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Japanese encephalitis ((日本語:日本脳炎, ''Nihon-nōen''))— abbreviated ''JE'', formerly known as Japanese B encephalitis to distinguish it from Economo's A encephalitis—is a disease caused by the mosquito-borne Japanese encephalitis virus (JEV). The Japanese encephalitis virus (JEV) itself is a virus from the family Flaviviridae, part of the ''Japanese encephalitis serocomplex'' of 9 genetically and antigenically related viruses,〔http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3337329/#R1〕 some which are particularly severe in horses, and four known to infect humans including West Nile virus. Domestic pigs and wild birds (especially herons) are reservoirs of the virus; transmission to humans may cause severe symptoms. Amongst the most important vectors of this disease are the mosquitoes ''Culex tritaeniorhynchus'' and ''Culex vishnui''. This disease is most prevalent in Southeast Asia and East Asia. ==Signs and symptoms== Japanese encephalitis has an incubation period of 5 to 15 days and the vast majority of infections are asymptomatic: only 1 in 250 infections develop into encephalitis. Severe rigors may mark the onset of this disease in humans. Fever, headache and malaise are other non-specific symptoms of this disease which may last for a period of between 1 and 6 days. Signs which develop during the acute encephalitic stage include neck rigidity, cachexia, hemiparesis, convulsions and a raised body temperature between . Mental retardation is usually developed. Mortality of this disease varies but is generally much higher in children. Transplacental spread has been noted. Lifelong neurological defects such as deafness, emotional lability and hemiparesis may occur in those who have had central nervous system involvement. In known cases some effects also include nausea, headache, fever, vomiting and sometimes swelling of the testicles. Increased microglial activation following Japanese Encephalitis infection has been found to influence the outcome of viral pathogenesis. Microglia are the resident immune cell In a murine model of JE, it was found that in the hippocampus and the striatum, the number of activated microglia was more than anywhere else in the brain closely followed by that in the thalamus. In the cortex, the number of activated microglia was significantly less when compared with other regions of the mouse brain. An overall induction of differential expression of proinflammatory cytokines and chemokines from different brain regions during a progressive Japanese Encephalitis infection was also observed. Although the net effect of the proinflammatory mediators is to kill infectious organisms and infected cells as well as to stimulate the production of molecules that amplify the mounting response to damage, it is also evident that in a nonregenerating organ such as brain, a dysregulated innate immune response would be deleterious. In JE the tight regulation of microglial activation appears to be disturbed, resulting in an autotoxic loop of microglial activation that possibly leads to bystander neuronal damage. In animals, key signs include infertility and abortion in pigs, neurological disease in horses and systemic signs including fever, lethargy and anorexia.〔(Japanese Encephalitis Virus ) reviewed and published by WikiVet, accessed 11 October 2011.〕 抄文引用元・出典: フリー百科事典『 ウィキペディア（Wikipedia）』 ■ウィキペディアで「Japanese encephalitis」の詳細全文を読む スポンサード リンク
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