Japanese Encephalitis

A special issue of Tropical Medicine and Infectious Disease (ISSN 2414-6366). This special issue belongs to the section "Vector-Borne Diseases".

Deadline for manuscript submissions: closed (16 June 2023) | Viewed by 1080

Special Issue Editor

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Guest Editor
Faculty of Health and Medical Sciences, Hokuriku University, Kanazawa 920-1180, Japan
Interests: Japanese encephalitis; vaccine; virology

Special Issue Information

Dear Colleagues,

This Special Issue focuses on the biology of Japanese encephalitis virus (JEV) and the wide range of recent advances in the diagnosis, epidemiology, and control of the infectious disease.

Japanese encephalitis is a viral infection caused by the Japanese encephalitis virus and results in severe acute encephalitis in humans. JEV belongs to the Flaviviridae family and was first isolated from an infected human brain in 1935 in Japan. Japanese encephalitis is widely distributed from the Far East to Southeast and South Asia. In recent years, outbreaks of Japanese encephalitis have been reported in Australia, where Japanese encephalitis had not been reported in the past, indicating the spread of the Japanese encephalitis virus outside of Asia.

In addition, 30,000 to 40,000 cases of Japanese encephalitis are reported annually worldwide, but the epidemic has already been largely prevented in Japan and South Korea due to routine vaccination.

Among the flaviviruses, JEV, West Nile virus, St. Louis encephalitis virus, and Murray Valley encephalitis virus are highly homologous and are called the Japanese encephalitis serotype group (Japanese encephalitis serocomplex). Therefore, there is a risk of cross-reactivity in the diagnosis of JEV infections in regions where these viruses are endemic.

Genotype shift of JEV in Southeast Asian countries and elsewhere has become apparent, and molecular studies are needed to analyze the ecology of JEV, especially the factors that contribute to its spread in infected countries.

An effective vaccine against JEV has been developed and proven to be effective, but other closely related flaviviruses can also protect against infection, and the development of a vaccine that is more effective as a single vaccination is expected.

Prof. Dr. Tomoyoshi Komiya
Guest Editor

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  • JEV
  • vaccines
  • epidemiology
  • immunology
  • treatment

Published Papers (1 paper)

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8 pages, 1920 KiB  
Characterization of Japanese Encephalitis Virus Isolated from Persistently Infected Mouse Embryo Cells
by Yume Kondo and Tomoyoshi Komiya
Trop. Med. Infect. Dis. 2024, 9(5), 117; https://doi.org/10.3390/tropicalmed9050117 - 16 May 2024
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Japanese encephalitis virus (JEV) has a positive-sense single-stranded RNA genome and belongs to the genus Flavivirus of the family Flaviviridae. Persistent JEV infection was previously shown in pig blood cells, which act as a natural reservoir of this virus. We aimed to [...] Read more.
Japanese encephalitis virus (JEV) has a positive-sense single-stranded RNA genome and belongs to the genus Flavivirus of the family Flaviviridae. Persistent JEV infection was previously shown in pig blood cells, which act as a natural reservoir of this virus. We aimed to determine the pathogenicity factors involved in persistent JEV infection by analyzing the pathogenicity and genome sequences of a virus isolated from a persistent infection model. We established persistent JEV infections in cells by inoculating mouse fetus primary cell cultures with the Beijing-1 strain of JEV and then performing repeated infected cell passages, harvesting viruses after each passage while monitoring the plaque size over 100 generations. The virus growth rate was compared among Vero, C6/36, and Neuro-2a cells. The pathogenicity was examined in female ICR mice at several ages. Additionally, we determined the whole-genome sequences. The 134th Beijing-1-derived persistent virus (ME134) grew in Vero cells at a similar rate to the parent strain but did not grow well in C6/36 or Neuro-2a cells. No differences were observed in pathogenicity after intracerebral inoculation in mice of different ages, but the survival time was extended in older mice. Mutations in the persistent virus genomes were found across all regions but were mainly focused in the NS3, NS4b, and 3′NCR regions, with a 34-base-pair deletion found in the variable region. The short deletion in the 3′NCR region appeared to be responsible for the reduced pathogenicity and growth efficiency. Full article
(This article belongs to the Special Issue Japanese Encephalitis)
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