Over 20 million individuals infected with hepatitis E in Asia and Africa
New research funded by the World Health Organization (WHO) estimates that 20.1 million individuals were infected with hepatitis E virus (HEV) genotypes 1 and 2 across 9 world regions in 2005. According to findings available in the April issue of Hepatology, a journal published by Wiley-Blackwell on behalf of the American Association for the Study of Liver Diseases, there were 3.4 million symptomatic cases, 70,000 deaths, and 3,000 stillbirths from HEV that year in countries throughout Asia and Africa.
Unlike hepatitis virus B and C strains that lead to chronic disease states, HEV causes acute illness. Previous studies show HEV genotypes 1 and 2 specifically infect humans, and are associated with large outbreaks in developing countries where sanitation conditions are poor. There is evidence that HEV increases mortality risk among pregnant women. While a safe and effective HEV vaccine has been developed, it has not been widely implemented.
“Our study represents the first attempt to estimate the annual global impact of hepatitis E,” said lead author Dr. David Rein of the social science research organization NORC at the University of Chicago. Estimates were created by modeling the disease burden of HEV genotypes 1 and 2 in the 9 regions, representing 71% of the world’s population. Based on published evidence the team - a collaboration between researchers from NORC, WHO and RTI International - also estimated annual incidence of infection to determine symptomatic, asymptomatic, and mortality cases.
The team determined that the prevalence pattern of HEV was consistent across the regions, with the largest incident increase occurring in those between the ages of 5 and 20 years. The average age of infection was 17 years with the lowest age of infection in North Africa (8 years) and highest in East Asia (21 years).
Of the more than 20 million people infected with HEV, 61% of the cases occurred in East and South Asia, two regions which also accounted for 65% of deaths from HEV. Researchers also noted that North Africa accounted for 14% of all global HEV infections, but only 8.3% of symptomatic cases and 8% of deaths, which the authors attribute to the younger average age of infection in that region.
Hepatitis E virus (HEV) is a major cause of hepatitis. We evaluated five HEV antibody diagnostic assays by using outbreak specimens. The Abbott immunoglobulin G (IgG), Genelabs IgG, and Walter Reed Army Institute of Research (WRAIR) IgM assays were about 90% sensitive; the Abbott IgG and WRAIR total Ig and IgM assays were more than 90% specific.
Hepatitis E virus (HEV) is the principal cause of acute hepatitis on the Indian subcontinent, in southeastern and central Asia, in the Middle East, in Mexico, and in parts of Africa. It is associated with the consumption of fecally contaminated drinking water. Recent outbreaks have occurred in Iraq, Chad, Sudan, and India. Although HEV is associated with a low case fatality rate in the general population, pregnant women in the second and third trimesters are at greater risk (case fatality rates of 10 to 24%) for fulminant hepatitis and fetal loss.
HEV has not been cultured in vitro, and most enzyme immunoassays (EIAs) for HEV infection are based on either recombinant HEV proteins or synthetic peptides. These assays have varied significantly, and assays based on open reading frame 2 (ORF2) were shown to be more sensitive in detecting anti-HEV than those based on ORF3. These recombinant-protein-based tests have detected anti-HEV in 90 to 95% of symptomatic HEV cases.
The authors caution there are limitations to the study which only estimated incidence of HEV genotypes 1 and 2, leaving out genotype 3 that prevalently occurs in Europe and the U.S., and genotype 4. “Future HEV estimates should include genotypes 3 and 4 to provide a complete picture of the global burden of HEV,” concludes Dr. Rein.
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HEV infection was first described as a waterborne disease, transmitted through drinking of fecally contaminated water. However, recent investigations have not consistently found well-defined water sources of HEV, suggesting other possible modes of transmission. These other transmission modes may be related to the level of population immunity, sanitary conditions, living conditions, and other factors. In sporadic hepatitis E, modes of transmission are even less clear and are generally not identified. Transmission by blood transfusion has been demonstrated, but this route of transmission is not thought to be frequent. There is growing evidence that HEV in outbreaks may be effectively transmitted person to person. It is also noteworthy that, in some populations, HEV appears to be easily transmissible, with up to 76% of persons aged >20 years having serological evidence of infection but not having significant disease.
HEV infection is a major public health problem in many developing countries. The first documented outbreak of hepatitis E in India resulted in 29,300 cases of jaundice. Other notable large outbreaks, resulting in significant morbidity, include outbreaks in India and China that resulted in 79,000 cases and 119,000 cases, respectively. Since genotyping of HEV strains became common in the mid-1990s, hepatitis outbreaks in developing countries have been caused primarily by HEV genotype 1, with outbreaks in Mexico and western Africa caused by genotype 2 and sporadic cases in Asia caused by genotype 4. In countries with suboptimal sanitary conditions, HEV is the single most important cause of sporadic and epidemic hepatitis. In susceptible populations, high attack rates have been observed. Case-fatality rates in epidemics range from 0.2% to 4%, but pregnant women, especially during the third trimester, may have a case-fatality rate of 10%–25%.
Full Citation: “The Global Burden of Hepatitis E Virus Genotypes 1 and 2 in 2005.” David B. Rein, Gretchen Stevens, Jordan Theaker, John S. Wittenborn and Steven T. Wiersma. Hepatology; Published Online: November 26, 2011 (DOI: 10.1002/hep.25505);
Author Contact: To arrange an interview with Dr. Rein, please contact Raymond Boyer at .(JavaScript must be enabled to view this email address) or at 312-330-6433.
This study is published in Hepatology. Media wishing to receive a PDF of the article may contact .(JavaScript must be enabled to view this email address).
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