Mir‐302c mediates influenza A virus‐induced IFNβ expression by targeting NF‐κB inducing kinase

Gui, Shulin; Chen, Xueyuan; Zhang, Mo; Zhao, Fanpeng; Wan, Yi; Wang, Li; Xu, Gang; Zhou, Li; Yue, Xin; Zhu, Ying; Shi, Liyi

doi:10.1016/j.febslet.2015.11.011

Cited by 43 publications

(35 citation statements)

References 29 publications

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“…Many viruses and viral proteins adopt microRNA mediated regulation of anti-viral pathways to alleviate their pathogenesis. Influenza A virus utilizes miR-302c to target NF-κB kinase activity in order to modulate IFN-β pathway20. Hepatitis B virus X protein has been reported to induce the expression of miR-21 to promote hepatocellular carcinoma in hepatocytes21.…”

Section: Discussionmentioning

confidence: 99%

Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5

Sharma

Kumawat

Rastogi

et al. 2016

Sci Rep

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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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Section: Discussionmentioning

confidence: 99%

Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5

Sharma

Kumawat

Rastogi

et al. 2016

Sci Rep

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show abstract

“…Previous evidence has demonstrated that several miRNAs, including miR‐33a, miR‐302c, and miR‐let‐7c, are involved in the replication of IAV . It has also been shown that miR‐146a is induced via a wide range of viral infections, and probably miR‐146a contributes to virus replication.…”

Section: Mir‐146a In Influenzamentioning

confidence: 99%

“…50 Previous evidence has demonstrated that several miRNAs, including miR-33a, miR-302c, and miR-let-7c, are involved in the replication of IAV. [99][100][101] It has also been shown that miR-146a is induced via a wide range of viral infections, and probably miR-146a contributes to virus replication. However, studies on the involvement of miR-146a in IAV infection are insufficient, and the related underlying molecular mechanisms of influenza infectious cycle remain unknown.…”

Section: Mir-146a In Influenzamentioning

confidence: 99%

The role of miR‐146a in viral infection

et al. 2019

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Cellular microRNAs (miRNAs) were identified as a key player in the posttranscriptional regulation of cellular‐genes regulatory pathways. They also emerged as a significant regulator of the immune response. In particular, miR‐146a acts as an importance modulator of function and differentiation cells of the innate and adaptive immunity. It has been associated with disorder including cancer and viral infections. Given its significance in the regulation of key cellular processes, it is not surprising which virus infection have found ways to dysregulation of miRNAs. miR‐146a has been identified in exosomes (exosomal miR‐146a). After the exosomes release from donor cells, they are taken up by the recipient cell and probably the exosomal miR‐146a is able to modulate the antiviral response in the recipient cell and result in making them more susceptible to virus infection. In this review, we discuss recent reports regarding miR‐146a expression levels, target genes, function, and contributing role in the pathogenesis of the viral infection and provide a clue to develop the new therapeutic and preventive strategies for viral disease in the future.

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“…Western blotting analyses were described in a previous study (34). Briefly, cells were harvested by low-speed centrifugation and washed with PBS.…”

Section: Western Blot Analysismentioning

confidence: 99%

Hepatitis B virus X protein–induced SH2 domain–containing 5 (SH2D5) expression promotes hepatoma cell growth via an SH2D5–transketolase interaction

Yang

Ming

Zhu

et al. 2019

Journal of Biological Chemistry

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Mir‐302c mediates influenza A virus‐induced IFNβ expression by targeting NF‐κB inducing kinase

Cited by 43 publications

References 29 publications

Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5

Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5

The role of miR‐146a in viral infection

Hepatitis B virus X protein–induced SH2 domain–containing 5 (SH2D5) expression promotes hepatoma cell growth via an SH2D5–transketolase interaction

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