MCPIP1 attenuates the innate immune response to influenza A virus by suppressing RIG‐I expression in lung epithelial cells

Sun, Xiaochuan; Feng, Wenjing; Guo, Yidi; Wang, Qi; Dong, Chunyan; Zhang, Maolin; Zhang, Guan; Duan, Ming

doi:10.1002/jmv.24944

Cited by 20 publications

(17 citation statements)

References 35 publications

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“…Some small RNAs facilitate influenza A virus (IAV) replication. For example, miR-141 suppresses transforming growth factor (TGF)-β2 and miR-9 targets monocyte chemoattractant protein 1-induced protein 1 (MCPIP1) to benefit IAV life cycle [2, 3]. On the other hand, several small RNAs participate in the host defensive response to IAV [4–8].…”

Section: Introductionmentioning

confidence: 99%

Exosome-delivered and Y RNA-derived small RNA suppresses influenza virus replication

et al. 2019

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Background Multiple interplays between viral and host factors are involved in influenza virus replication and pathogenesis. Several small RNAs have recently emerged as important regulators of host response to viral infections. The aim of this study was to characterize the functional role of hsa-miR-1975, a Y5 RNA-derived small RNA, in defending influenza virus and delineate the mechanisms. Methods We performed high throughput sequencing of small RNAs in influenza virus-infected cells to identify up- or down- regulated small RNA species. The expression of the most abundant RNA species (hsa-miR-1975) was validated by stem-loop reverse transcription-polymerase chain reaction (RT-PCR). Antiviral effects of hsa-miR-1975 were confirmed by Western Blot, RT-PCR and plaque assay. In vitro perturbation of hsa-miR-1975 combined with exosomes isolation was used to elucidate the role and mechanism of hsa-miR-1975 in the context of antiviral immunity. Results Small RNA sequencing revealed that hsa-miR-1975 was the most up-regulated small RNA in influenza virus-infected cells. The amount of intracellular hsa-miR-1975 increased in the late stage of the influenza virus replication cycle. The increased hsa-miR-1975 was at least partially derived from degradation of Y5RNA as a result of cellular apoptosis. Unexpectedly, hsa-miR-1975 mimics inhibited influenza virus replication while hsa-miR-1975 sponges enhanced the virus replication. Moreover, hsa-miR-1975 was secreted in exosomes and taken up by the neighboring cells to induce interferon expression. Conclusions Our findings unravel a critical role of Y-class small RNA in host’s defense against influenza virus infection and reveal its antiviral mechanism through exosome delivery. This may provide a new candidate for targeting influenza virus. Electronic supplementary material The online version of this article (10.1186/s12929-019-0553-6) contains supplementary material, which is available to authorized users.

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Section: Introductionmentioning

confidence: 99%

Exosome-delivered and Y RNA-derived small RNA suppresses influenza virus replication

et al. 2019

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“…MCPIP1 potently promotes type I IFN signalling by enhancing ISRE promoter activity and ISG expression. On the other hand, the other two studies suggest a negative regulatory role for MCPIP1 in IFN production, thereby serving a pro-viral function (Chen et al 2018;Sun et al 2018). MCPIP1…”

Section: Mcpip1mentioning

confidence: 99%

“…for zinc finger CCCH-type containing 12A, is a CCCH-type zinc-finger protein belonging to the MCPIP family, which has originally been identified as a gene induced by MCP-1 (Zhou et al 2006). With RNase activity, MCPIP1 has subsequently been shown to degrade mRNA of various pro-inflammatory cytokines and is thus implicated as a negative regulator of the cellular inflammatory responses (Matsushita et al 2009;Lin et al 2013;Sun et al 2018).…”

Section: Mcpip1mentioning

confidence: 99%

Cytoplasmic RNA sensors and their interplay with RNA-binding partners in innate antiviral response: theme and variations

Chan

Jin

2022

RNA

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Sensing of pathogen-associated molecular patterns including viral RNA by innate immunity represents the first line of defense against viral infection. In addition to RIG-I-like receptors and NOD-like receptors, several other RNA sensors are known to mediate innate antiviral response in the cytoplasm. Double-stranded RNA-binding protein PACT interacts with prototypic RNA sensor RIG-I to facilitate its recognition of viral RNA and induction of host interferon response, but variations of this theme are seen when the functions of RNA sensors are modulated by other RNA-binding proteins to impinge on antiviral defense, proinflammatory cytokine production and cell death programs. Their discrete and coordinated actions are crucial to protect the host from infection. In this review, we will focus on cytoplasmic RNA sensors with an emphasis on their interplay with RNA-binding partners. Classical sensors such as RIG-I will be briefly reviewed. More attention will be brought to the new insights on how RNA-binding partners of RNA sensors modulate innate RNA sensing and how viruses perturb the functions of RNA-binding partners.

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“…IAV NS1 protein can induce host cells to express MCPIP1, which can negatively regulate cellular inflammatory response. MCPIP1 degrades RIG-I mRNA through its RNase activity, then inhibits the phosphorylation of IRF3, the expression of IFN and ISG genes, and finally promotes the replication and proliferation of IAV ( Sun et al., 2018 ).…”

Section: Four “Tricks” Played By Ns1 Against Innate Immunitymentioning

confidence: 99%

NS1: A Key Protein in the “Game” Between Influenza A Virus and Host in Innate Immunity

Wang

Liu

2021

Front. Cell. Infect. Microbiol.

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Since the influenza pandemic occurred in 1918, people have recognized the perniciousness of this virus. It can cause mild to severe infections in animals and humans worldwide, with extremely high morbidity and mortality. Since the first day of human discovery of it, the “game” between the influenza virus and the host has never stopped. NS1 protein is the key protein of the influenza virus against host innate immunity. The interaction between viruses and organisms is a complex and dynamic process, in which they restrict each other, but retain their own advantages. In this review, we start by introducing the structure and biological characteristics of NS1, and then investigate the factors that affect pathogenicity of influenza which determined by NS1. In order to uncover the importance of NS1, we analyze the interaction of NS1 protein with interferon system in innate immunity and the molecular mechanism of host antagonism to NS1 protein, highlight the unique biological function of NS1 protein in cell cycle.

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MCPIP1 attenuates the innate immune response to influenza A virus by suppressing RIG‐I expression in lung epithelial cells

Cited by 20 publications

References 35 publications

Exosome-delivered and Y RNA-derived small RNA suppresses influenza virus replication

Exosome-delivered and Y RNA-derived small RNA suppresses influenza virus replication

Cytoplasmic RNA sensors and their interplay with RNA-binding partners in innate antiviral response: theme and variations

NS1: A Key Protein in the “Game” Between Influenza A Virus and Host in Innate Immunity

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