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Table of Contents

Published May 29, 2002

Talal Adhami, MD

Department of
Gastroenterology
and Hepatology

Gavin
Levinthal, MD

Department of
Gastroenterology
and Hepatology

Print Chapter

Viral liver disease, particularly with the current hepatitis C epidemic, presents a challenging and frequently encountered problem for practicing physicians. The literature on this subject is vast and rapidly increasing and new and promising therapies are being offered to patients.

Five viruses designated hepatitis A, B, C, D and E infect the liver and produce hepatitis as their primary clinical manifestation. Hepatitis G virus has been identified more recently, but its role in causing liver disease is not clearly defined. Other viruses, such as Epstein-Barr (EBV) and cytomegalovirus (CMV), may cause hepatitis as part of their clinical presentation but the liver is usually not the primary target organ.

This chapter covers hepatitis E and G/GBV-C. The other hepatitis viruses are discussed in separate chapters and can be viewed by clicking on the hyperlinks on the right-hand side of this page.

HEPATITIS E

Definition

Prevalence

Pathophysiology

Signs and
Symptoms

Diagnosis

Therapy

Outcomes

HEPATITIS G/GBV-C

Definition

Prevalence

Pathophysiology

Signs and
Symptoms

Diagnosis

Therapy

Outcomes

References

RELATED
CHAPTERS

Hepatitis A

Hepatitis B

Hepatitis C

Hepatitis D

Hepatitis E virus (HEV) is a 32 nm non-enveloped, single-strand RNA virus. It belongs to the family Calciviridae and genus Calcivirus. It is largely a waterborne epidemic disease.

HEV replicates in the hepatocytes and is excreted in stool. Transmission is predominantly by the fecal-oral route, usually through contaminated water. Although person-to-person transmission is rare, maternal-neonatal transmission has been documented.

The incubation period ranges from 15 to 60 days. The virus is detected in stools as early as 1 week prior to onset of clinical illness and persists for 1 to 2 weeks afterwards, during which stools are highly infectious.

Anti HBE antibody (IgM) appears soon after the onset of the clinical infection, immunoglobulin G (IgG) soon after that and IgG remains detectable for as long as 20 months.^1-3

HEV causes acute hepatitis. Constitutional and gastrointestinal symptoms are similar to those found in other types of viral hepatitis. The onset of symptoms tends to be abrupt and fever is uncommon. Prodromal symptoms improve or disappear with the onset of jaundice, although anorexia, malaise, and weakness may persist.

In the United States hepatitis E infection should be considered in all patients who present with acute hepatitis and have recently traveled to endemic areas. The disease is frequently cholestatic, with bilirubin and alkaline phosphatase elevations. The presence of anti-HBE antibody (IgM) in the serum confirms the disease and persists for at least 6 weeks after the peak of the illness. IgG antibody peaks soon after that and remains detectable for as long as 20 months.

Individuals traveling to endemic areas should be aware of the virus and avoid water, uncooked food, and contact with contaminated substances. Vaccination and immune globulin are not currently available but tests have been conducted in human volunteers. Treatment of the acute infection is supportive.

The course of HEV is usually more severe than other forms of epidemic jaundice. The fatality rate is generally 1% to 2%. It is, however, a very concerning illness in pregnant women as it may cause liver failure with a mortality rate of 20%. Prolonged viremia or fecal shedding are unusual and chronic infection does not occur.^4,5

Persistent HGV infection and chronic viremia have been documented, but there is no information on the nature or frequency of the acute infection or the consequences of persistent viremia.^7-9

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1. Buti M, Jardi R, Cotrina M, et al. Hepatitis E virus infection in acute hepatitis in Spain. J Virol Methods. 1995;55:49-54.
   
   
2. Mateos ML, Camarero C, Lasa E, Teruel JL, Mir N, Baquero F. Hepatitis E virus: relevance in blood donors and other risk groups. Vox Sang. 1998;75:267-269.
   
   
3. Arankalle VA, Chadha MS, Mehendale SM, Tungatkar SP. Epidemic hepatitis E: serological evidence for lack of intrafamilial spread. Indian J Gastroenterol. 2000;19:24-28.
   
   
4. Mast EE, Purdy MA, Krawczynski K. Hepatitis E. Baillieres Clin Gastroenterol. 1996;10:227-242.
   
   
5. Mast EE, Krawczynski K. Hepatitis E: an overview. Annu Rev Med. 1996;47:257-266.
   
   
6. Yoshiba M, Okamoto H, Mishiro S. Detection of the GBV-C hepatitis virus genome in serum from patients with fulminant hepatitis of unknown aetiology. Lancet. 1995;346:1131-1132.
   
   
7. Bricaire F. Hepatitis G virus: a new agent responsible for viral hepatitis. Bull Soc Pathol Exot. 1998;91:34-36.
   
   
8. Cheung RC, Keeffe EB, Greenberg HB. Hepatitis G virus: is it a hepatitis virus? West J Med. 1997;167:23-33.
   
   
9. Linnen J, Wages J Jr, Zhang-Keck ZY, et al. Molecular cloning and disease association of hepatitis G virus: a transfusion-transmissible agent. Science. 1996;271:505-508.
   

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