About: SARS-CoV Pathogenesis Is Regulated by a STAT1 Dependent but a Type I, II and III Interferon Receptor Independent Mechanism

Facets (new session)
Description
Metadata
Settings
- owl:sameAs
- Inference Rule:

About: SARS-CoV Pathogenesis Is Regulated by a STAT1 Dependent but a Type I, II and III Interferon Receptor Independent Mechanism Goto Sponge NotDistinct Permalink

An Entity of Type : schema:ScholarlyArticle, within Data Space : wasabi.inria.fr associated with source document(s)

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	SARS-CoV Pathogenesis Is Regulated by a STAT1 Dependent but a Type I, II and III Interferon Receptor Independent Mechanism
Creator	Baric, Ralph Frieman, Matthew Subbarao, Kanta Whitmore, Alan Roberts, Anjeanette Heise, Mark Funkhouser, William Lamirande, Elaine Chen, Ward, Jerrold Morrison,
Source	Medline; PMC
abstract	Severe acute respiratory syndrome coronavirus (SARS-CoV) infection often caused severe end stage lung disease and organizing phase diffuse alveolar damage, especially in the elderly. The virus-host interactions that governed development of these acute end stage lung diseases and death are unknown. To address this question, we evaluated the role of innate immune signaling in protection from human (Urbani) and a recombinant mouse adapted SARS-CoV, designated rMA15. In contrast to most models of viral pathogenesis, infection of type I, type II or type III interferon knockout mice (129 background) with either Urbani or MA15 viruses resulted in clinical disease outcomes, including transient weight loss, denuding bronchiolitis and alveolar inflammation and recovery, identical to that seen in infection of wildtype mice. This suggests that type I, II and III interferon signaling play minor roles in regulating SARS pathogenesis in mouse models. In contrast, infection of STAT1−/− mice resulted in severe disease, high virus titer, extensive pulmonary lesions and 100% mortality by day 9 and 30 post-infection with rMA15 or Urbani viruses, respectively. Non-lethal in BALB/c mice, Urbani SARS-CoV infection in STAT1−/− mice caused disseminated infection involving the liver, spleen and other tissues after day 9. These findings demonstrated that SARS-CoV pathogenesis is regulated by a STAT1 dependent but type I, II and III interferon receptor independent, mechanism. In contrast to a well documented role in innate immunity, we propose that STAT1 also protects mice via its role as an antagonist of unrestrained cell proliferation.
has issue date	2010-04-08(xsd:dateTime)
bibo:doi	10.1371/journal.ppat.1000849
bibo:pmid	20386712
has license	cc0
sha1sum (hex)	68ac410cd36c5699f58d2b76b0eeb84956573f77
schema:url	https://doi.org/10.1371/journal.ppat.1000849
resource representing a document's title	SARS-CoV Pathogenesis Is Regulated by a STAT1 Dependent but a Type I, II and III Interferon Receptor Independent Mechanism
has PubMed Central identifier	PMC2851658
has PubMed identifier	20386712
schema:publication	PLoS Pathog
resource representing a document's body	covid:68ac410cd36c5699f58d2b76b0eeb84956573f77#body_text
is schema:about of	named entity 'DIFFUSE ALVEOLAR DAMAGE' named entity 'WEIGHT LOSS' named entity 'TITER' named entity 'HOST' named entity 'HIGH' named entity 'INDEPENDENT' named entity 'PHASE' named entity 'INFECTION' named entity 'BACKGROUND' named entity 'CONTRAST' named entity 'TYPE II' named entity 'PULMONARY' named entity 'QUESTION' named entity 'STAT1' named entity 'MECHANISM' named entity 'LIVER' named entity 'IMMUNE' named entity 'CITATION' named entity 'ALVEOLAR INFLAMMATION' named entity 'CAUSED' named entity 'INTERFERON SIGNALING' named entity 'ADDRESS' named entity 'SPLEEN' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS' named entity 'MINOR' named entity 'BALB' named entity 'MICE' named entity 'VIRAL PATHOGENESIS' named entity 'DOCUMENTED' named entity 'SEVERE DISEASE' named entity 'VIRUSES' named entity 'MODELS' named entity 'EXTENSIVE' named entity 'DEATH' named entity 'TYPE III INTERFERON' named entity 'DISSEMINATED' named entity 'FINDINGS' named entity 'diffuse alveolar damage' named entity 'viruses' named entity 'receptor' named entity 'mice' named entity '2010' named entity 'pathogenesis' named entity 'mice' named entity 'Chen' named entity 'Type I' named entity 'Dependent' named entity 'III' named entity 'BUT' named entity 'SARS-COV' named entity 'LESIONS' named entity 'OUTCOMES' named entity '28129' named entity 'ORGANIZING' named entity 'DEVELOPMENT' named entity 'ROLE' named entity 'END STAGE LUNG DISEASE' named entity 'BRONCHIOLITIS' named entity 'DISEASE' named entity 'SEVERE' named entity 'HUMAN' named entity 'NON-LETHAL' named entity 'RECOVERY' named entity 'TRANSIENT' named entity 'CHEN' named entity 'ITS' named entity 'DEPENDENT' named entity 'DAY' named entity 'SEEN' named entity 'PLAY' named entity 'PROTECTION'

Faceted Search & Find service v1.13.91 as of Mar 24 2020

Alternative Linked Data Documents: Sponger | ODE Content Formats:

RDF

ODATA

Microdata

About

OpenLink Virtuoso version 07.20.3229 as of Jul 10 2020, on Linux (x86_64-pc-linux-gnu), Single-Server Edition (94 GB total memory)
Data on this page belongs to its respective rights holders.
Virtuoso Faceted Browser Copyright © 2009-2024 OpenLink Software