Viremia, fecal shedding and antibody responses to hepatitis E virus (HEV) infections are poorly understood. To better characterize HEV infections, these responses were examined in 67 patients with acute markers for hepatitis E who were admitted to the Infectious Disease Hospital in Kathmandu, Nepal in 1993. A single stool and multiple sera from each patient were examined using polymerase chain reaction to detect HEV RNA. Sera were also examined for antibodies to HEV. Viremia, fecal shedding, and IgM and IgG to HEV were detected in 93%, 70%, 79%, and 87% of 67 patients, respectively. Viremia or fecal shedding (or both) were detected in 14 patients from whom IgM and IgG to HEV were not detected. Viremia lasted at least 2 weeks in nearly all subjects and at least 39 days in 1 subject. Our results suggest that viremia is a common occurrence in patients infected with HEV.

No abstract

and Bruce L. InnisTo determine hepatitis E virus (HEV) infection and disease rates in the Kathmandu Valley of Nepal, serum was collected from 757 healthy Nepalese (ages 12 -48 years) during March and September 1992 and September 1993. At each visit, reports of interval illness were obtained. Sera were examined for IgG to HEV, using a commercially available kit. Seroconversion was used as a marker for HEV infection, and an episode of hepatitis E was defined as a history of jaundice with seroconversion. Seroprevalence ranged from 16% to 31% and increased with age, whereas both infection and disease rates decreased with age. Infection and disease rates were as high as 99/1000 and 45/1000 person-years, respectively. These results highlight the importance of sporadic hepatitis E as a public health problem among adolescents and young adults in this region. Hepatitis E virus (HEV) is believed to be the primary agentStudies to characterize the prevalence of IgG to HEV began as a result of the recent development of serologic assays for responsible for enterically transmitted non-A, non-B hepatitis. The most commonly reported signs and symptoms of this dis-HEV. Generally, the prevalence of antibody against HEV is low (0% -3%) in areas where no outbreaks have been reported ease include malaise, jaundice, dark urine, nausea, abdominal pain, fever, hepatomegaly, and vomiting [1]. The mortality rate and sporadic cases are rare (e.g., in the United States, Europe, Australia, Japan, New Zealand, South Africa, and Thailand) for hepatitis E is higher than for hepatitis A and ranges from 1% -3% among men and nonpregnant women to 12% -42% [5 -8]. By contrast, the prevalence of antibody against HEV is higher (10% -40%) in regions where outbreaks have been among pregnant women [2]. High rates of perinatal death are also associated with this disease [3,4]. Hepatitis E is an imreported and sporadic transmission occurs regularly, such as India, Nepal, and Tajikistan [6,7,9, 10]. Age-specific antibody portant health concern in nearly all under-developed regions of the world. No vaccines for hepatitis E have been developed, prevalence has been examined in India and Nepal [9, 10]. In both studies, antibody prevalence was found to increase with and prophylaxis with immune serum globulin appears to have little or no protective effect [2]. age until about age 30 years. No increase in antibody prevalence was apparent after age 30. No sex-dependent differences in antibody prevalence were observed; on the other hand, in older age groups, the numbers of women were too small to NOTE. Serum and medical histories were collected from 757 persons during March and September 1992 and September 1993. Case of hepatitis E was defined as episode of jaundice (self-reported during interview) along with acquisition of IgG to HEV during period examined. Infection was based on acquisition of HEV antibody during period examined. IgG to HEV was detected using ELISA developed by Diagnostic Biotechnology (Singapore). All 3 serum specimens from each individual were ...

No abstract

We have investigated the process of release of simian virus 40 (SV40) virions from several monkey kidney cell lines. High levels of virus release were observed prior to any significantly cytopathic effects in all cell lines examined, indicating that SV40 utilizes a mechanism for escape from the host cell which does not involve cell lysis. We demonstrate that SV40 release was polarized in two epithelial cell types (Vero C1008 and primary African green monkey kidney cells) grown on permeable supports; release of virus occurs almost exclusively at apical surfaces. In contrast, equivalent amounts of SV40 virions were recovered from apical and basal culture fluids of nonpolarized CV-1 cells. SV40 virions were observed in large numbers on apical surfaces of epithelial cells and in cytoplasmic smooth membrane vesicles. The sodium ionophore monensin, an inhibitor of vesicular transport, was found to inhibit SV40 release without altering viral protein synthesis or infectious virus production.