tetano
Editor, Senior Moderator
Cell Rep
. 2021 Sep 17;109793.
doi: 10.1016/j.celrep.2021.109793. Online ahead of print.
Single-cell analysis of COVID-19, sepsis, and HIV infection reveals hyperinflammatory and immunosuppressive signatures in monocytes
Nianping Liu[SUP] 1 [/SUP], Chen Jiang[SUP] 1 [/SUP], Pengfei Cai[SUP] 1 [/SUP], Zhuoqiao Shen[SUP] 2 [/SUP], Wujianan Sun[SUP] 3 [/SUP], Hao Xu[SUP] 3 [/SUP], Minghao Fang[SUP] 4 [/SUP], Xinfeng Yao[SUP] 5 [/SUP], Lin Zhu[SUP] 3 [/SUP], Xuyuan Gao[SUP] 3 [/SUP], Jingwen Fang[SUP] 6 [/SUP], Jun Lin[SUP] 1 [/SUP], Chuang Guo[SUP] 7 [/SUP], Kun Qu[SUP] 8 [/SUP]
Affiliations
Abstract
The mortality risk of coronavirus disease 2019 (COVID-19) patients has been linked to the cytokine storm caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Understanding the inflammatory responses shared between COVID-19 and other infectious diseases that feature cytokine storms may therefore help in developing improved therapeutic strategies. Here, we use integrative analysis of single-cell transcriptomes to characterize the inflammatory signatures of peripheral blood mononuclear cells from patients with COVID-19, sepsis, and HIV infection. We identify ten hyperinflammatory cell subtypes in which monocytes are the main contributors to the transcriptional differences in these infections. Monocytes from COVID-19 patients share hyperinflammatory signatures with HIV infection and immunosuppressive signatures with sepsis. Finally, we construct a "three-stage" model of heterogeneity among COVID-19 patients, related to the hyperinflammatory and immunosuppressive signatures in monocytes. Our study thus reveals cellular and molecular insights about inflammatory responses to SARS-CoV-2 infection and provides therapeutic guidance to improve treatments for subsets of COVID-19 patients.
Keywords: COVID-19; SARS-CoV-2; immunosuppression; inflammation.
. 2021 Sep 17;109793.
doi: 10.1016/j.celrep.2021.109793. Online ahead of print.
Single-cell analysis of COVID-19, sepsis, and HIV infection reveals hyperinflammatory and immunosuppressive signatures in monocytes
Nianping Liu[SUP] 1 [/SUP], Chen Jiang[SUP] 1 [/SUP], Pengfei Cai[SUP] 1 [/SUP], Zhuoqiao Shen[SUP] 2 [/SUP], Wujianan Sun[SUP] 3 [/SUP], Hao Xu[SUP] 3 [/SUP], Minghao Fang[SUP] 4 [/SUP], Xinfeng Yao[SUP] 5 [/SUP], Lin Zhu[SUP] 3 [/SUP], Xuyuan Gao[SUP] 3 [/SUP], Jingwen Fang[SUP] 6 [/SUP], Jun Lin[SUP] 1 [/SUP], Chuang Guo[SUP] 7 [/SUP], Kun Qu[SUP] 8 [/SUP]
Affiliations
- PMID: 34587478
- PMCID: PMC8445774
- DOI: 10.1016/j.celrep.2021.109793
Abstract
The mortality risk of coronavirus disease 2019 (COVID-19) patients has been linked to the cytokine storm caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Understanding the inflammatory responses shared between COVID-19 and other infectious diseases that feature cytokine storms may therefore help in developing improved therapeutic strategies. Here, we use integrative analysis of single-cell transcriptomes to characterize the inflammatory signatures of peripheral blood mononuclear cells from patients with COVID-19, sepsis, and HIV infection. We identify ten hyperinflammatory cell subtypes in which monocytes are the main contributors to the transcriptional differences in these infections. Monocytes from COVID-19 patients share hyperinflammatory signatures with HIV infection and immunosuppressive signatures with sepsis. Finally, we construct a "three-stage" model of heterogeneity among COVID-19 patients, related to the hyperinflammatory and immunosuppressive signatures in monocytes. Our study thus reveals cellular and molecular insights about inflammatory responses to SARS-CoV-2 infection and provides therapeutic guidance to improve treatments for subsets of COVID-19 patients.
Keywords: COVID-19; SARS-CoV-2; immunosuppression; inflammation.