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Chapter 4 : The Global Impact of Hepatitis E: New Horizons for an Emerging Virus

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Abstract:

An appreciation of the role of the fifth human hepatitis virus, hepatitis E virus (HEV), as an important cause of acute, and occasionally chronic, hepatitis in humans has increased in recent years. Hepatitis viruses have long been implicated as the cause of substantial morbidity and mortality in the developing world, through both sporadic and epidemic disease. The predictable seasonal outbreaks, coincident with the monsoon rains, have provided numerous opportunities to study risk factors for HEV infection, the clinical course of hepatitis E disease, and the characteristics of the virus. In 1980, by excluding hepatitis A virus (HAV) and hepatitis B virus (HBV) as causes of a large 1955 to 1956 hepatitis epidemic in India, two groups independently reported the hypothesis of a novel, enterically transmitted non-A, non-B (ET-NANB) virus. As HEV shares certain morphologic and biophysical properties with members of the family, it was initially classified as a calicivirus. Electron microscopy has been used to detect virus-like particles in the livers of patients with HEV-attributable fulminant hepatitis. The age- and gender-matched control group in a case control study in Sudan found a high (18%) anti-HEV IgG seroprevalence among children in the general population. Immunologic changes of pregnancy, such as the down-regulation of TH1 cytokines, and hormonal changes may also influence pathogenesis. A recent case report of fulminant hepatitis due to infection with an HEV genotype 3 strain in a patient in Spain has suggested that an important cofactor was the usage of hormonal contraceptives.

Citation: Labrique A, Kuniholm M, Nelson K. 2010. The Global Impact of Hepatitis E: New Horizons for an Emerging Virus, p 53-93. In Scheld W, Grayson M, Hughes J (ed), Emerging Infections 9. ASM Press, Washington, DC. doi: 10.1128/9781555816803.ch4

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Hepatitis E virus
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Figures

Image of Figure 1.
Figure 1.

Phylogenetic tree of complete genomic sequences of HEV, representing all four genotypes of HEV. Swine (Sw) and human (Hu) sources of strains are indicated by a suffix following the country in which the isolate was identified. Genotype assignments are indicated in black circles on each primary branch. The novel avian group has been indicated as an outgroup, and the line showing the actual distance from the four HEV genotypes has been truncated. A horizontal scale bar has been included to indicate relative genetic distances. Figure drawn with MEGA software, reprinted with permission from reference .

Citation: Labrique A, Kuniholm M, Nelson K. 2010. The Global Impact of Hepatitis E: New Horizons for an Emerging Virus, p 53-93. In Scheld W, Grayson M, Hughes J (ed), Emerging Infections 9. ASM Press, Washington, DC. doi: 10.1128/9781555816803.ch4
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Image of Figure 2.
Figure 2.

IEM of HEV particles and a suggested structural model. Acute-phase HEV by IEM reveals ~27- to 34-nm-diameter antibody-coated particles. The micrograph was modified from CDC internet resources (http://www.cdc.gov/ncidod/diseases/hepatitis/slideset/index.htm). The structural cartoon was modified with permission from reference .

Citation: Labrique A, Kuniholm M, Nelson K. 2010. The Global Impact of Hepatitis E: New Horizons for an Emerging Virus, p 53-93. In Scheld W, Grayson M, Hughes J (ed), Emerging Infections 9. ASM Press, Washington, DC. doi: 10.1128/9781555816803.ch4
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Image of Figure 3.
Figure 3.

Schematic diagram of the HEV genome, illustrating the three ORFs (ORF1 to ORF3), a 5′ cap, and a 3’ poly(A) tail. Indicated are the regions of ORF1 which encode nonstructural proteins such as methyltransferase (MTR), protease (PRO), helicase (HEL), and RNA-dependent RNA polymerase (POL) and, in ORF2, the structural capsid (CP) domain. Modified with permission from reference .

Citation: Labrique A, Kuniholm M, Nelson K. 2010. The Global Impact of Hepatitis E: New Horizons for an Emerging Virus, p 53-93. In Scheld W, Grayson M, Hughes J (ed), Emerging Infections 9. ASM Press, Washington, DC. doi: 10.1128/9781555816803.ch4
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Image of Figure 4.
Figure 4.

An overview of the course of HEV infection based on studies of nonhuman primates, human volunteers, and human outbreak studies. The dotted line represents the trajectory of anti-HEV IgM after infection at 0 months. The dashed line follows the course of anti-HEV IgG up to 5 months postinfection. The top arrows define the acute and convalescent phases of the clinical illness. The gray bar shows the time during which HEV particles may be detectable in an infected patient’s stool, the black bar represents the period when HEV antigen may be detectable in the liver, and the hatched bar represents the period of serum viremia, as detectable by PCR. The earliest sign of infection is viral replication in the liver, detectable by immunofluorescence of HEV antigen, IEM of HEV particles, or PCR of HEV RNA. Used with permission from reference .

Citation: Labrique A, Kuniholm M, Nelson K. 2010. The Global Impact of Hepatitis E: New Horizons for an Emerging Virus, p 53-93. In Scheld W, Grayson M, Hughes J (ed), Emerging Infections 9. ASM Press, Washington, DC. doi: 10.1128/9781555816803.ch4
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Image of Figure 5.
Figure 5.

Epidemic curve of new clinical cases of hepatitis E, as recorded during the landmark 1955 to 1956 Delhi outbreak, indicating a clear point source exposure with no secondary peak following the initial exposure. The outbreak was caused by severe contamination of the drinking water supply by fecal waste, resulting in over 29,000 cases of hepatitis E. Modified with permission from reference .

Citation: Labrique A, Kuniholm M, Nelson K. 2010. The Global Impact of Hepatitis E: New Horizons for an Emerging Virus, p 53-93. In Scheld W, Grayson M, Hughes J (ed), Emerging Infections 9. ASM Press, Washington, DC. doi: 10.1128/9781555816803.ch4
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Image of Figure 6.
Figure 6.

Age-specific seroprevalence of anti-HEV (by quantitative total Ig assay) in a representative rural population of Bangladesh. This pattern is typical of seroepidemiologic studies conducted in most of South Asia, showing relatively low levels of antibodies in early infancy and childhood and peaking in the third and fourth decades of life after a sharp rise in adolescence. Modified with permission from reference .

Citation: Labrique A, Kuniholm M, Nelson K. 2010. The Global Impact of Hepatitis E: New Horizons for an Emerging Virus, p 53-93. In Scheld W, Grayson M, Hughes J (ed), Emerging Infections 9. ASM Press, Washington, DC. doi: 10.1128/9781555816803.ch4
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