis E, and the underlying pathological immune processes.
