Japanese encephalitis virus (JEV) is an enveloped, positive-sense single-stranded RNA virus belonging to the genus Flavivirus. It is transmitted primarily by Culex tritaeniorhynchus mosquitoes and is the leading cause of viral encephalitis in Asia.
Genome and Virology
The JEV genome is approximately 11 kilobases long and encodes a single open reading frame. Translation of the genome produces a polyprotein that is co- and post-translationally cleaved into three structural proteins—capsid, premembrane/membrane and envelope—and seven nonstructural proteins (NS1, NS2A, NS2B, NS3, NS4A, NS4B and NS5). The envelope protein facilitates attachment to host cell receptors such as glycosaminoglycans and laminin receptors; viral entry occurs via clathrin-mediated endocytosis, and low endosomal pH triggers membrane fusion. Replication takes place on endoplasmic reticulum-derived membranes; NS3 functions as a serine protease and helicase, and NS5 acts as the RNA-dependent RNA polymerase and methyltransferase synthesising negative-strand intermediates and progeny genomes. Virions assemble in the endoplasmic reticulum, mature in the Golgi and are secreted by exocytosis. JEV exhibits genotype diversity (I–V) with geographic and temporal variation; genotypes I and III are currently dominant. The virus infects a range of cells including neurons, astrocytes and microglia in the central nervous system, as well as endothelial cells and mononuclear phagocytes.
Epidemiology and Public Health
JEV is maintained in an enzootic cycle involving wading birds and pigs as amplifying hosts and Culex mosquitoes as vectors. Human infection is incidental and occurs mainly in rural areas of East, Southeast and South Asia. An estimated 68 000 cases of Japanese encephalitis occur annually, with a fatality rate of 20 % to 30 % and neurologic sequelae in up to half of survivors. Clinical disease develops after an incubation period of 5‑15 days and begins with fever, headache and gastrointestinal symptoms; progression to encephalitis includes altered consciousness, seizures, focal neurologic deficits and movement disorders. Children are disproportionately affected. There is no specific antiviral therapy; management is supportive. Several effective vaccines are available, including inactivated mouse-brain-derived vaccines, cell culture‑derived inactivated vaccines and live attenuated vaccines such as SA14‑14‑2. Vaccination programmes in endemic countries have dramatically reduced disease incidence. Preventive measures also include vector control, pig immunisation and improved agricultural practices to reduce mosquito breeding.
Japanese encephalitis virus remains a serious threat in parts of Asia despite the availability of vaccines. Continued surveillance, vaccination and integrated vector management are essential to control this neurotropic arbovirus.
Related Terms: West Nile Virus, Tick-Borne Encephalitis Virus, Murray Valley Encephalitis Virus, Flavivirus, Culex tritaeniorhynchus