ArticleMicrobiology spectrum2022
Increased Cleavage of Japanese Encephalitis Virus prM Protein Promotes Viral Replication but Attenuates Virulence.
Article in Microbiology spectrum, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 16 citations in OpenAlex.
- Host-specific ubiquitination of prM orchestrates ESCRT recruitment to mediate efficient Japanese Encephalitis Virus assembly in vertebrates.PLoS pathogens · 2026Article
- Article
- The alarming spread of Japanese encephalitis: A growing public health concern.Open veterinary journal · 2025Review
- Natural products and derivatives as Japanese encephalitis virus antivirals.Pathogens and disease · 2024Review
- N6-methyladenosine modification positively regulate Japanese encephalitis virus replication.Virology journal · 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
Corrections and comments
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Authors and funding
9 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In flavivirus, the furin-mediated cleavage of prM is mandatory to produce infectious particles, and the immature particles containing uncleaved prM cannot undergo membrane fusion and release to the extracellular environment. However, the detailed relationship between viral replication or pathogenicity and furin in Japanese encephalitis virus (JEV) hasn't been clarified. Here, JEV with the mutations in furin cleavage sites and its nearby were constructed. Compared with WT virus, the mutant virus showed enhanced cleavage efficiency of prM protein and increased replication ability. Furthermore, we found that the mutations mainly promote genomic replication and assembly of JEV. However, the mutant formed smaller plaques than WT virus in plaque forming assay, indicating the lower cytopathogenicity of mutant virus. To assess the virulence of JEV mutant, an
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