Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2019 Jul 1;9(7):a031872.
doi: 10.1101/cshperspect.a031872.

Acute and Persistent Hepatitis E Virus Genotype 3 and 4 Infection: Clinical Features, Pathogenesis, and Treatment

Nassim Kamar  1 , Sven Pischke  2
Affiliations
Review

Acute and Persistent Hepatitis E Virus Genotype 3 and 4 Infection: Clinical Features, Pathogenesis, and Treatment

Nassim Kamar et al. Cold Spring Harb Perspect Med. .

Abstract

Hepatitis E virus (HEV) genotype (gt)3 and 4 infections are prevalent in industrialized and high-income countries. Although most HEV gt3 and gt4 infections are clinically silent, acute infection may be symptomatic in some patients. In persons with underlying liver disease and in elderly men, HEV infections may present as acute or acute-on-chronic liver failure. Chronic hepatitis may develop in immunosuppressed individuals, including transplant recipients, human immunodeficiency virus (HIV)-infected patients, and persons with hematologic malignancy undergoing chemotherapy, and may progress to life-threatening liver cirrhosis. Extrahepatic manifestations of infection may include neurological and renal disease. Although there is no approved specific therapy for the treatment of acute or chronic HEV gt3 or gt4 infection, off-label use of ribavirin appears to be capable of eliminating chronic HEV infection, and may reduce disease severity in patients suffering from acute liver failure.

PubMed Disclaimer

Figures

Figure 1.
Figure 1.
Possible clinical outcomes of genotype (gt)3/4 hepatitis E virus (HEV) infections.
Figure 2.
Figure 2.
Potential extrahepatic manifestations of genotype (gt)3/4 HEV infection. (A) Extrahepatic disease manifestations reported in the context of acute HEV infection. Underlying mechanisms of pathogenesis are unclear but could involve either (B) virus replication in tissues other than the liver, or (C) collateral damage from immune responses to HEV infection in the liver including, for example, immune complex formation or molecular mimicry resulting in nerve injury. (From Pischke et al. 2017; adapted, with permission, from Elsevier © 2017.)
See this image and copyright information in PMC

References

    1. Abravanel F, Lhomme S, Rostaing L, Kamar N, Izopet J. 2015. Protracted fecal shedding of HEV during ribavirin therapy predicts treatment relapse. Clin Infect Dis 60: 96–99. - PubMed
    1. Abravanel F, Barrague H, Dorr G, Saune K, Peron JM, Alric L, Kamar N, Izopet J, Champagne E. 2016. Conventional and innate lymphocytes response at the acute phase of HEV infection in transplanted patients. J Infect 72: 723–730. - PubMed
    1. Acharya SK, Dasarathy S, Kumer TL, Sushma S, Prasanna KS, Tandon A, Sreenivas V, Nijhawan S, Panda SK, Nanda SK, et al. 1996. Fulminant hepatitis in a tropical population: Clinical course, cause, and early predictors of outcome. Hepatology 23: 1448–1455. - PubMed
    1. Aggarwal R, Jameel S. 2011. Hepatitis E. Hepatology 54: 2218–2226. - PubMed
    1. Aggarwal R, Kini D, Sofat S, Naik SR, Krawczynski K. 2000. Duration of viraemia and faecal viral excretion in acute hepatitis E. Lancet 356: 1081–1082. - PubMed

LinkOut - more resources