ArticleJournal of virology2009
3' cis-acting elements that contribute to the competence and efficiency of Japanese encephalitis virus genome replication: functional importance of sequence duplications, deletions, and substitutions.
Article in Journal of virology, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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Who cites it
33 citing papers in PubMed, 49 citations in OpenAlex.
- The SL-I structural element of the 3' UTR region of West Nile virus participates in the regulation of viral translation.The Journal of general virology · 2026Article
- 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
- Cellular NONO protein binds to the flavivirus replication complex and promotes positive-strand RNA synthesis.Journal of virology · 2024Article
- Mice as an Animal Model for Japanese Encephalitis Virus Research: Mouse Susceptibility, Infection Route, and Viral Pathogenesis.Pathogens (Basel, Switzerland) · 2023Review
- Sequence duplication in 3' UTR modulates virus replication and virulence of Japanese encephalitis virus.Emerging microbes & infections · 2022Article
- Molecular Mechanism and Role of Japanese Encephalitis Virus Infection in Central Nervous System-Mediated Diseases.Viruses · 2022Review
- FUSE binding protein FUBP3 is a potent regulator in Japanese encephalitis virus infection.Virology journal · 2021Article
- Rational design of West Nile virus vaccine through large replacement of 3' UTR with internal poly(A).EMBO molecular medicine · 2021Article
- 3'UTR SL-IV and DB1 Regions Contribute to Japanese Encephalitis Virus Replication and Pathogenicity.Frontiers in veterinary science · 2021Article
- Proline-Rich Hypervariable Region of Hepatitis E Virus: Arranging the Disorder.Microorganisms · 2020Article
- Development, Characterization, and Application of Two Reporter-Expressing Recombinant Zika Viruses.Viruses · 2020Article
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- Early Events in Japanese Encephalitis Virus Infection: Viral Entry.Pathogens (Basel, Switzerland) · 2018Review
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- Genomic changes in an attenuated genotype I Japanese encephalitis virus and comparison with virulent parental strain.Virus genes · 2018Article
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- Zika virus: An emerging flavivirus.Journal of microbiology (Seoul, Korea) · 2017Review
- ADP-ribosylation Factor-related Protein 1 Interacts with NS5A and Regulates Hepatitis C Virus Propagation.Scientific reports · 2016Article
- RNA Structure Duplications and Flavivirus Host Adaptation.Trends in microbiology · 2016Review
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The positive-strand RNA genome of Japanese encephalitis virus (JEV) terminates in a highly conserved 3'-noncoding region (3'NCR) of six domains (V, X, I, II-1, II-2, and III in the 5'-to-3' direction). By manipulating the JEV genomic RNA, we have identified important roles for RNA elements present within the 574-nucleotide 3'NCR in viral replication. The two 3'-proximal domains (II-2 and III) were sufficient for RNA replication and virus production, whereas the remaining four (V, X, I, and II-1) were dispensable for RNA replication competence but required for maximal replication efficiency. Surprisingly, a lethal mutant lacking all of the 3'NCR except domain III regained viability through pseudoreversion by duplicating an 83-nucleotide sequence from the 3'-terminal region of the viral open reading frame. Also, two viable mutants displayed severe genetic instability; these two mutants rapidly developed 12 point mutations in domain II-2 in the mutant lacking domains V, X, I, and II-1 and showed the duplication of seven upstream sequences of various sizes at the junction between domains II-1 and II-2 in the mutant lacking domains V, X, and I. In all cases, the introduction of these spontaneous mutations led to an increase in RNA production that paralleled the level of protein accumulation and virus yield. Interestingly, the mutant lacking domains V, X, I, and II-1 was able to replicate in hamster BHK-21 and human neuroblastoma SH-SY5Y cells but not in mosquito C6/36 cells, indicating a cell type-specific restriction of its viral replication. Thus, our findings provide the basis for a detailed map of the 3' cis-acting elements in JEV genomic RNA, which play an essential role in viral replication. They also provide experimental evidence for the function of 3' direct repeat sequences and suggest possible mechanisms for the emergence of these sequences in the 3'NCR of JEV and perhaps in other flaviviruses.
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