*Gretchen Stevens and Steven T. Wiersma are staff members of WHO. The authors alone are responsible for the views expressed in this publication and they do not necessarily represent the decisions, policy, or views of WHO.
Article first published online: 27 MAR 2012
Copyright © 2011 American Association for the Study of Liver Diseases
Volume 55, Issue 4, pages 988–997, April 2012
How to Cite
Rein, D. B., Stevens, G. A., Theaker, J., Wittenborn, J. S. and Wiersma, S. T. (2012), The global burden of hepatitis E virus genotypes 1 and 2 in 2005. Hepatology, 55: 988–997. doi: 10.1002/hep.25505
Potential conflict of interest: Nothing to report.
Supported by the Expanded Programme on Immunization (EPI), Department of Immunization, Vaccines and Biologicals (IVB), Family and Community Health (FCH), World Health Organization, through Agreement for Performance of Work (APW) Ref. no. I8-APW-189.
- Issue published online: 27 MAR 2012
- Article first published online: 27 MAR 2012
- Accepted manuscript online: 26 NOV 2011 06:45AM EST
- Manuscript Accepted: 13 NOV 2011
- Manuscript Received: 6 SEP 2011
We estimated the global burden of hepatitis E virus (HEV) genotypes 1 and 2 in 2005. HEV is an emergent waterborne infection that causes source-originated epidemics of acute disease with a case fatality rate thought to vary by age and pregnancy status. To create our estimates, we modeled the annual disease burden of HEV genotypes 1 and 2 for 9 of 21 regions defined for the Global Burden of Diseases, Injuries, and Risk Factors Study (the GBD 2010 Study), which represent 71% of the world's population. We estimated the seroprevalence of anti-HEV antibody and annual incidence of infection for each region using data from 37 published national studies and the DISMOD 3, a generic disease model designed for the GBD Study. We converted incident infections into three mutually exclusive results of infection: (1) asymptomatic episodes, (2) symptomatic disease, and (3) death from HEV. We also estimated incremental cases of stillbirths among infected pregnant women. For 2005, we estimated 20.1 (95% credible interval [Cr.I.]: 2.8-37.0) million incident HEV infections across the nine GBD Regions, resulting in 3.4 (95% Cr.I.: 0.5-6.5) million symptomatic cases, 70,000 (95% Cr.I.: 12,400-132,732) deaths, and 3,000 (95% Cr.I.: 1,892-4,424) stillbirths. We estimated a probability of symptomatic illness given infection of 0.198 (95% Cr.I.: 0.167-0.229) and a probability of death given symptomatic illness of 0.019 (95% Cr.I.: 0.017-0.021) for nonpregnant cases and 0.198 (95% Cr.I.: 0.169-0.227) for pregnant cases. Conclusion: The model was most sensitive to estimates of age-specific incidence of HEV disease. (HEPATOLOGY 2012)