ArticleJournal of biomedical science2025
A non-structural protein 1 substitution of dengue virus enhances viral replication by interfering with the antiviral signaling pathway.
Article in Journal of biomedical science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- The Role of Natural Killer (NK) Cells in Dengue Virus Infection: A Narrative Review.Health science reports · 2026Article
- CLEC5A/TLR2 bispecific antibody suppresses dengue virus-induced pro-inflammatory cytokines production from macrophages.Journal of biomedical science · 2026Article
- Roles of non-structural protein 1 in dengue virus replication and immunomodulation in vivo.The Journal of veterinary medical science · 2026Article
- Molecular epidemiology and evolutionary trends of dengue virus serotype-2 strains in Sri Lanka.BMC microbiology · 2025Article
- Transcriptome Analysis of Monocytes Treated With Dengue Virus Nonstructural Protein 1 Revealed a Shift in Transcripts Involved in Self-Propagated Proinflammation and Antiviral Responses.The Journal of infectious diseases · 2025Article
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Authors and funding
12 authors.
Funding
Abstract
backgroundThe largest dengue virus 2 (DENV2) outbreak occurred in Taiwan in 2015, resulting in many fatalities. We therefore aim to identify crucial genetic variations which determine the virulence of the 2015 Taiwan outbreak strains.
methodsWe compared the 2015 Taiwan DENV2 sequences to the pre-2015 sequences. Reverse genetics (rg) viruses with substitutions were produced and the viral growth kinetics were investigated. We treated A549 cells with interferon (IFN) to determine the interferon-stimulated genes (ISGs) expression and STAT1 phosphorylation in the rg viral infection and plasmid transfection systems. IFN and pro-inflammatory cytokines levels were measured upon DENV infection using ELISA.
resultsThe rgNS1-K272R mutant showed faster replication in IFN-I producing cells compared to wildtype (WT) virus. Results revealed that NS1-K272R substitution contributed to higher soluble NS1 secretion and evade the antiviral response by suppressing the expression of ISGs and STAT1 phosphorylation compared to NS1-WT. Infection with rgNS1-K272R induced higher secretion of pro-inflammatory cytokines through the activation of canonical nuclear factor-kappa B (NF-κB) signaling pathway.
conclusionsOur results revealed that the DENV NS1 amino acid substitution affects the NS1 ability in immune evasion, which may contribute to the largest dengue outbreak in Taiwan since the 1990s.
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