ArticlePLoS pathogens2019
NS2B/NS3 mutations enhance the infectivity of genotype I Japanese encephalitis virus in amplifying hosts.
Article in PLoS pathogens, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers, 1 of them a synthesis that pooled it.
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Who cites it
23 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Mosquito vector competence for Japanese encephalitis virus: a systematic review and meta-analysis update.Parasites & vectors · 2025Pooled it
- Article
- Superinfection Exclusion Between Japanese Encephalitis Virus Genotypes I and III Occurs During Viral Entry.Archives of virology · 2026Article
- Detection of Japanese encephalitis virus inParasite epidemiology and control · 2026Article
- Host-specific ubiquitination of prM orchestrates ESCRT recruitment to mediate efficient Japanese Encephalitis Virus assembly in vertebrates.PLoS pathogens · 2026Article
- Discerning dangerous gain of function: most gain of function (GoF) research does not involve infectious microbes.Frontiers in bioengineering and biotechnology · 2026Review
- Construction and Evaluation of a Chimeric Japanese Encephalitis Virus Vaccine Candidate Strain with Chaoyang Virus as the Backbone.Vaccines · 2025Article
- A Japanese encephalitis virus biological clone with anThe Journal of general virology · 2025Article
- DDX3 Regulates the Cap-Independent Translation of the Japanese Encephalitis Virus via Its Interactions with PABP1 and the Untranslated Regions of the Viral Genome.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025Article
- NS2B-D55E and NS2B-E65D Variations Are Responsible for Differences in NS2B-NS3 Protease Activities Between Japanese Encephalitis Virus Genotype I and III in Fluorogenic Peptide Model.International journal of molecular sciences · 2024Article
- Epitope(s) involving amino acids of the fusion loop of Japanese encephalitis virus envelope protein is(are) important to elicit protective immunity.Journal of virology · 2024Article
- Comparative genomics of Japanese encephalitis virus shows low rates of recombination and a small subset of codon positions under episodic diversifying selection.PLoS neglected tropical diseases · 2024Article
- Advances in viral encephalitis: Viral transmission, host immunity, and experimental animal models.Zoological research · 2023Review
- Article
- Re-Examining the Importance of Pigs in the Transmission of Japanese Encephalitis Virus.Pathogens (Basel, Switzerland) · 2022Review
- Article
- Review
- The feasibility of field collected pig oronasal secretions as specimens for the virologic surveillance of Japanese encephalitis virus.PLoS neglected tropical diseases · 2021Article
- Japanese Encephalitis Virus NS2B-3 Protein Complex Promotes Cell Apoptosis and Viral Particle Release by Down-Regulating the Expression of AXL.Virologica Sinica · 2021Article
- Potential Role of Birds in Japanese Encephalitis Virus Zoonotic Transmission and Genotype Shift.Viruses · 2021Review
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Authors and funding
13 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Genotype I (GI) virus has replaced genotype III (GIII) virus as the dominant Japanese encephalitis virus (JEV) in the epidemic area of Asia. The mechanism underlying the genotype replacement remains unclear. Therefore, we focused our current study on investigating the roles of mosquito vector and amplifying host(s) in JEV genotype replacement by comparing the replication ability of GI and GIII viruses. GI and GIII viruses had similar infection rates and replicated to similar viral titers after blood meal feedings in Culex tritaeniorhynchus. However, GI virus yielded a higher viral titer in amplifying host-derived cells, especially at an elevated temperature, and produced an earlier and higher viremia in experimentally inoculated pigs, ducklings, and young chickens. Subsequently we identified the amplification advantage of viral genetic determinants from GI viruses by utilizing chimeric and recombinant JEVs (rJEVs). Compared to the recombinant GIII virus (rGIII virus), we observed that both the recombinant GI virus and the chimeric rJEVs encoding GI virus-derived NS1-3 genes supported higher replication ability in amplifying hosts. The replication advantage of the chimeric rJEVs was lost after introduction of a single substitution from a GIII viral mutation (NS2B-L99V, NS3-S78A, or NS3-D177E). In addition, the gain-of-function assay further elucidated that rGIII virus encoding GI virus NS2B-V99L/NS3-A78S/E177E substitutions re-gained the enhanced replication ability. Thus, we conclude that the replication advantage of GI virus in pigs and poultry is the result of three critical NS2B/NS3 substitutions. This may lead to more efficient transmission of GI virus than GIII virus in the amplifying host-mosquito cycle.
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