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

Severe Acute Respiratory Syndrome Coronavirus Open Reading Frame (ORF) 3b, ORF 6, and Nucleocapsid Proteins Function as Interferon Antagonists

16 Nov 2006

Abstract excerpt

The severe acute respiratory syndrome coronavirus (SARS-CoV) is highly pathogenic in humans, with a death rate near 10%. This high pathogenicity suggests that SARS-CoV has developed mechanisms to overcome the host innate immune response. It has now been determined that SARS-CoV open reading frame (ORF) 3b, ORF 6, and N proteins antagonize interferon, a key component of the innate immune response. All three...

Read the complete abstract on PubMed

Topics

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

Share to Animal Virus Infections Studies
Share to interferon and immune responses
Share to SARS-CoV-2 and COVID-19 Research

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Source

Identifiers

PMID: 17108024
DOI: 10.1128/jvi.01782-06

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 8 Sept 2026.

Related research

Semantic proximity does not establish scientific evidence.

Research trail→

Click a neighbor to travelStep 1 · 12 closest

Severe Acute Respiratory Syndrome Coronavirus Open Reading Frame (ORF) 3b, ORF 6, and Nucleocapsid Proteins Function as Interferon AntagonistsPMID 17108024Read ↗

The structural and accessory proteins M, ORF 4a, ORF 4b, and ORF 5 of Middle East respiratory syndrome coronavirus (MERS-CoV) are potent interferon antagonistsSemantic proximity Read ↗

Activation and evasion of type I interferon responses by SARS-CoV-2.Semantic proximity Read ↗

Bat severe acute respiratory syndrome-like coronavirus ORF3b homologues display different interferon antagonist activitiesSemantic proximity Read ↗

Manipulation of innate immune signaling pathways by SARS-CoV-2 non-structural proteinsSemantic proximity Read ↗

Evasion of Type I Interferon by SARS-CoV-2Semantic proximity Read ↗

Inhibition of Beta Interferon Induction by Severe Acute Respiratory Syndrome Coronavirus Suggests a Two-Step Model for Activation of Interferon Regulatory Factor 3Semantic proximity Read ↗

Activation of interferon regulatory factor 3 is inhibited by the influenza A virus NS1 protein.Semantic proximity Read ↗

SARS-CoV-2 nsp12 attenuates type I interferon production by inhibiting IRF3 nuclear translocation.Semantic proximity Read ↗

Antagonism of Type I Interferon by Severe Acute Respiratory Syndrome Coronavirus 2.Semantic proximity Read ↗

Middle East Respiratory Syndrome Coronavirus Accessory Protein 4a Is a Type I Interferon AntagonistSemantic proximity Read ↗

Middle East respiratory syndrome coronavirus M protein suppresses type I interferon expression through the inhibition of TBK1-dependent phosphorylation of IRF3Semantic proximity Read ↗

Sarbecovirus ORF6 proteins hamper induction of interferon signalingSemantic proximity Read ↗

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