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

Enterovirus D68 infection upregulates SOCS3 expression to inhibit JAK-STAT3 signaling and antagonize the innate interferon response of the host

30 Aug 2023

Abstract excerpt

Enterovirus D68 (EV-D68) can cause respiratory diseases and acute flaccid paralysis, posing a great threat to public health. Interferons are cytokines secreted by host cells that have broad-spectrum antiviral effects, inducing the expression of hundreds of interferon-stimulated genes (ISGs). EV-D68 activates ISG expression early in infection, but at a later stage, the virus suppresses ISG expression, a strategy...

Read the complete abstract on PubMed

Topics

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

Share to Cytokine Signaling Pathways and Interactions
Share to interferon and immune responses
Share to Viral Infections and Immunology Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 37657555
DOI: 10.1016/j.virs.2023.08.007

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 5 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Enterovirus D68 infection upregulates SOCS3 expression to inhibit JAK-STAT3 signaling and antagonize the innate interferon response of the hostPMID 37657555Read ↗

Enterovirus D68 3C protease antagonizes type I interferon signaling by cleaving signal transducer and activator of transcription 1Semantic proximity Read ↗

Enterovirus D68 Antivirals: Past, Present, and FutureSemantic proximity Read ↗

The structural protein VP3 of enterovirus D68 interacts with MAVS to inhibit the NF-κB signaling pathwaySemantic proximity Read ↗

An update on enterovirus 71 infection and interferon type I responseSemantic proximity Read ↗

SOCS, Intrinsic Virulence Factors, and Treatment of COVID-19Semantic proximity Read ↗

The Coronavirus Transmissible Gastroenteritis Virus Evades the Type I Interferon Response through IRE1α-Mediated Manipulation of the MicroRNA miR-30a-5p/SOCS1/3 AxisSemantic proximity Read ↗

Japanese Encephalitis Virus exploits the microRNA-432 to regulate the expression of Suppressor of Cytokine Signaling (SOCS) 5Semantic proximity Read ↗

Viral Exploitation of Host SOCS Protein FunctionsSemantic proximity Read ↗

Beclin1 Binds to Enterovirus 71 3D Protein to Promote the Virus ReplicationSemantic proximity Read ↗

Downregulation of miR-155-5p facilitates enterovirus 71 replication through suppression of type I IFN response by targeting FOXO3/IRF7 pathwaySemantic proximity Read ↗

Inhibition of EV71 replication by an interferon-stimulated gene product L3HYPDHSemantic proximity Read ↗

Transcription factor EB (TFEB) interaction with RagC is disrupted during enterovirus D68 infectionSemantic proximity Read ↗

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