Japanese encephalitis 医学文献 百度医学 brain anoxia

Abstract japanese encephalitis (JE) is a disease of the CNS caused by japanese encephalitis virus (JEV). The disease appears in the form of frequent outbreaks in most south- and southeast asian countries and the virus has become endemic in several areas. There is no licensed therapy available and disease control by vaccination is considered to be most effective. Mouse brain-derived inactivated JE vaccines, although immunogenic, have several limitations in terms of safety, availability and requirement for multiple doses. Owing to these drawbacks, the WHO called for the development of novel, safe and more efficacious JE vaccines.


Several candidate vaccines have been developed and at least three of them that demonstrated strong immunogenicity after one or two doses of the vaccine in animal models were subsequently tested in various clinical trials.Brain anoxia one of these vaccines, IMOJEV(®) (JE-CV and previously known as chimerivax™-JE), is a novel recombinant chimeric virus vaccine, developed using the yellow fever virus (YFV) vaccine vector YFV17D, by replacing the cdna encoding the envelope proteins of YFV with that of an attenuated JEV strain SA14-14-2. IMOJEV was found to be safe, highly immunogenic and capable of inducing long-lasting immunity in both preclinical and clinical trials. Moreover, a single dose of IMOJEV was sufficient to induce protective immunity, which was similar to that induced in adults by three doses of JE-VAX(®), a mouse brain-derived inactivated JE vaccine. Recently, phase III trials evaluating the immunogenicity and safety of the chimeric virus vaccine have been successfully completed in some JE-endemic countries and the vaccine manufacturers have filed an application for vaccine registration.Brain anoxia IMOJEV may thus be licensed for use in humans as an improved alternative to the currently licensed JE vaccines.

Japanese encephalitis virus (JEV) is the principal cause of viral encephalitis. The predominance of children among patients with encephalitis in areas where JEV is endemic that do not have immunization programs suggests that acquired immunity is critical in protecting adults against symptomatic JEV encephalitis. We characterized and compared the T cell response to nonstructural (NS) protein 3 between healthy individuals naturally exposed to JEV and patients in the convalescent phase of JEV encephalitis. The NS3 protein, used as a fusion to the 11-amino acid protein transduction domain of human immunodeficiency virus tat, elicited CD4(+) and T helper-dependent CD8(+) T cell responses.Brain anoxia the production of interferon (IFN)- gamma by responding T cells was significantly higher in healthy donors than in patients, correlating strongly with acquired protective immunity to JEV. Furthermore, a striking inverse association between IFN- gamma levels and the severity of postencephalitic sequelae in patients implicated a role of IFN- gamma in recovery.

Griffithsin (GRFT) is a broad-spectrum antiviral protein that is effective against several glycosylated viruses. Here, we have evaluated the in vitro and in vivo antiviral activities of GRFT against japanese encephalitis virus (JEV) infection. In vitro experiments showed that treatment of JEV with GRFT before inoculation of BHK-21 cells inhibited infection in a dose-dependent manner, with 99% inhibition at 100μg/ml and a 50% inhibitory concentration (IC(50)) of 265ng/ml (20 nm).Brain anoxia binding assays suggested that binding of GRFT to JEV virions inhibited JEV infection. In vivo experiment showed that GRFT (5mg/kg) administered intraperitoneally before virus infection could completely prevent mortality in mice challenged intraperitoneally with a lethal dose of JEV. Our study also suggested that GRFT prevents JEV infection at the entry phase by targeting the virus. Collectively, our data demonstrate that GRFT is an antiviral agent with potential application in the development of therapeutics against JEV or other flavivirus infections.

ABSTRACT human serum was collected from a sample cohort of 494 persons residing in the five study areas in the chiangmai valley, thailand. The sample was bled before the start of the 1970 japanese encephalitis epidemic, and three times during the epidemic year.Brain anoxia the purpose was to define the degree of past and present human exposure to japanese encephalitis virus (JEV), and to study the seroepidemiologic interrelationships existing between dengue and JEV. Analysis of village and urban sera revealed that JEV transmission had probably been occurring for many years. JEV antibody prevalence rose with age; by age 30 nearly everyone of both sexes had been infected. Serologic and entomologic data further revealed that dengue transmission before 1970 had been occurring more in and near chiangmai city than in rural districts, but there was no clinical or serologic evidence of dengue infections occurring during 1970. Inapparent JEV infections occurred in 6% of the sample cohort.Brain anoxia fevers and respiratory illnesses occurred only slightly more frequently in persons having JEV infections than in those not infected. The valley residence, age, sex, and antibody response patterns of persons experiencing inapparent JEV infections were very similar to the 1970 encephalitis cases. Inapparent JEV infections occurred throughout the study year. The ratio of inapparent to apparent JEV infections was estimated to be 300: 1 under age 40. Primary or secondary-type hemagglutination-inhibition antibody responses after JEV infection occurred in individuals in each age group depending upon the absence or presence, respectively, of pre-existing dengue antibody. Evidence is presented which suggests that the incidence rate of JEV infections in persons with previous dengue infections) was at least as great as that in persons without previous dengue exposure.Brain anoxia

Aims: to investigate if two important epidemic viral encephalitis in children, enterovirus 71 (EV71) encephalomyelitis and japanese encephalitis (JE) whose clinical and pathological features may be nonspecific and overlapping, could be distinguished. Methods: tissue sections from the central nervous system of infected cases were examined by light microscopy. Immunohistochemistry and in situ hybridization. Results: all 13 cases of EV71 encephalomyelitis collected from asia and france invariably showed stereotyped distribution of inflammation in the spinal cord, brainstem, hypothalamus, cerebellar dentate nucleus and, to a lesser extent, cerebral cortex and meninges. Anterior pons. Corpus striatum, thalamus, temporal lobe, hippocampus and cerebellar cortex were always uninflamed.Brain anoxia in contrast, the eight JE cases studied showed inflammation involving most neuronal areas of the central nervous system, including the areas that were uninflamed in EV71 encephalomyelitis. Lesions in both infections were nonspecific, consisting of perivascular and parenchymal infiltration by inflammatory cells, oedematous/necrolytic areas. Microglial nodules and neuronophagia. Viral inclusions were absent. Conclusions: immunohistochemistry and in situ hybridization assays were useful to identify the causative virus, localizing viral antigens and RNA, respectively, almost exclusively to neurones. The stereotyped distribution of inflammatory lesions in EV71 encephalomyelitis appears to be very useful to help distinguish it from JE.Brain anoxia