7% of deaths from HEV infection. Although the North Africa region accounted for 14.3% of all global infections, it only contributed 8.3% of global symptomatic cases and 8.1% of global deaths due to the younger average age of infection in that region. This article represents the first attempt to estimate the annual global impact of HEV infections caused by HEV genotypes 1 and 2 in Africa and Asia. We found that in 2005 HEV genotypes 1 and 2 accounted for approximately 20.1 million incident HEV infections, 3.4 Selleckchem Small molecule library million cases of symptomatic disease, 70,000 deaths, and 3,000 stillbirths. Incident infections increased through childhood to peak levels between the ages of 15 and 19 and fell thereafter to lower

levels in adulthood and disease

outcomes followed a similar pattern. This article is also the first to use meta-analytic techniques to summarize published reports into estimates of the rate of symptomatic illness given infection and the rate of death given symptomatic illness. We found strong evidence that the death rate differed between nonpregnant and pregnant symptomatic individuals, but we did not find evidence that the rate differed by continent of infection (Africa versus Asia). This study is limited in several respects. First, we did not attempt to estimate the burden of HEV genotypes 3 and 4. HEV genotype 3 is most prevalent Angiogenesis inhibitor in Europe and the United States, but its capacity to cause symptomatic illness and disease is not extensively documented.56, 57 If evidence becomes available, future

estimates of the burden of HEV should incorporate additional genotypes to create complete global estimates. Second, the data used to estimate the prevalence and incidence of HEV infection are sparse and uncertain. Disease incidence was by far the dominant source of uncertainty in our model, and this uncertainty led to wide credible intervals for our estimates of annual infections and outcomes. A large degree of uncertainty is inherent in the measurement of any emergent infection, and assuming interest in HEV increases, prevalence and incidence estimates of HEV infection will likely improve over time as the disease is increasingly recognized and measured across different countries. Third, our estimate of incidence and symptomatic illness relied on assumptions about HEV that are yet to be verified. selleck chemical Specifically, we assumed that all infections lead to seroconversion that can be detected by way of anti-HEV tests and that the presence of anti-HEV antibodies is lifelong. These assumptions were necessary to convert seroprevalence evidence into annual incidence estimates, but they may not be accurate. Several studies that we reviewed identified individuals during HEV outbreaks who reported jaundice and/or other symptoms indicative of infection but who exhibited no detectable serologic signs of infection.4, 38, 39 Furthermore, anti-HEV protection may not be lifelong.