Corpus overview


MeSH Disease

HGNC Genes

SARS-CoV-2 proteins

There are no SARS-CoV-2 protein terms in the subcorpus


SARS-CoV-2 Proteins
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    SARS-CoV-2 activates lung epithelia cell proinflammatory signaling and leads to immune dysregulation in COVID-19 MESHD patients by single-cell sequencing

    Authors: Huarong Chen; Weixin Liu; Dabin Liu; Liuyang Zhao; Jun Yu

    doi:10.1101/2020.05.08.20096024 Date: 2020-05-13 Source: medRxiv

    Objective: The outbreak of Coronavirus disease 2019 MESHD ( COVID-19 MESHD) caused by SARS-CoV-2 infection MESHD has become a global health emergency. We aim to decipher SARS-CoV-2 infected MESHD cell types, the consequent host immune response and their interplay in the lung of COVID-19 MESHD patients. Design: We analyzed single-cell RNA sequencing (scRNA-seq) data of lung samples from 17 subjects (6 severe COVID-19 MESHD patients, 3 mild patients who recovered and 8 healthy controls). The expression of SARS-CoV-2 receptors ( ACE2 HGNC and TMPRSS2 HGNC) was examined among different cell types in the lung. The immune cells infiltration patterns, their gene expression profiles, and the interplay of immune cells and SARS-CoV-2 target cells were further investigated. Results: Compared to healthy controls, the overall ACE2 HGNC (receptor of SARS-CoV-2) expression was significantly higher in lung epithelial cells of COVID-19 MESHD patients, in particular in ciliated cell, club cell and basal cell. Comparative transcriptome analysis of these lung epithelial cells of COVID-19 MESHD patients and healthy controls identified that SARS-CoV-2 infection MESHD activated pro-inflammatory signaling including interferon pathway and cytokine signaling. Moreover, we identified dysregulation of immune response in patients with COVID-19 MESHD. In severe COVID-19 MESHD patients, significantly higher neutrophil, but lower T and NK cells in lung were observed along with markedly increased cytokines ( CCL2 HGNC, CCL3 HGNC, CCL4 HGNC, CCL7 HGNC, CCL3L1 HGNC and CCL4L2 HGNC) compared with healthy controls as well as mild patients who recovered. The cytotoxic phenotypes were shown in lung T and NK cells of severe patients as evidenced by enhanced IFN{gamma HGNC}, Granulysin HGNC, Granzyme B HGNC and Perforin expression. Moreover, SARS-CoV-2 infection MESHD altered the community interplay of lung epithelial cells and immune cells: the interaction between epithelial cells with macrophage, T and NK cell was stronger, but their interaction with neutrophils was lost in COVID-19 MESHD patients compared to healthy controls. Conclusions: SARS-CoV-2 infection MESHD activates pro-inflammatory signaling in lung epithelial cells expressing ACE2 HGNC and causes dysregulation of immune response to release more pro-inflammatory cytokines. Moreover, SARS-CoV-2 infection MESHD breaks the interplay of lung epithelial cells and immune cells.

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MeSH Disease
HGNC Genes
SARS-CoV-2 Proteins

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