Discover Community Create You

Loading publication...

Noodle always counts identifier-free feature events for service operation. With your permission, Google Analytics can also estimate audience and engagement. Search text, publication identifiers, cookies, IP addresses and browser fingerprints are never included in Noodle's first-party event counters.

Privacy details

Article

Npro of Classical Swine Fever Virus Suppresses Type III Interferon Production by Inhibiting IRF1 Expression and Its Nuclear Translocation.

Viruses - 31 Oct 2019

Cao Tong, Li Xiaoye, Xu Yonghao, Zhang Shengnan, Wang Zuohuan, Shan Ying, Sun Jianhe, Fang Weihuan, Li Xiaoliang

Abstract excerpt

Classical swine fever virus (CSFV) causes a contagious disease of pigs. The virus can break the mucosal barrier to establish its infection. Type III interferons (IFN-λs) play a crucial role in maintaining the antiviral state in epithelial cells. Limited information is available on whether or how CSFV modulates IFN-λs production. We found that IFN-λ3 showed dose-dependent suppression of CSFV replication in IPEC-J2...

Read the complete abstract on PubMed

Topics

Share this publication in a Topic to start or enrich a Post.

Share to Active Transport, Cell Nucleus
Share to Classical Swine Fever

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Classical Swine Fever Virus

Share to Endopeptidases

Share to Host-Pathogen Interactions

Share to Interferon Regulatory Factor-1

Share to Interferons

Share to Swine Diseases

Source

Open in PubMed Open full text

Identifiers

PMID: 31683525
DOI: 10.3390/v11110998
PMCID: PMC6893713

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Npro of Classical Swine Fever Virus Suppresses Type III Interferon Production by Inhibiting IRF1 Expression and Its Nuclear Translocation.PMID 31683525Read ↗

Npro of classical swine fever virus contributes to pathogenicity in pigs by preventing type I interferon induction at local replication sitesSemantic proximity Read ↗

Swine acute diarrhea syndrome coronavirus Nsp1 suppresses IFN-λ1 production by degrading IRF1 via ubiquitin–proteasome pathwaySemantic proximity Read ↗

Type III Interferon Restriction by Porcine Epidemic Diarrhea Virus and the Role of Viral Protein nsp1 in IRF1 Signaling.Semantic proximity Read ↗

N(pro) of classical swine fever virus prevents type I interferon-mediated priming of conventional dendritic cells for enhanced interferon-α response.Semantic proximity Read ↗

Intracellular Vimentin Regulates the Formation of Classical Swine Fever Virus Replication Complex through Interaction with NS5A ProteinSemantic proximity Read ↗

Classical Swine Fever Virus NproLimits Type I Interferon Induction in Plasmacytoid Dendritic Cells by Interacting with Interferon Regulatory Factor 7Semantic proximity Read ↗

Guanylate-Binding Protein 1, an Interferon-Induced GTPase, Exerts an Antiviral Activity against Classical Swine Fever Virus Depending on Its GTPase ActivitySemantic proximity Read ↗

Immune Responses Against Classical Swine Fever Virus: Between Ignorance and LunacySemantic proximity Read ↗

African Swine Fever Virus MGF505-7R Interacts with Interferon Regulatory Factor 9 to Evade the Type I Interferon Signaling Pathway and Promote Viral ReplicationSemantic proximity Read ↗

Investigation of porcine interferons as a metaphylactic intervention against classical swine fever virusSemantic proximity Read ↗

pK205R targets the proximal element of IFN-I signaling pathway to assist African swine fever virus to escape host innate immunity at the early stage of infectionSemantic proximity Read ↗

Antiviral Role of IFITM Proteins in Classical Swine Fever Virus InfectionSemantic proximity Read ↗

⌁Select a neighboring publication to make it the new centre.