ArticleScientific reports2016
Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5.
Article in Scientific reports, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.
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Who cites it
42 citing papers in PubMed, 73 citations in OpenAlex.
- Article
- Pyruvate kinase M2 modulates Japanese encephalitis virus replication in neuronal cells.The Journal of general virology · 2025Article
- Regulatory role of microRNAs in virus-mediated inflammation.Journal of inflammation (London, England) · 2024Review
- Research progress on miRNAs function in the interaction between human infectious viruses and hosts: A review.Biomolecules & biomedicine · 2024Review
- Article
- Review
- A Review of miRNA Regulation in Japanese Encephalitis (JEV) Virus Infection.Current pharmaceutical biotechnology · 2024Review
- Exaggerated levels of some specific TLRs, cytokines and chemokines in Japanese encephalitis infected BV2 and neuro 2A cell lines associated with worst outcome.Virology journal · 2023Article
- Suppressor of Cytokine Signalling 5 (SOCS5) Modulates Inflammatory Responses during Alphavirus Infection.Viruses · 2022Article
- Neurotropic RNA Virus Modulation of Immune Responses within the Central Nervous System.International journal of molecular sciences · 2022Review
- Regulatory Role of Host MicroRNAs in Flaviviruses Infection.Frontiers in microbiology · 2022Review
- Involvement of host microRNAs in flavivirus-induced neuropathology: An update.Journal of biosciences · 2022Review
- Pathogenicity and virulence of Japanese encephalitis virus: Neuroinflammation and neuronal cell damage.Virulence · 2021Review
- Chandipura virus dysregulates the expression of hsa-miR-21-5p to activate NF-κB in human microglial cells.Journal of biomedical science · 2021Article
- Alteration of miRNA Biogenesis Regulating Proteins in the Human Microglial Cell Line HMC-3 After Ischemic Stress.Molecular neurobiology · 2021Article
- Degradation of MicroRNA miR-466d-3p by Japanese Encephalitis Virus NS3 Facilitates Viral Replication and Interleukin-1β Expression.Journal of virology · 2020Article
- An HBV-encoded miRNA activates innate immunity to restrict HBV replication.Journal of molecular cell biology · 2020Article
- miR-802 participates in the inflammatory process of inflammatory bowel disease by suppressing SOCS5.Bioscience reports · 2020Article
- Porcine Reproductive and Respiratory Syndrome Virus Enhances Self-Replication via AP-1-Dependent Induction of SOCS1.Journal of immunology (Baltimore, Md. : 1950) · 2020Article
- The Coronavirus PEDV Evades Type III Interferon Response Through the miR-30c-5p/SOCS1 Axis.Frontiers in microbiology · 2020Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Japanese encephalitis virus (JEV) is a plus strand RNA virus, which infects brain. MicroRNAs are regulatory non-coding RNAs which regulate the expression of various genes in cells. Viruses modulate the expression of various microRNAs to suppress anti-viral signaling and evade the immune response. SOCS (Suppressor of cytokine signalling) family of proteins are negative regulators of anti-viral Jak-STAT pathway. In this study, we demonstrated the regulatory role of SOCS5 in Jak-STAT signaling and its exploitation by JEV through a microRNA mediated mechanism. JEV infection in human brain microglial cells (CHME3) downregulated the expression of miR-432, and upregulated SOCS5 levels. SOCS5 was validated as a target of miR-432 by using 3'UTR clone of SOCS5 in luciferase vector along with miR-432 mimic. The overexpression of miR-432 prior to JEV infection enhanced the phosphorylation of STAT1 resulting into increased ISRE activity and cellular inflammatory response resulting into diminished viral replication. The knockdown of SOCS5 resulted into increased STAT1 phosphorylation and suppressed viral replication. JEV infection mediated downregulation of miR-432 leads to SOCS5 upregulation, which helps the virus to evade cellular anti-viral response. This study demonstrated that JEV utilizes this microRNA mediated strategy to manipulate cellular immune response promoting JEV pathogenesis.
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