About: Rationale for targeting Complement in COVID‐19

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About: Rationale for targeting Complement in COVID‐19 Goto Sponge NotDistinct Permalink

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

Attributes	Values
type	Academic Article research paper schema:ScholarlyArticle
isDefinedBy	Covid-on-the-Web dataset
has title	Rationale for targeting Complement in COVID‐19
Creator	Fanelli, Giorgia Farrar, Conrad Greenlaw, Roseanna Howard, Mark Klavinskis, Linda Polycarpou, Anastasia Sacks, Steven Wallis, Russell
topic	covid:501cacc32f36759c08bceffdab3a52d7af2e5a07#this
Source	Medline; PMC
abstract	A novel coronavirus, SARS‐CoV‐2, has recently emerged in China and spread internationally, posing a health emergency to the global community. COVID‐19 caused by SARS‐CoV‐2 is associated with an acute respiratory illness that varies from mild to the life‐threatening acute respiratory distress syndrome (ARDS). The complement system is part of the innate immune arsenal against pathogens, which many viruses can evade or employ to mediate cell entry. The immunopathology and acute lung injury orchestrated through the influx of pro‐inflammatory macrophages and neutrophils can be directly activated by complement components to prime an overzealous cytokine storm. The manifestations of severe COVID‐19 such as the ARDS, sepsis and multiorgan failure have an established relationship with activation of the complement cascade. We have collected evidence from all the current studies we are aware of on SARS‐CoV‐2 immunopathogenesis and the preceding literature on SARS‐CoV‐1 and MERS‐CoV infection linking severe COVID‐19 disease directly with dysfunction of the complement pathways. This information lends support for a therapeutic anti‐inflammatory strategy against complement, where a number of clinically ready potential therapeutic agents are available.
has issue date	2020-06-19(xsd:dateTime)
bibo:doi	10.15252/emmm.202012642
bibo:pmid	32559343
has license	no-cc
sha1sum (hex)	501cacc32f36759c08bceffdab3a52d7af2e5a07
schema:url	https://doi.org/10.15252/emmm.202012642
resource representing a document's title	Rationale for targeting Complement in COVID‐19
has PubMed Central identifier	PMC7323084
has PubMed identifier	32559343
schema:publication	EMBO Mol Med
resource representing a document's body	covid:501cacc32f36759c08bceffdab3a52d7af2e5a07#body_text
is http://vocab.deri.ie/void#inDataset of	proxy:http/ns.inria.fr/covid19/501cacc32f36759c08bceffdab3a52d7af2e5a07
is schema:about of	named entity 'mediate' named entity 'COVID-19' named entity 'innate immune' named entity 'SARS-CoV-2' named entity 'PATHOGENS' named entity 'PART OF' named entity 'EMERGENCY' named entity 'viruses' named entity 'acute respiratory distress syndrome (ARDS)' named entity 'acute lung injury' named entity 'varies' named entity 'macrophages' named entity 'COVID-19' named entity 'ARDS' named entity 'pro-inflammatory' named entity 'China' named entity 'coronavirus' named entity 'macrophages' named entity 'pathogens' named entity 'acute lung injury' named entity 'fibrinogen' named entity 'binding site' named entity 'ARDS' named entity 'infectious bronchitis virus' named entity 'Complement activation' named entity 'fibrinogen' named entity 'COVID-19' named entity 'Canna' named entity 'IL-10' named entity 'thrombosis' named entity 'fibrinogen' named entity 'Numis' named entity 'C3 convertase' named entity 'coagulation' named entity 'virus' named entity 'collectins' named entity 'proteolytic cleavage' named entity 'lectin complement pathway' named entity 'TNF' named entity 'viruses' named entity 'monocytes' named entity 'L-fucose' named entity 'alternative pathway' named entity 'complement' named entity 'C3a' named entity 'lung' named entity 'systemic administration' named entity 'complement' named entity 'macrophages' named entity 'Intercellular adhesion molecule' named entity 'viral load' named entity 'serine protease' named entity 'anticoagulant therapy' named entity 'murine' named entity 'deficient mice' named entity 'proximal tubule' named entity 'Angiotensin II' named entity 'viral infection' named entity 'virus' named entity 'Almansa' named entity 'glycosylation' named entity 'lectin' named entity 'coagulopathy' named entity 'complement activation pathway' named entity 'membrane attack complex' named entity 'infection' named entity 'glycans' named entity 'erythrocytes' named entity 'COVID' named entity 'off-label treatment' named entity 'structural proteins' named entity 'ligand'

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