Eriocheir sinensis microRNA-7 targets crab Myd88 to enhance white spot syndrome virus replication

Huang, Ying; Wang, Wen; Xu, Zhiqiang; Pan, Jianlin; Zhao, Zhe; Ren, Qian

doi:10.1016/j.fsi.2018.05.028

Cited by 38 publications

(20 citation statements)

References 48 publications

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“…In this study, we initially show that ILF2 downregulates EV71 TCID50 and attenuates EV71 PFU, thereby repressing EV71 infection. Although this result is similar to previous reports showing that ILF2 regulates the replication of other viruses [28][29][30][31][32][33], this is the first study providing evidence that ILF2 represses EV71 infection. And although ILF2 plays critical roles in the repression of viral infection, the mechanism by which virus antagonizes ILF2-mediated antiviral effects was unknown until this study.…”

Section: Discussionsupporting

confidence: 92%

“…ILF2 also plays a role in the progression of pancreatic carcinoma [21,22], hepatocellular carcinoma [20,23], lung cancer [24], esophageal squamous cell carcinoma [25], gastric cancer [26], and breast cancer [27]. Moreover, ILF2 regulates the replication of immunodeficiency virus type 1 [28], hepatitis C virus [29], rhinovirus type 2 [30], white spot syndrome virus [31], human papilloma virus [32], and respiratory syndrome virus [33]. However, the mechanisms underlying the control of ILF2-mediated antiviral effects have not been reported, and the role of ILF2 in EV71 replication is unknown.…”

Section: Introductionmentioning

confidence: 99%

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Enterovirus 71 Represses Interleukin Enhancer-Binding Factor 2 Production and Nucleus Translocation to Antagonize ILF2 Antiviral Effects

Jin

Wang

et al. 2019

Viruses

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Enterovirus 71 (EV71) infection causes hand-foot-mouth disease (HFMD), meningoencephalitis, neonatal sepsis, and even fatal encephalitis in children, thereby presenting a serious risk to public health. It is important to determine the mechanisms underlying the regulation of EV71 infection. In this study, we initially show that the interleukin enhancer-binding factor 2 (ILF2) reduces EV71 50% tissue culture infective dose (TCID50) and attenuates EV71 plaque-formation unit (PFU), thereby repressing EV71 infection. Microarray data analyses show that ILF2 mRNA is reduced upon EV71 infection. Cellular studies indicate that EV71 infection represses ILF2 mRNA expression and protein production in human leukemic monocytes (THP-1) -differentiated macrophages and human rhabdomyosarcoma (RD) cells. In addition, EV71 nonstructural protein 2B interacts with ILF2 in human embryonic kidney (HEK293T) cells. Interestingly, in the presence of EV71 2B, ILF2 is translocated from the nucleus to the cytoplasm, and it colocalizes with 2B in the cytoplasm. Therefore, we present a distinct mechanism by which EV71 antagonizes ILF2-mediated antiviral effects by inhibiting ILF2 expression and promoting ILF2 translocation from the nucleus to the cytoplasm through its 2B protein.

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Section: Discussionsupporting

confidence: 92%

Section: Introductionmentioning

confidence: 99%

Enterovirus 71 Represses Interleukin Enhancer-Binding Factor 2 Production and Nucleus Translocation to Antagonize ILF2 Antiviral Effects

Jin

Wang

et al. 2019

Viruses

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“…was targeted by miR-7 and miR-21 during several viruses infection enabling these viruses to evade the immune surveillance system to enhance their proliferation [42][43][44]. It is important to note that, Evidence is accumulating that host miRNAs can bind to a broad range of RNA viruses, directly regulating their pathogenesis [18].…”

Section: Discussionmentioning

confidence: 99%

Immune-related miRNA-mRNA regulation network in the livers of DHAV-3-infected ducklings

Fan

et al. 2019

Preprint

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Background: Duck hepatitis A virus type 3 (DHAV-3) is one of the most harmful pathogens in the duck industry. However, the molecular mechanism underlying DHAV-3 infection in ducklings is remain poorly understood. To elucidate the genetic regulatory network for miRNA-mRNA and the signaling pathways involved in DHAV-3 infection in ducklings, we conducted global miRNA and mRNA expression profiling of duckling liver tissues infected with lethal DHAV-3 using high-throughput sequencing. Results: We found 156 differentially expressed miRNAs (DEMs) and 7717 differentially expressed miRNAs (DEGs) between mock-infected and DHAV-3-infected duckling livers. A total of 19,606 miRNA-mRNA pairs with negatively correlated expression patterns were identified in miRNA-mRNA networks constructed on the basis of these DEMs and DEGs. Moreover, immune-related pathways including the cytokine-cytokine receptor interaction, apoptosis, Toll-like receptor, Jak-STAT, and RIG-I-like receptor signaling pathway were significantly enriched through analyzing functions of mRNAs in the network in response to DHAV-3 infection. Besides, apl-miR-32-5p, apl-miR-125-5p, apl-miR-128-3p, apl-miR-460-5p, and novel-m0012-3p were identified as potential regulators in the immune-related signaling pathways during the DHAV-3 infection. Conclusions: To our knowledge, this is the first report on integrated analysis of miRNA-seq and mRNA-seq in DHAV-3-infected ducklings. The results indicated the important roles of miRNAs in regulating immune response genes and revealed the immune related miRNA-mRNA regulation network in the DHAV-3-infected duckling liver. Our findings may provide valuable information to further investigate the roles of miRNAs and their target genes in DHAV-3 replication and pathogenesis; additionally, they may offer clues for further understanding host-virus interactions.

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“…during several viruses infection that led these viruses to evade the immune surveillance system to enhance them proliferation [42][43][44]. It is important to note that, apl-miR-32-5p had multiple target genes in the Toll-like receptor signaling pathway, including TLR2, TOLLP (toll-interacting protein), TRAF3 (TNF receptor-associated factor 3), and TBK1 (TANK-binding kinase 1).…”

Section: Discussionmentioning

confidence: 99%

Integrated analysis of miRNA-seq and mRNA-seq reveals immune related miRNA-mRNA regulation network in the DHAV-3-infected duckling liver

Fan

et al. 2019

Preprint

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KEYWORDSDuck hepatitis A virus type 3, miRNA-seq, mRNA-seq, miRNA-mRNA network, Innate immune response, Host-virus interactions 2 Abstract Background: Duck hepatitis A virus type 3 (DHAV-3) is one of the most harmful pathogens in the duck industry. However, the molecular mechanism underlying DHAV-3 infection in ducklings is remain poorly understood. To elucidate the genetic regulatory network for miRNA-mRNA and the signaling pathways involved in DHAV-3 infection in ducklings, we conducted global miRNA and mRNA expression profiling of duckling liver tissues infected with lethal DHAV-3 using high-throughput sequencing. Results: We found 156 differentially expressed miRNAs (DEMs) and 7717 differentially expressed miRNAs (DEGs) between mock-infected and DHAV-3-infected duckling livers. A total of 19,606 miRNA-mRNA pairs with negatively correlated expression patterns were identified in miRNA-mRNA networks constructed on the basis of these DEMs and DEGs. Moreover, immune-related pathways including the cytokine-cytokine receptor interaction, apoptosis, Toll-like receptor, Jak-STAT, and RIG-I-like receptor signaling pathway were significantly enriched through analyzing functions of mRNAs in the network in response to DHAV-3 infection. Besides, apl-miR-32-5p, apl-miR-125-5p, apl-miR-128-3p, apl-miR-460-5p, and novel-m0012-3p were identified as potential regulators in the immune-related signaling pathways during the DHAV-3 infection. Conclusions: To our knowledge, this is the first report on integrated analysis of miRNA-seq and mRNA-seq in DHAV-3-infected ducklings.The results indicated the important roles of miRNAs in regulating immune response genes and revealed the immune related miRNA-mRNA regulation network in the DHAV-3-infected duckling liver.Our findings may provide valuable information to further investigate the roles of miRNAs and their target genes in DHAV-3 replication and pathogenesis; additionally, they may offer clues for further understanding host-virus interactions.

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Eriocheir sinensis microRNA-7 targets crab Myd88 to enhance white spot syndrome virus replication

Cited by 38 publications

References 48 publications

Enterovirus 71 Represses Interleukin Enhancer-Binding Factor 2 Production and Nucleus Translocation to Antagonize ILF2 Antiviral Effects

Enterovirus 71 Represses Interleukin Enhancer-Binding Factor 2 Production and Nucleus Translocation to Antagonize ILF2 Antiviral Effects

Immune-related miRNA-mRNA regulation network in the livers of DHAV-3-infected ducklings

Integrated analysis of miRNA-seq and mRNA-seq reveals immune related miRNA-mRNA regulation network in the DHAV-3-infected duckling liver

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