Muscovy duck reovirus infection rapidly activates host innate immune signaling and induces an effective antiviral immune response involving critical interferons

Chen, Zhilong; Luo, Guifeng; Wang, Quanxi; Wang, Song; Chi, Xiaojuan; Huang, Yifan; Wei, Haitao; Wu, Benhong; Huang, Shile; Chen, Ji‐Long

doi:10.1016/j.vetmic.2014.12.004

Cited by 14 publications

(11 citation statements)

References 39 publications

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“…The host TLR-3, 7, and 8 are responsible for sensing the RNA viruses ( Kawai and Akira, 2006 ). TLR-7 binds with the ssRNA derived from CSFV and TLR-3 senses the replication intermediate dsRNAs ( Diebold et al, 2004 ; Sen and Sarkar, 2005 ; Chen et al, 2015 ). Intracellular detection of ssRNA by TLR-7 triggers the activation of transcription factors IRF-7 and NF-κB, which ultimately initiate the expression of type I IFNs including IFNα and IFNβ ( Lund et al, 2004 ; Cao et al, 2015 ).…”

Section: Introductionmentioning

confidence: 99%

“…Intracellular detection of ssRNA by TLR-7 triggers the activation of transcription factors IRF-7 and NF-κB, which ultimately initiate the expression of type I IFNs including IFNα and IFNβ ( Lund et al, 2004 ; Cao et al, 2015 ). TLR-3 signaling activates the transcription factor IRF-3, which induces expression of the IFN-β and type III IFNs upon its entrance into the nucleus of cells ( Kawai and Akira, 2006 ; Chen et al, 2015 ). It has been established that the presence of viral RNA in the cytoplasm can be detected by cellular RIG-I and MDA-5 ( Yoneyama et al, 2005 ).…”

Section: Introductionmentioning

confidence: 99%

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Infection with Classical Swine Fever Virus Induces Expression of Type III Interferons and Activates Innate Immune Signaling

et al. 2017

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Classical swine fever virus (CSFV) commonly infects the lymphatic tissues and immune cells of pigs and could cause a lethal disease in the animals. The process and release of cytokines like type III interferons (IFNs) is one of the important responses of the host innate immunity to viral infection. However, little information is available about type III IFN response to the CSFV infection. In this study, we investigated the expression of type III IFNs including interleukin-28B (IL-28B) and IL-29 in PK-15 cells and pigs following CSFV infection. We found that infection with CSFV was able to induce expression of IL-28B and IL-29 in PK-15 cells, although the increased levels of type III IFNs were limited. Importantly, up-regulation of IL-28B and IL-29 was further observed in CSFV infected animal tissues. The production of IL-28B and IL-29 was reduced by the inactivation of NF-κB in cells, indicating that activated NF-κB is required for efficient expression of type III IFNs induced by CSFV. Moreover, our experiments demonstrated that infection with CSFV strongly stimulated the downstream of STAT1 signaling in vitro and in vivo. In addition, several critical IFN-stimulated genes (ISGs) including IFITM3, OASL, OAS1, and ISG15 were significantly upregulated at both mRNA and protein levels in PK-15 cells and infected pigs. Together, these results reveal that CSFV can trigger host antiviral immune responses including production of type III IFNs, activation of STAT1, and induction of some critical ISGs.

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Section: Introductionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

Infection with Classical Swine Fever Virus Induces Expression of Type III Interferons and Activates Innate Immune Signaling

et al. 2017

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“…Interestingly, human 293T cells exhibited similar innate immune response to ATMUV infection as CEF did (such as PRR and interferon up-expression). Because we have previously generated 293T cell lines stably expressing specific shRNA targeting either MDA5, RIG-I, TLR3, IPS-1, IRF3, IRF7, or luciferase control [ 33 , 39 , 42 ], 293T cell was selected as a model cell system to perform experimentation in this study. Our results reveal that both TLR3 and MDA5 are involved in host innate immune response to ATMUV infection.…”

Section: Discussionmentioning

confidence: 99%

“…Equal amounts of RNA (4 μg) was used for reverse-transcription PCR to prepare cDNA using M-MLV Reverse Transcriptase (Promega, USA), followed by PCR using rTaq DNA polymerase and quantitative real-time PCR using TransStart Green qPCR SuperMix (TransGen). The primers for ATMUV and chicken IFN-β, IFN-λ gene were designed using the Primer 5 software; other sequences of the primers used in this study have been described previously [ 39 – 41 ]. All primers are shown in Table 1 .…”

Section: Methodsmentioning

confidence: 99%

“…NC-siRNA sense sequence: 5′-UUCUCCGAACGUGUCACGUTT-3′; NC-siRNA antisense sequence: 5′-ACGUGACACGUUCGGAGAATT-3′. Cell lines stably expressing short hairpin RNA (shRNA) specifically targeting either MDA5, TLR3, IPS-1, IRF3, IRF7, or luciferase control were generated by infection of 293T cells with lentiviruses encoding these shRNA in pSIH-H1-GFP vector as previously described [ 33 , 39 , 42 ].…”

Section: Methodsmentioning

confidence: 99%

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Avian Tembusu virus infection effectively triggers host innate immune response through MDA5 and TLR3-dependent signaling pathways

Chen

Luo

Zhou

et al. 2016

Vet Res

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Avian Tembusu virus (ATMUV) is a newly emerged flavivirus that belongs to the Ntaya virus group. ATMUV is a highly pathogenic virus causing significant economic loss to the Chinese poultry industry. However, little is known about the role of host innate immune mechanism in defending against ATMUV infection. In this study, we found that ATMUV infection significantly up-regulated the expression of type I and type III interferons (IFN) and some critical IFN-stimulated genes (ISG) in vivo and in vitro. This innate immune response was induced by genomic RNA of ATMUV. Furthermore, we observed that ATMUV infection triggered IFN response mainly through MDA5 and TLR3-dependent signaling pathways. Strikingly, shRNA-based disruption of IPS-1, IRF3 or IRF7 expression significantly reduced the production of IFN in the 293T cell model. Moreover, NF-κB was shown to be activated in both chicken and human cells during the ATMUV infection. Inhibition of NF-κB signaling also resulted in a clear decrease in expression of IFN. Importantly, experiments revealed that treatment with IFN significantly impaired ATMUV replication in the chicken cell. Consistently, type I IFN also exhibited promising antiviral activity against ATMUV replication in the human cell. Together, these data indicate that ATMUV infection triggers host innate immune response through MDA5 and TLR3-dependent signaling that controls IFN production, and thereby induces an effective antiviral immunity.Electronic supplementary materialThe online version of this article (doi:10.1186/s13567-016-0358-5) contains supplementary material, which is available to authorized users.

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Effects of Hericium erinaceus polysaccharide on immunity and apoptosis of the main immune organs in Muscovy duck reovirus-infected ducklings

Liu

Liao

Chen

et al. 2021

International Journal of Biological Macromolecules

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Muscovy duck reovirus infection rapidly activates host innate immune signaling and induces an effective antiviral immune response involving critical interferons

Cited by 14 publications

References 39 publications

Infection with Classical Swine Fever Virus Induces Expression of Type III Interferons and Activates Innate Immune Signaling

Infection with Classical Swine Fever Virus Induces Expression of Type III Interferons and Activates Innate Immune Signaling

Avian Tembusu virus infection effectively triggers host innate immune response through MDA5 and TLR3-dependent signaling pathways

Effects of Hericium erinaceus polysaccharide on immunity and apoptosis of the main immune organs in Muscovy duck reovirus-infected ducklings

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