About: Heightened innate immune responses in the respiratory tract of COVID-19 patients

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About: Heightened innate immune responses in the respiratory tract of COVID-19 patients 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	Heightened innate immune responses in the respiratory tract of COVID-19 patients
Creator	Yang, Jian Zhang, Li Ren, Lili Wang, Jianwei Xiao, Yan Yang, Jing Chen, Mingwei Gao, Zhancheng Guo, Li Li, Hongru Li, Mingkun Xu, Yu Yang, Donghong Zhang, Guoliang Zhong, Jiaxin Zhou, Zhuo Wang, Weidong Jin, Qi Liu, Bo Zhou, Z Dong, Jie Jiang, Shuai Chen, H Wang, X Zhang, L Wang, Chun Chen, Y He, Kunlun Li, Q Liu, J Wang, J Zhang, Guo, Z Jiang, C Li, G Yang, S Ren, L Zhang, B Jia, Y Jia, Zhilong Xiao, J Chen, Fuhui Gao, M Guoliang, Xu, F Zhang, Xiannian
Source	Elsevier; Medline; PMC; WHO
abstract	Summary The outbreaks of 2019 novel coronavirus disease (COVID-19) caused by SARS-CoV-2 infection has posed a severe threat to global public health. It is unclear how the human immune system responds to this infection. Here, we used metatranscriptomic sequencing to profile immune signatures in the bronchoalveolar lavage fluid of eight COVID-19 cases. The expression of proinflammatory genes, especially chemokines, was markedly elevated in COVID-19 cases compared to community-acquired pneumonia patients and healthy controls, suggesting that SARS-CoV-2 infection causes hypercytokinemia. Compared to SARS-CoV, which is thought to induce inadequate interferon (IFN) responses, SARS-CoV-2 robustly triggered expression of numerous IFN-inducible genes (ISGs). These ISGs exhibit immunopathogenic potential, with overrepresentation of genes involved in inflammation. The transcriptome data was also used to estimate immune cell populations, revealing increases in activated dendritic cells and neutrophils. Collectively, these host responses to SARS-CoV-2 infection could further our understanding of disease pathogenesis and point towards antiviral strategies.
has issue date	2020-05-04(xsd:dateTime)
bibo:doi	10.1016/j.chom.2020.04.017
bibo:pmid	32407669
has license	els-covid
sha1sum (hex)	0e10bd6e8479cc0809b6b38cc8961b160749246c
schema:url	https://doi.org/10.1016/j.chom.2020.04.017
resource representing a document's title	Heightened innate immune responses in the respiratory tract of COVID-19 patients
has PubMed Central identifier	PMC7196896
has PubMed identifier	32407669
schema:publication	Cell Host Microbe
resource representing a document's body	covid:0e10bd6e8479cc0809b6b38cc8961b160749246c#body_text
is schema:about of	named entity 'coronavirus' named entity 'neutrophils' named entity 'These' named entity 'HUMAN' named entity 'EXHIBIT' named entity 'SARS-COV-2 INFECTION' named entity 'genes' named entity 'cases' named entity 'signatures' named entity 'expression' named entity 'cases' named entity 'innate immune responses' named entity 'COVID' named entity 'SARS-CoV' named entity 'SARS-CoV-2' named entity 'IFN' named entity 'global public health' named entity 'COVID' named entity 'inflammation' named entity 'infection' named entity 'chemokines' named entity 'antiviral' named entity 'IPA' named entity 'z-score' named entity 'q-value' named entity 'KEGG' named entity '1.6' named entity 'Endocannabinoid' named entity 'cytokine' named entity 'Interleukin' named entity 'CXCL8' named entity 'HBP1' named entity 'OSMR' named entity 'CCR1' named entity 'IFITM1' named entity 'IFIH1'

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