Molecular cloning and functional analysis of duck ubiquitin-specific protease 18 (USP18) gene

Qian, Wei; Wei, Xiaojian; Jin, Meilin

doi:10.1016/j.dci.2016.04.008

Cited by 12 publications

(9 citation statements)

References 47 publications

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“…In ducks and chickens, OASL is the only protein of this family, and it possesses both oligoadenylate synthase activity and the ability to restrict flavivirus replication in an RNaseL independent manner [253,254]. Duck embryonic fibroblasts produce OASL in response to poly(I:C) [255], and it is upregulated in the brain, lung, and spleen tissues of ducks infected with HPAI H5N1 viruses [37,99]. Rong and colleagues recently demonstrated that duck OASL can potentially activate both RNase-L and RIG-I pathways [252].…”

Section: Interferon-stimulated Genes (Isgs)mentioning

confidence: 99%

“…Qian et al cloned and characterized the duck ubiquitin-specific protease 18 (USP18) and proposed that it is involved in controlling inflammatory responses in ducks [255]. In humans USP18 maintains homeostasis by removing ISG15 labels from proteins [285,286].…”

Section: Other Potential Mechanisms Of Influenza Disease Resistanmentioning

confidence: 99%

“…However, USP18 can also oppose pro-inflammatory NF-κB signaling by cleaving K63-linked ubiquitin chains [287]. Qian et al found that duck USP18 is broadly expressed in duck tissues, particularly abundant in lung, spleen, and kidney, and that it is inducible by the viral RNA analog poly(I:C) [255]. Overexpression of recombinant duck USP18 suppressed pro-inflammatory cytokine secretion in duck embryonic fibroblasts (DEFs).…”

Section: Other Potential Mechanisms Of Influenza Disease Resistanmentioning

confidence: 99%

“…It would be interesting to know if duck USP18 can negatively regulate RIG-I signaling by removing the K63-linked ubiquitin chains furnished by TRIM25. When Qian et al overexpressed duck USP18 in DEFs they found that it inhibited IFN-β production along with pro-inflammatory cytokines, but that the cells still induced ISGs in response to poly(I:C) [255].…”

Section: Other Potential Mechanisms Of Influenza Disease Resistanmentioning

confidence: 99%

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Innate Immune Responses to Avian Influenza Viruses in Ducks and Chickens

Evseev

Magor

2019

Veterinary Sciences

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Mallard ducks are important natural hosts of low pathogenic avian influenza (LPAI) viruses and many strains circulate in this reservoir and cause little harm. Some strains can be transmitted to other hosts, including chickens, and cause respiratory and systemic disease. Rarely, these highly pathogenic avian influenza (HPAI) viruses cause disease in mallards, while chickens are highly susceptible. The long co-evolution of mallard ducks with influenza viruses has undoubtedly fine-tuned many immunological host–pathogen interactions to confer resistance to disease, which are poorly understood. Here, we compare innate responses to different avian influenza viruses in ducks and chickens to reveal differences that point to potential mechanisms of disease resistance. Mallard ducks are permissive to LPAI replication in their intestinal tissues without overtly compromising their fitness. In contrast, the mallard response to HPAI infection reflects an immediate and robust induction of type I interferon and antiviral interferon stimulated genes, highlighting the importance of the RIG-I pathway. Ducks also appear to limit the duration of the response, particularly of pro-inflammatory cytokine expression. Chickens lack RIG-I, and some modulators of the signaling pathway and may be compromised in initiating an early interferon response, allowing more viral replication and consequent damage. We review current knowledge about innate response mediators to influenza infection in mallard ducks compared to chickens to gain insight into protective immune responses, and open questions for future research.

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Section: Interferon-stimulated Genes (Isgs)mentioning

confidence: 99%

Section: Other Potential Mechanisms Of Influenza Disease Resistanmentioning

confidence: 99%

Section: Other Potential Mechanisms Of Influenza Disease Resistanmentioning

confidence: 99%

Section: Other Potential Mechanisms Of Influenza Disease Resistanmentioning

confidence: 99%

See 2 more Smart Citations

Innate Immune Responses to Avian Influenza Viruses in Ducks and Chickens

Evseev

Magor

2019

Veterinary Sciences

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“…Recently, several studies have suggested that USP18 acts as a negative regulator in mammals, birds and fish (Chen, Zhang, & Gui, 2015;Kang, Jiang, Wu, Pestka, & Fisher, 2001;Malakhova et al, 2006;Wei, Wei, & Zhou, 2016). In mice, USP18 negatively regulates IFN signaling, independent of its isopeptidase activity associated with ISG15, by binding to the IFNAR2 receptor subunit and blocking the interaction between Janus kinase and the IFN receptor (Malakhova et al, 2006).…”

mentioning

confidence: 99%

Negative regulation of the RLR‐mediated IFN signaling pathway by duck ubiquitin‐specific protease 18 (USP18)

et al. 2018

Journal Cellular Physiology

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Ubiquitin-specific protease 18 (USP18) plays an important role in regulating type I interferon (IFN) signaling in innate immunity, and has a crucial impact on the IFN therapeutic effect. Although significant progress has been made in elucidating USP18 function in mammals, the role of USP18 in ducks (duUSP18) remains poorly understood. In this study, we cloned the USP18 gene from white crested ducks by reverse transcription polymerase chain reaction (RT-PCR) and rapid amplification of complementary DNA (cDNA) ends. We determined that duUSP18 cDNA contains a 52-bp 5'UTR, a 1,131-bp open reading frame and a 356-bp 3'UTR, and encodes a 376-amino acid protein. Multiple sequence alignments showed that duUSP18 shares high similarity with USP18 from other vertebrates. Overexpression of duUSP18 inhibited nuclear factor-κB (NF-κB) and interferon regulatory factor 1 (IRF1) activity, and reduced IFN-β production following 5' triphosphate double-stranded RNA (5'ppp dsRNA) or lipopolysaccharide (LPS) stimulation. duUSP18 knockdown significantly activated 5'ppp dsRNA-induced and LPS-induced NF-κB and IRF1 activation, and induced IFN-β expression in duck embryo fibroblasts. Furthermore, Quantitative real-time PCR (qRT-PCR) revealed that overexpression or knockdown of duUSP18 could alter the expression of genes related to the RLR-mediated IFN signaling pathway following the treatment with 5'ppp dsRNA. In addition, site-directed mutation analysis revealed that cysteine 66 (C66), histidine 313 (H313), and histidine 321 (H321) of duUSP18 were critical for inhibiting IFN-β activity. Taken together, these results suggest that duck USP18 plays an important role in innate immune responses against double-stranded RNA viruses in the RLR-mediated IFN signaling pathway, and that further studies are warranted to elucidate its underlying mechanisms, which could provide molecular insights into the effect of the treatment of duck diseases.

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