Goose RIG-I functions in innate immunity against Newcastle disease virus infections

Sun, Yingjie; Ding, Na; Ding, Serena; Yu, Shuang; Meng, C.; Chen, Hongjun; Qiu, Xusheng; Zhang, Shilei; Yu, Yong; Zhan, Yuan; Ding, Chan

doi:10.1016/j.molimm.2012.08.022

Cited by 61 publications

(62 citation statements)

References 28 publications

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“…The ability of dRIG-I and gRIG-I to induce IFN production was also significantly reduced compared with hRIG-I and mRIG-I. Surprisingly, gRIG-I blocked IFN-b, Mx1 and PKR mRNA production during influenza infection, which is almost the opposite effect reported for gRIG-I in 293T cells after NDV infection (Sun et al, 2013). One possible cause of this inhibitory effect is that gRIG-I could compete with endogenous hRIG-I to bind influenza vRNA.…”

Section: Ifn-bmentioning

confidence: 72%

“…Previous studies revealed that duck and goose CARDs activate IFN-b in chicken cells, suggesting that chicken cells contain all the proteins required for the activation and downstream signalling of RIG-I (Miranzo-Navarro & Magor, 2014;Sun et al, 2013). Recent in vitro studies demonstrated that human TRIM25 did not interact with, ubiquitinate or activate human CARDs that were cotransfected into chicken DF-1 cells (Miranzo-Navarro & Magor, 2014).…”

Section: Ifn-bmentioning

confidence: 99%

“…Sun et al (2013) demonstrated that Newcastle disease virus (NDV) infection in gRIG-I-transfected 293T/17 cells resulted in upregulated activity of the IFN-b promoter and IRF-3 and IFIT1 mRNA levels, but decreased viral titres. Consistent with these reports, in this study dCARDs, gCARDs, dRIG-I and gRIG-I promoted IFN expression in mock-treated 293T and A549 cells.…”

Section: Ifn-bmentioning

confidence: 99%

“…As a natural reservoir of most influenza A strains, waterfowl have a crucial role in the ecology and evolution of influenza A viruses (IAVs) (Webster et al, 1992). As with hRIG-I and mRIG-I, duck RIG-I (dRIG-I) and goose RIG-I (gRIG-I) also induce type I IFN after influenza infection and poly I : C transfection Sun et al, 2013). Although dRIG-I and gRIG-I share similar CARDs and a helicase domain with hRIG-I and mRIG-I, the amino acids Ser8 and Thr170, which are critical for phosphorylation, and Thr55 and Lys172, which are essential for interaction and polyubiquitination by the tripartite motif containing 25 (TRIM25) in humans, are not conserved in mice, ducks or geese.…”

Section: Introductionmentioning

confidence: 99%

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RIG-I from waterfowl and mammals differ in their abilities to induce antiviral responses against influenza A viruses

Shao

Guo

et al. 2015

Journal of General Virology

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The retinoic acid-induced gene I (RIG-I) plays a crucial role in sensing viral RNA and IFN-b production. RIG-I varies in length and sequence between different species. We assessed the functional differences between RIG-I proteins derived from mammals and birds. The transfection of duck caspase recruitment domains (CARDs) and duck RIG-I (dCARDs and dRIG-I) and goose CARDs and goose RIG-I (gCARDs and gRIG-I) into chicken DF-1 cells increased the production of IFN-b mRNA and IFN-stimulated genes and decreased influenza A virus (IAV) replication; whereas human CARDs and RIG-I (hCARDs and hRIG-I) and mouse CARDs and RIG-I (mCARDs and mRIG-I) had no effect. In human 293T and A549 cells, hCARDs had the strongest IFN-inducing activity, followed by mCARDs, dCARDs and gCARDs. The IFN-inducing activity of hRIG-I was stronger than that of mRIG-I, dRIG-I and gRIG-I, in that order. The results showed that, although the ability of dCARDs to activate IFN was stronger than that of gCARDs in DF-1, 293T and A549 cells, dRIG-I had a weaker ability to activate IFN than gRIG-I in DF-1 cells with or without IAV infection. These data suggest that RIG-I proteins from different species have different amino acid sequences and functions. This genetic and functional diversity renders RIG-I flexible, adaptable and capable of recognizing many viruses in different species.

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Section: Ifn-bmentioning

confidence: 72%

Section: Ifn-bmentioning

confidence: 99%

Section: Ifn-bmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

RIG-I from waterfowl and mammals differ in their abilities to induce antiviral responses against influenza A viruses

Shao

Guo

et al. 2015

Journal of General Virology

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“…At 48 h posttreatment, chicken tissues were subjected to Western blotting to measure the conversion of LC3-I to LC3-II. The mRNA level of the NDV P gene in the tissue was used for evaluation of the quantity of NDV and measured by real-time quantitative reverse transcription-PCR (qRT-PCR) as described previously (26). The ␤-actin gene was used as an endogenous control.…”

Section: Temmentioning

confidence: 99%

Autophagy Benefits the Replication of Newcastle Disease Virus in Chicken Cells and Tissues

Sun

Ding

et al. 2014

J Virol

Self Cite

102

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bNewcastle disease virus (NDV) is an important avian pathogen. We previously reported that NDV triggers autophagy in U251 glioma cells, resulting in enhanced virus replication. In this study, we investigated whether NDV triggers autophagy in chicken cells and tissues to enhance virus replication. We demonstrated that NDV infection induced steady-state autophagy in chickenderived DF-1 cells and in primary chicken embryo fibroblast (CEF) cells, evident through increased double-or single-membrane vesicles, the accumulation of green fluorescent protein (GFP)-LC3 dots, and the conversion of LC3-I to LC3-II. In addition, we measured autophagic flux by monitoring p62/SQSTM1 degradation, LC3-II turnover, and GFP-LC3 lysosomal delivery and proteolysis, to confirm that NDV infection induced the complete autophagic process. Inhibition of autophagy by pharmacological inhibitors and RNA interference reduced virus replication, indicating an important role for autophagy in NDV infection. Furthermore, we conducted in vivo experiments and observed the conversion of LC3-I to LC3-II in heart, liver, spleen, lung, and kidney of NDV-infected chickens. Regulation of the induction of autophagy with wortmannin, chloroquine, or starvation treatment affects NDV production and pathogenesis in tissues of both lung and intestine; however, treatment with rapamycin, an autophagy inducer of mammalian cells, showed no detectable changes in chicken cells and tissues. Moreover, administration of the autophagy inhibitor wortmannin increased the survival rate of NDV-infected chickens. Our studies provide strong evidence that NDV infection induces autophagy which benefits NDV replication in chicken cells and tissues.

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Evolution of RNA sensing receptors in birds

Magor

2022

Immunogenetics

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Birds are important hosts for many RNA viruses, including influenza A virus, Newcastle disease virus, West Nile virus and coronaviruses. Innate defense against RNA viruses in birds involves detection of viral RNA by pattern recognition receptors. Several receptors of different classes are involved, such as endosomal toll-like receptors and cytoplasmic retinoic acid-inducible gene I-like receptors, and their downstream adaptor proteins. The function of these receptors and their antagonism by viruses is well established in mammals; however, this has received less attention in birds. These receptors have been characterized in a few bird species, and the completion of avian genomes will permit study of their evolution. For each receptor, functional work has established ligand specificity and activation by viral infection. Engagement of adaptors, regulation by modulators and the supramolecular organization of proteins required for activation are incompletely understood in both mammals and birds. These receptors bind conserved nucleic acid agonists such as single-or double-stranded RNA and generally show purifying selection, particularly the ligand binding regions. However, in birds, these receptors and adaptors differ between species, and between individuals, suggesting that they are under selection for diversification over time. Avian receptors and signalling pathways, like their mammalian counterparts, are targets for antagonism by a variety of viruses, intent on escape from innate immune responses.

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Goose RIG-I functions in innate immunity against Newcastle disease virus infections

Cited by 61 publications

References 28 publications

RIG-I from waterfowl and mammals differ in their abilities to induce antiviral responses against influenza A viruses

RIG-I from waterfowl and mammals differ in their abilities to induce antiviral responses against influenza A viruses

Autophagy Benefits the Replication of Newcastle Disease Virus in Chicken Cells and Tissues

Evolution of RNA sensing receptors in birds

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