About: Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection

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About: Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection 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	Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection
Creator	Baric, Ralph Schäfer, Alexandra Agnihothram, Sudhakar Whitmore, Alan Heise, Mark Totura, Allison Katze, Michael Lipkin, Editor
Source	Medline; PMC
abstract	Toll-like receptors (TLRs) are sensors that recognize molecular patterns from viruses, bacteria, and fungi to initiate innate immune responses to invading pathogens. The emergence of highly pathogenic coronaviruses severe acute respiratory syndrome coronavirus (SARS-CoV) and Middle East respiratory syndrome coronavirus (MERS-CoV) is a concern for global public health, as there is a lack of efficacious vaccine platforms and antiviral therapeutic strategies. Previously, it was shown that MyD88, an adaptor protein necessary for signaling by multiple TLRs, is a required component of the innate immune response to mouse-adapted SARS-CoV infection in vivo. Here, we demonstrate that TLR3(−/−), TLR4(−/−), and TRAM(−/−) mice are more susceptible to SARS-CoV than wild-type mice but experience only transient weight loss with no mortality in response to infection. In contrast, mice deficient in the TLR3/TLR4 adaptor TRIF are highly susceptible to SARS-CoV infection, showing increased weight loss, mortality, reduced lung function, increased lung pathology, and higher viral titers. Distinct alterations in inflammation were present in TRIF(−/−) mice infected with SARS-CoV, including excess infiltration of neutrophils and inflammatory cell types that correlate with increased pathology of other known causes of acute respiratory distress syndrome (ARDS), including influenza virus infections. Aberrant proinflammatory cytokine, chemokine, and interferon-stimulated gene (ISG) signaling programs were also noted following infection of TRIF(−/−) mice that were similar to those seen in human patients with poor disease outcome following SARS-CoV or MERS-CoV infection. These findings highlight the importance of TLR adaptor signaling in generating a balanced protective innate immune response to highly pathogenic coronavirus infections.
has issue date	2015-05-26(xsd:dateTime)
bibo:doi	10.1128/mbio.00638-15
bibo:pmid	26015500
has license	cc-by-nc-sa
sha1sum (hex)	dcce6e45fd562d7a15633fc5a55aed8d3ce37f49
schema:url	https://doi.org/10.1128/mbio.00638-15
resource representing a document's title	Toll-Like Receptor 3 Signaling via TRIF Contributes to a Protective Innate Immune Response to Severe Acute Respiratory Syndrome Coronavirus Infection
has PubMed Central identifier	PMC4447251
has PubMed identifier	26015500
schema:publication	mBio
resource representing a document's body	covid:dcce6e45fd562d7a15633fc5a55aed8d3ce37f49#body_text
is schema:about of	named entity 'TOLL-LIKE RECEPTOR 3' named entity 'VIRUSES' named entity 'PATHOGENS' named entity 'TRANSIENT' named entity 'TLR4' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS' named entity 'CORONAVIRUSES' named entity 'BACTERIA' named entity 'MOUSE' named entity 'ADAPTOR PROTEIN' named entity 'MOLECULAR' named entity 'GLOBAL' named entity 'THERAPEUTIC' named entity 'TLR3' named entity 'WEIGHT LOSS' named entity 'HIGHLY' named entity 'PREVIOUSLY' named entity 'PATHOGENIC' named entity 'EXPERIENCE' named entity 'MULTIPLE' named entity 'LACK' named entity 'CONCERN' named entity 'weight loss' named entity 'innate immune response' named entity 'highly' named entity 'SARS-CoV' named entity 'experience' covid:arg/dcce6e45fd562d7a15633fc5a55aed8d3ce37f49 named entity 'INNATE IMMUNE RESPONSE' named entity 'CORONAVIRUS INFECTION' named entity 'ADAPTED' named entity 'PATTERNS' named entity 'SARS-COV INFECTION' named entity 'COMPONENT' named entity 'NECESSARY' named entity 'WILD-TYPE' named entity 'HERE' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS' named entity 'SIGNALING' named entity 'RESPONSE TO' named entity 'INITIATE' named entity 'SARS-COV' named entity 'TRAM' named entity 'MIDDLE EAST RESPIRATORY SYNDROME CORONAVIRUS' named entity 'REQUIRED' named entity 'RESPONSE TO' named entity 'STRATEGIES' named entity 'PROTEIN ' named entity 'EMERGENCE' named entity 'SIGNALING' named entity 'TRIF' named entity 'MYD88' named entity 'FUNGI ' named entity 'INFECTION' named entity 'IMMUNE RESPONSES' named entity 'SENSORS' named entity 'SUSCEPTIBLE' named entity 'INNATE IMMUNE RESPONSE' named entity 'BUT' named entity 'MORTALITY' named entity 'RECOGNIZE' named entity 'IN VIVO' named entity 'TOLL-LIKE RECEPTORS' named entity 'PUBLIC HEALTH' named entity 'ANTIVIRAL' named entity 'IS A' named entity 'VACCINE' named entity 'MICE' named entity 'Middle East respiratory syndrome' named entity 'TRAM' named entity 'MERS-CoV' named entity 'initiate' named entity 'therapeutic' named entity 'mice'

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