About: Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2-mediated complement over-activation

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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
title	Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2-mediated complement over-activation
Creator	Chen, Wei Cao, Cheng Li, Ping Ma, Qingjun Zhang, Lu Yang, Weihong Gao, Ting Hu, Yong Jin, Yanwen Liu, Xuan Mao, Qing Zhang, Zhang Peng, Jing Zhu, Lin Liu, Yue Li, Liu, Junli Bian, Xiuwu Chen, Xiaoyu Dong, Qincai Fu, Yangbo Hu, Mingdong Li, Kaitong Li, Lufeng Liu, Hainan Liu, Yaoning Luo, Shuping Song, Jibo Wang, Zhongyi Xiao, Yongjiu Xie, Yonghong Zhang, Xiaopeng Zhao, Huailong Zhao, Lingfang Zhao, Songtao
source	MedRxiv
abstract	An excessive immune response contributes to SARS-CoV, MERS-CoV and SARS-CoV-2 pathogenesis and lethality, but the mechanism remains unclear. In this study, the N proteins of SARS-CoV, MERS-CoV and SARS-CoV-2 were found to bind to MASP-2, the key serine protease in the lectin pathway of complement activation, resulting in aberrant complement activation and aggravated inflammatory lung injury. Either blocking the N protein:MASP-2 interaction or suppressing complement activation can significantly alleviate N protein-induced complement hyper-activation and lung injury in vitro and in vivo. Complement hyper-activation was also observed in COVID-19 patients, and a promising suppressive effect was observed when the deteriorating patients were treated with anti-C5a monoclonal antibody. Complement suppression may represent a common therapeutic approach for pneumonia induced by these highly pathogenic coronaviruses.
has issue date	2020-03-30(xsd:dateTime)
bibo:doi	10.1101/2020.03.29.20041962
has license	medrxiv
sha1sum (hex)	26cc3f38f54d8bb124682d382d7b5ffa4df0a257
schema:url	https://doi.org/10.1101/2020.03.29.20041962
resource representing a document's title	Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2-mediated complement over-activation
resource representing a document's body	covid:26cc3f38f54d8bb124682d382d7b5ffa4df0a257#body_text
is schema:about of	covid:arg/26cc3f38f54d8bb124682d382d7b5ffa4df0a257 named entity 'coronavirus' named entity 'Qing' named entity '+86' named entity 'lung injury' named entity 'protein' named entity 'MASP-2' named entity 'Qing' named entity 'Mao' named entity 'pathogenic' named entity 'complement' named entity 'lung injury' named entity 'mediated' named entity 'protein' named entity 'MASP-2' nodeID://b56431982 nodeID://b57734162 nodeID://b57885506 nodeID://b58020010
is wasQuotedFrom of	covid:arg/26cc3f38f54d8bb124682d382d7b5ffa4df0a257/0 covid:arg/26cc3f38f54d8bb124682d382d7b5ffa4df0a257/1 covid:arg/26cc3f38f54d8bb124682d382d7b5ffa4df0a257/2
is part of of	Highly pathogenic coronavirus N protein aggravates lung injury by MASP-2-mediated complement over-activation An excessive immune response contributes to SARS-CoV, MERS-CoV and SARS-CoV-2 pathogenesis and lethality, but the mechanism remains unclear. In this study, the N proteins of SARS-CoV, MERS-CoV and SARS-CoV-2 were found to bind to MASP-2, the key serine protease in the lectin pathway of complement activation, resulting in aberrant complement activation and aggravated inflammatory lung injury. Either blocking the N protein:MASP-2 interaction or suppressing complement activation can significantly alleviate N protein-induced complement hyper-activation and lung injury in vitro and in vivo. Complement hyper-activation was also observed in COVID-19 patients, and a promising suppressive effect was observed when the deteriorating patients were treated with anti-C5a monoclonal antibody. Complement suppression may represent a common therapeutic approach for pneumonia induced by these highly pathogenic coronaviruses. covid:26cc3f38f54d8bb124682d382d7b5ffa4df0a257#body_text

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