ArticleVirology journal2025
Signaling pathway of DNA replication and toll-like receptors was inhibited in C6/36 cells infected with Japanese encephalitis virus.
Article in Virology journal, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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Who cites it
1 citing paper in PubMed.
- Neuroinflammation and blood-brain barrier disruption in Japanese encephalitis virus infection: mechanisms, therapeutic targets, and intervention strategies.Archives of pharmacal research · 2026Review
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12 authors.
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Abstract
backgroundThe Aedes albopictus C6/36 cell line is model system for studying mosquito-borne viruses. These cells exhibit high permissiveness to Japanese encephalitis virus (JEV), supporting robust viral replication and producing a significant viral load.
methodsGiven C6/36 cells established susceptibility, this study employed 4D label-free quantitative proteomics to investigate the underlying mechanisms that enable C6/36 cells to be readily cultured and facilitate efficient JEV infection. C6/36 cells were infected with JEV at MOI of 0.5 and harvested at 0,6,12, and 24 hours post-infection (HPI) for 4D label-free quantitative proteomics analysis.
resultsProteomic data analysis revealed that differentially expressed proteins were primarily involved in signal transduction mechanisms, innate immune responses, metabolism, and the synthesis, transport, and catabolism of secondary metabolites. JEV infection downregulated several proteins involved in DNA replication, including proliferating cell nuclear antigen (PCNA), DNA polymerase epsilon subunit 3 (POLε3), and DNA primase large subunit (PRI2), thereby inhibiting DNA replication signaling pathways and contributing to increased JEV replication. JEV infection also suppressed Toll-like receptors (TLRs), key components of the innate immune system. Specifically, TLR2, TLR4, TLR7, and TLR13 were significantly downregulated, thereby suppressing the innate immune response.
conclusionOur results suggest that JEV infection impairs DNA replication and innate immune responses, particularly the inhibition of PRI2 and POLε3, leading to increased JEV replication and potentially a key mechanism of JEV pathogenesis. Elucidating the interactions between JEV and the host DNA replication and immune system will facilitate the development of more effective JEV prevention and treatment strategies.
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