MicroRNA-30c targets the interferon–alpha/beta receptor beta chain to promote type 2 PRRSV infection

Liu, Fang; Wang, Honglei; Du, Lijun; Wei, Zeyu; Zhang, Qiong; Feng, Wen-hai

doi:10.1099/jgv.0.001166

Cited by 24 publications

(17 citation statements)

References 57 publications

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“…miR-30c also targets IFNs-α/β receptor beta-chain (IFNAR2) and downregulates IFNAR2 expression. miR-30c J o u r n a l P r e -p r o o f and IFNAR2 mRNA co-localize in RNA-induced silencing complex (RISC), and by targeting IFNAR2, miR-30c impairs the production of ISGs and promotes PRRSV replication (Liu et al, 2018). These findings add a new strategy of PRRSV to evasion of IFN-mediated antiviral immunity by engaging miR-30c.…”

Section: Mirnas Promoting Prrsv Replicationmentioning

confidence: 88%

Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection

et al. 2020

Virus Research

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Section: Mirnas Promoting Prrsv Replicationmentioning

confidence: 88%

Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection

et al. 2020

Virus Research

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“…MiRNA plays a vital role in regulating gene expression through post-transcription modification. Increasing evidence demonstrates that viruses escape IFN antiviral activity for optimal infection by modifying the cellular abundance of miRNA targeting vital components of the IFN response (Zhu et al, 2014;Liu et al, 2018;Ma et al, 2018). JEV infection downregulates the expression of miRNA miR-432, which directly targets the suppressor of cytokine signaling protein 5 (SOCS5) and manipulates the JAK-STAT1 signaling cascade (Sharma et al, 2016).…”

Section: Discussionmentioning

confidence: 99%

“…The porcine miR-30 family (five members: miR30a-e) has been demonstrated to modulate host type I IFN response during virus infection (Zhu et al, 2014;Liu et al, 2018;Ma et al, 2018). The TargetScan (http://www.targetscan.…”

Section: Pedv Upregulated Socs1 Expression By Modulating Mir-30c-5pmentioning

confidence: 99%

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The Coronavirus PEDV Evades Type III Interferon Response Through the miR-30c-5p/SOCS1 Axis

Shan

Xue

et al. 2020

Front. Microbiol.

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Porcine epidemic diarrhea virus (PEDV) is an economically important pathogen that has evolved several mechanisms to evade type I IFN responses. Type III interferon (IFN-λ), an innate cytokine that primarily targets the mucosal epithelia, is critical in fighting mucosal infection in the host and has been reported to potently inhibit PEDV infection in vitro. However, how PEDV escapes IFN-λ antiviral response remains unclear. In this study, we found that PEDV infection induced significant IFN-λ expression in type I IFN-defective Vero E6 cells, but virus-induced endogenous IFN-λ did not reduce PEDV titers. Moreover, we demonstrated that PEDV escaped IFN-λ responses by substantially upregulating the suppressor of cytokine signaling protein 1 (SOCS1) expression, which impaired the induction of IFN-stimulated genes (ISGs) and dampened the IFN-λ antiviral response and facilitated PEDV replication in Vero E6 cells. We further showed that PEDV infection increased SOCS1 expression by decreasing host miR-30c-5p expression. MiR-30c-5p suppressed SOCS1 expression through targeting the 3 ′ untranslated region (UTR) of SOCS1. The inhibition of IFN-λ elicited ISGs expression by SOCS1 was specifically rescued by overexpression of miR-30c-5p. Collectively, our findings identify a new strategy by PEDV to escape IFN-λ-mediated antiviral immune responses by engaging the SOCS1/miR-30c axis, thus improving our understanding of its pathogenesis.

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“…It has been reported that miR-135a regulates Hepatitis C virus (HCV) replication by targeting C-X-C motif chemokine ligand 12 (CXCL12) and receptor-interacting serine/threonine kinase 2 (RIPK2) [27]. MiR-30 c promotes porcine reproductive and respiratory syndrome (PRRSV) replication by targeting interferon-alpha/beta receptor beta chain (IFNAR2) [28]. In addition, miR-122 repress porcine circovirus type 2 (PCV2) by down-regulating the expression of nuclear factor of activated T-cells 5 (NFAT5) and aminopeptidase puromycin sensitive (NPEPPS) [29].…”

Section: Discussionmentioning

confidence: 99%

MiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells

Jia

Wang

et al. 2020

Virulence

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Classical swine fever virus (CSFV) is one of the most important viral pathogens leading worldwide threats to pig industry. MicroRNAs (miRNAs) play important roles in regulating virus replication, but whether miRNAs affect CSFV infection is still poorly understood. In previous study, we identified four miRNAs that were down-regulated by CSFV in swine umbilical vein endothelial cells (SUVEC). In this study, miR-140, one of the most potently down-regulated genes was investigated. We found that the miRNA expression was significantly inhibited by CSFV infection. Subsequent studies revealed that miR-140 mimics significantly inhibited CSFV replication, while the inhibition of endogenous miR-140 enhanced CSFV replication. By using bioinformatics prediction, luciferase reporter system, real-time fluorescence quantitative PCR (RT-qPCR) and Western blot assays, we further demonstrated that miR-140 bind to the 3ʹ UTR of Rab25 mRNA to regulate its expression. We also analyzed the expression pattern of Rab25 in SUVECs after CSFV infection. The results showed that CSFV infection induced Rab25 expression. Finally, Rab25 was found to promote CSFV replication. In conclusion, this study demonstrated that CSFV inhibits miR-140 expression and miR-140 inhibits replication by binding to host factor Rab25.

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MicroRNA-30c targets the interferon–alpha/beta receptor beta chain to promote type 2 PRRSV infection

Cited by 24 publications

References 57 publications

Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection

Molecular and Cellular Mechanisms for PRRSV Pathogenesis and Host Response to Infection

The Coronavirus PEDV Evades Type III Interferon Response Through the miR-30c-5p/SOCS1 Axis

MiR-140 inhibits classical swine fever virus replication by targeting Rab25 in swine umbilical vein endothelial cells

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