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Published on: November 1, 2011
E and prM proteins of genotype V Japanese encephalitis virus are required for its increased virulence in mice
Shigeru Tajima1, Ken-Ichi Shibasaki1, Satoshi Taniguchi1
1Department of Virology 1, National Institute of Infectious Diseases, 1-23-1 Toyama, Shinjuku, Tokyo, 162-8640, Japan.
Abstract:
We previously showed that the Japanese encephalitis virus (JEV) genotype V (GV) strain Muar exhibits significantly higher virulence in mice than the genotype I (GI) JEV strain Mie/41/2002. In this study, we attempted to identify the region responsible for the increased virulence of GV JEV using recombinant intertypic and single mutant JEVs. Intertypic viruses containing the GV E region in the Mie/41/2002 backbone showed increased pathogenicity in mice. The amino acid at position 123 in the E protein (E123) of the Mie/41/2002 and GV JEVs was serine and histidine, respectively. A serine-to-histidine substitution at E123 of the Mie/41/2002 increased its virulence. However, histidine-to-serine changes at E123 in the intertypic mutants with the GV E region remained highly virulent. GV Muar prM-bearing mutants were also highly pathogenic in mice. Our results suggest that the E and prM proteins of GV JEV are responsible for the highly virulent characteristics of GV JEV.
Insights
Japanese encephalitis virus (JEV) genotype V (GV) shows higher virulence than genotype I (GI). The E and prM proteins of GV JEV are identified as key factors contributing to its increased pathogenicity in mice.
Area of Science:
- Virology
- Molecular Biology
- Pathogenesis
Background:
- Japanese encephalitis virus (JEV) exhibits varying virulence across genotypes.
- Genotype V (GV) JEV strain Muar is significantly more virulent in mice than Genotype I (GI) JEV strain Mie/41/2002.
Purpose of the Study:
- To identify the genetic regions responsible for the increased virulence of GV JEV.
- To elucidate the roles of specific viral proteins in JEV pathogenesis.
Main Methods:
- Construction and analysis of recombinant intertypic and single mutant JEV strains.
- Assessment of viral pathogenicity in murine models.
- Amino acid substitution analysis at position 123 of the E protein.
Main Results:
- Intertypic viruses with the GV E region in a GI backbone demonstrated increased pathogenicity.
- A serine-to-histidine substitution at E123 in the GI strain increased virulence.
- GV Muar prM-bearing mutants also exhibited high pathogenicity.
Conclusions:
- The E and prM proteins of GV JEV are critical determinants of its high virulence.
- Specific amino acid residues within these proteins contribute significantly to JEV pathogenesis.
