Molecular Characterizations of Subcellular Localization Signals in the Nucleocapsid Protein of Porcine Epidemic Diarrhea Virus

Da, Shi; Lv, Maojie; Chen, Jianfei; Shi, Hongyan; Zhang, Sha; Zhang, Xin; Feng, Li

doi:10.3390/v6031253

Cited by 33 publications

(40 citation statements)

References 58 publications

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“…In other study, the N protein blocks the IFN-␤ production and ISGs expression, leading to suppression of the IRF3 and NF-B activities (Ding et al, 2014b). The N protein is an RNA-binding protein and shuttles between the cytoplasm and nucleus (Shi et al, 2014b). Furthermore, N interacts with TBK1 and sequesters its association with IRF3 to block the phosphorylation and nuclear translocation of IRF3 leading to inhibition of IRF3-mediated IFN production (Ding et al, 2014b).…”

Section: Evasion Of Ifn Response By Pedvmentioning

confidence: 96%

Immune evasion of porcine enteric coronaviruses and viral modulation of antiviral innate signaling

Zhang

Yoo

2016

Virus Research

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Porcine epidemic diarrhea virus (PEDV) and porcine deltacoronavirus (PDCoV) are emerged and reemerging viruses in pigs, and together with transmissible gastroenteritis virus (TGEV), pose significant economic concerns to the swine industry. These viruses infect epithelial cells of the small intestine and cause watery diarrhea, dehydration, and a high mortality in neonatal piglets. Type I interferons (IFN-α/β) are major antiviral cytokines forming host innate immunity, and in turn, these enteric coronaviruses have evolved to modulate the host innate immune signaling during infection. Accumulating evidence however suggests that IFN induction and signaling in the intestinal epithelial cells differ from other epithelial cells, largely due to distinct features of the gut epithelial mucosal surface and commensal microflora, and it appears that type III interferon (IFN-λ) plays a key role to maintain the antiviral state in the gut. This review describes the recent understanding on the immune evasion strategies of porcine enteric coronaviruses and the role of different types of IFNs for intestinal antiviral innate immunity.

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Section: Evasion Of Ifn Response By Pedvmentioning

confidence: 96%

Immune evasion of porcine enteric coronaviruses and viral modulation of antiviral innate signaling

Zhang

Yoo

2016

Virus Research

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“…The PEDV N protein contains a nucleolar localization signal (NoLS) sequence located at aa 71-90, and two nuclear export signal (NES) sequences at aa 221-236 (NES-1) and 325-364 (NES-2) (Shi et al, 2014). We analysed the structure of the PEDV N protein using Lasergene DNASTAR Protean 9.0 software, finding that the immunodominant region of the PEDV N protein is mainly localized to aa 136-289 and that this region has high hydrophilicity and flexibility.…”

Section: Pedv-encoded Nucleocapsid Protein Activates Nf-kbmentioning

confidence: 99%

Porcine epidemic diarrhea virus infection induces NF-κB activation through the TLR2, TLR3 and TLR9 pathways in porcine intestinal epithelial cells

Cao

Gao

et al. 2015

Journal of General Virology

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Porcine epidemic diarrhea virus (PEDV) is a coronavirus that induces persistent diarrhoea in swine, resulting in severe economic losses in swine-producing countries. Insights into the interplay between PEDV infection and the innate immune system are necessary for understanding the associated mechanism of pathogenesis. The transcription factor NF-kB plays an important role in regulating host immune responses. Here, we elucidated for the first time to our knowledge the potential mechanism of PEDV-mediated NF-kB activation in porcine small intestinal epithelial cells (IECs). During PEDV infection, NF-kB p65 was found to translocate from the cytoplasm to the nucleus, and PEDV-dependent NF-kB activity was associated with viral dose and active replication. Using small interfering RNAs to screen different mRNA components of the Toll-like receptor (TLR) or RIG-I-like receptor signalling pathways, we demonstrated that TLR2, TLR3 and TLR9 contribute to NF-kB activation in response to PEDV infection, but not RIG-I. By screening PEDV structural proteins for their ability to induce NF-kB activities, we found that PEDV nucleocapsid protein (N) could activate NF-kB and that the central region of N was essential for NF-kB activation. Furthermore, TLR2 was involved in PEDV N-induced NF-kB activation in IECs. Collectively, these findings provide new avenues of investigation into the molecular mechanisms of NF-kB activation induced by PEDV infection.

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“…Mouse anti-PEDV spike protein (PEDV-S) monoclonal antibody (3F12) was purchased from Median Diagnostics Inc (Chuncheon, South Korea). Mouse polyclonal antibody against PEDV nucleocapsid protein (PEDV-N) was prepared by our team in our previous study (Shi et al, 2014). The human IFN-beta ELISA Kit was purchased from R&D (Minneapolis, USA).…”

Section: Plasmids Antibodies and Reagentsmentioning

confidence: 99%

Tumor suppressor p53 inhibits porcine epidemic diarrhea virus infection via interferon-mediated antiviral immunity

Hao

Cao

et al. 2019

Molecular Immunology

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A B S T R A C T p53 is a tumor suppressor gene that can be activated in many contexts, such as DNA damage or stressful conditions. p53 has also been shown to be important for responses to certain viral infections. Porcine epidemic diarrhea virus (PEDV) is a major enteric pathogen of the coronavirus family that causes extensive mortality among piglets. The involvement of p53 during PEDV infection has not previously been investigated. In this study, we detected p53 upregulation in response to PEDV infection. Treatment with a p53 specific activator or p53 overexpression markedly decreased viral replication, and we showed that there was more viral progeny produced in p53 knock-out cells than in p53 wild-type cells. Finally, we demonstrated that inhibition of viral infection by p53 was mediated via p53-dependent IFN signaling, leading to IFN-stimulated response element (ISRE) activation, as well as the upregulation of IFN-stimulated genes (ISGs) and IFN-β released from infected cells. These findings demonstrate that p53 suppresses PEDV infection, offering a novel therapeutic strategy for combatting this deadly disease in piglets. as a central regulator of the innate immune response (Rivas et al., https://doi.

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Molecular Characterizations of Subcellular Localization Signals in the Nucleocapsid Protein of Porcine Epidemic Diarrhea Virus

Cited by 33 publications

References 58 publications

Immune evasion of porcine enteric coronaviruses and viral modulation of antiviral innate signaling

Immune evasion of porcine enteric coronaviruses and viral modulation of antiviral innate signaling

Porcine epidemic diarrhea virus infection induces NF-κB activation through the TLR2, TLR3 and TLR9 pathways in porcine intestinal epithelial cells

Tumor suppressor p53 inhibits porcine epidemic diarrhea virus infection via interferon-mediated antiviral immunity

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