Japanese Encephalitis is a disease caused by the mosquito-borne Japanese Encephalitis Virus (JEV). JE is a mosquito-borne viral infection of the central nervous system in humans and animals, specifically horses and cattle. Infectious mosquito can spread the virus to humans when humans were bitten. Japanese Encephalitis can cause fever, headache, confusion, seizures, and, in some cases, death.
Japanese encephalitis virus (JEV) is the leading cause of vaccine-preventable encephalitis in Asia and the western Pacific. JEV is a flavivirus, which is closely related to Dengue, Yellow Fever and West Nile Encephalitis. There are five genotypes and one serotype of JEV: GI-GV. Genotypes GIb and GII are associated with temperate climates. GIb is believed to be the dominant JEV genotype in Asia. The genomic RNA of JEV encodes a single long open reading frame(ORF), and a polyprotein translated from the genome is cleaved co- and posttranslationally by host and viral proteases to yield 3 structural proteins: the core, precursor membrane (prM), and envelope (E) proteins, and seven nonstructural proteins, NS1, NS2A, NS2B, NS3, NS4A, NS4B, and NS5.
- Capsid protein (C protein) Plays a role in virus budding by binding to the cell membrane and gathering the viral RNA into a nucleocapsid that forms the core of a mature virus particle. During virus entry, may induce genome penetration into the host cytoplasm after hemifusion induced by the surface proteins. Can migrate to the cell nucleus where it modulates host functions. Overcomes the anti-viral effects of host EXOC1 by sequestering and degrading the latter through the proteasome degradation pathway.
- Envelope protein (E protein) Binds to host cell surface receptor and mediates fusion between viral and cellular membranes. Envelope protein is synthesized in the endoplasmic reticulum in the form of heterodimer with protein prM. They play a role in virion budding in the ER, and the newly formed immature particle is covered with 60 spikes composed of heterodimer between precursor prM and envelope protein E. The virion is transported to the Golgi apparatus where the low pH causes dissociation of PrM-E heterodimers and formation of E homodimers. prM-E cleavage is inefficient, and many virions are only partially matured. These uncleaved prM would play a role in immune evasion.
- Nonstructural protein (NS protein) Non-structural protein 1: Involved in immune evasion, pathogenesis and viral replication. Once cleaved off the polyprotein, is targeted to three destinations: the viral replication cycle, the plasma membrane and the extracellular compartment; Non-structural protein 2A: Component of the viral RNA replication complex that functions in virion assembly and antagonizes the host alpha/beta interferon antiviral response; Non-structural protein 4A: Regulates the ATPase activity of the NS3 helicase activity; Non-structural protein 4B: Induces the formation of ER-derived membrane vesicles where the viral replication takes place.
- pre-Membrane/ Membrane (PreM/M protein) Acts as a chaperone for envelope protein E during intracellular virion assembly by masking and inactivating envelope protein E fusion peptide. prM is the only viral peptide matured by host furin in the trans-Golgi network probably to avoid catastrophic activation of the viral fusion activity in acidic Golgi compartment prior to virion release. prM-E cleavage is inefficient, and many virions are only partially matured. These uncleaved prM would play a role in immune evasion.
Japanese encephalitis virus (JEV) is an enveloped, single-stranded RNA virus, it belongs to the genus Flavivirus within the family Flaviviridae. Generally, JEV occurs as a single serotype, but considerable antigenic variation is also observed. Scientists have been isolated more than 50 strains in Japan. There are several diagnostic methods to detect JEV. According to a latest report, more and more scientists prefer to use fewer materials and less technical skills to detect the virus. More attention was given to PCR, RT-LAMP, ELISA, and immunochromatography. Flavivirus-specific monoclonal antibodies can also be used to detect JEV antigen in serum, and immunohistochemistry (IHC) can be used to detect JEV antigen in fetal tissues. Meanwhile, serological tests which including immunofluorescent antibody (IFA), virus neutralization (VN), complement fixation (CF), hemagglutination inhibition (HI), and ELISA can be used to establish the prevalence of infection in a population or individual diagnosis purpose. Therefore, serological diagnoses should be carried out very careful because cross-reactivity with other flaviviruses might occur and the maternal antibodies may be present for up to 8 weeks in piglets.
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