About: Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis

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

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type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
title	Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis
Creator	Baric, Ralph Gralinski, Lisa Whitmore, Alan Heise, Mark Sheahan, Timothy Jensen, Kara Menachery, Vineet Leist, Sarah Morrison, Thomas
source	Medline; PMC
abstract	Acute respiratory distress syndrome (ARDS) is immune-driven pathologies that are observed in severe cases of severe acute respiratory syndrome coronavirus (SARS-CoV) infection. SARS-CoV emerged in 2002 to 2003 and led to a global outbreak of SARS. As with the outcome of human infection, intranasal infection of C57BL/6J mice with mouse-adapted SARS-CoV results in high-titer virus replication within the lung, induction of inflammatory cytokines and chemokines, and immune cell infiltration within the lung. Using this model, we investigated the role of the complement system during SARS-CoV infection. We observed activation of the complement cascade in the lung as early as day 1 following SARS-CoV infection. To test whether this activation contributed to protective or pathologic outcomes, we utilized mice deficient in C3 (C3(–/–)), the central component of the complement system. Relative to C57BL/6J control mice, SARS-CoV-infected C3(–/–) mice exhibited significantly less weight loss and less respiratory dysfunction despite equivalent viral loads in the lung. Significantly fewer neutrophils and inflammatory monocytes were present in the lungs of C3(–/–) mice than in C56BL/6J controls, and subsequent studies revealed reduced lung pathology and lower cytokine and chemokine levels in both the lungs and the sera of C3(–/–) mice than in controls. These studies identify the complement system as an important host mediator of SARS-CoV-induced disease and suggest that complement activation regulates a systemic proinflammatory response to SARS-CoV infection. Furthermore, these data suggest that SARS-CoV-mediated disease is largely immune driven and that inhibiting complement signaling after SARS-CoV infection might function as an effective immune therapeutic.
has issue date	2018-10-09(xsd:dateTime)
bibo:doi	10.1128/mbio.01753-18
bibo:pmid	30301856
has license	cc-by
sha1sum (hex)	948028bf6ac0f66ea490a476c599db04fb42a50f
schema:url	https://doi.org/10.1128/mbio.01753-18
resource representing a document's title	Complement Activation Contributes to Severe Acute Respiratory Syndrome Coronavirus Pathogenesis
has PubMed Central identifier	PMC6178621
has PubMed identifier	30301856
schema:publication	mBio
resource representing a document's body	covid:948028bf6ac0f66ea490a476c599db04fb42a50f#body_text
is schema:about of	named entity 'LED' named entity 'VIRAL LOAD' named entity 'FOLLOWING' named entity 'SARS' named entity 'REVEALED' named entity 'OBSERVED' named entity 'PRESENT' named entity 'PATHOLOGIES' named entity 'CHEMOKINE' named entity 'DIRECTLY' named entity 'VIRAL' named entity 'THE LUNGS' named entity 'MONOCYTES' named entity 'DISEASE' named entity 'NEUTROPHILS' named entity 'SUBSEQUENT' named entity 'RESULTS' named entity 'ADVANCE' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS' named entity 'TITER' named entity 'THEIR' covid:arg/948028bf6ac0f66ea490a476c599db04fb42a50f named entity 'CONTROL' named entity 'RELATIVE TO' named entity 'WEIGHT LOSS' named entity 'MICE' named entity 'TO TEST' named entity 'SEVERE' named entity 'FUNGAL INFECTIONS' named entity 'IMMUNE' named entity 'FUNCTION' named entity 'CONSISTENT WITH' named entity 'RESPIRATORY DISEASE' named entity 'ACUTE RESPIRATORY DISTRESS SYNDROME' named entity 'LARGELY' named entity 'IDENTIFY' named entity 'HOST DEFENSE' named entity 'INFECTION' named entity 'ABSENCE OF' named entity 'ACTIVATION' named entity 'MEDIATED' named entity 'EQUIVALENT' named entity 'CELL INFILTRATION ' named entity 'RESPIRATORY DYSFUNCTION' named entity 'THESE' named entity 'INDUCED' named entity 'EARLY' named entity 'GLOBAL' named entity 'COMPLEMENT ACTIVATION' named entity 'SEVERE ACUTE RESPIRATORY SYNDROME CORONAVIRUS' named entity 'LUNG' named entity 'INFECTED' named entity 'OBSERVATION' named entity 'COMPLEMENT' named entity 'USING' named entity 'OUTCOMES' named entity 'TEST' named entity 'HAVE' named entity 'DAY 1' named entity 'MIGHT BE' named entity 'SIGNALING' named entity 'SARS-COV' named entity 'MODEL' named entity 'SARS-COV INFECTION' named entity 'IS A' named entity 'PATHOLOGY' named entity 'MOUSE MODEL' named entity 'CORONAVIRUS INFECTION' named entity 'LEVELS' named entity 'STUDY' named entity 'HOST' named entity 'OUTBREAK' named entity 'INHIBITION'

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