Longitudinal Peripheral Blood Transcriptional Analysis Reveals Molecular Signatures of Disease Progression in COVID-19 Patients
Copyright © 2021 by The American Association of Immunologists, Inc..
Coronavirus disease 2019 (COVID-19) is caused by a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with some patients developing severe illness or even death. Disease severity has been associated with increased levels of proinflammatory cytokines and lymphopenia. To elucidate the atlas of peripheral immune response and pathways that might lead to immunopathology during COVID-19 disease course, we performed a peripheral blood RNA sequencing analysis of the same patient's samples collected from symptom onset to full recovery. We found that PBMCs at different disease stages exhibited unique transcriptome characteristics. We observed that SARS-CoV-2 infection caused excessive release of inflammatory cytokines and lipid mediators as well as an aberrant increase of low-density neutrophils. Further analysis revealed an increased expression of RNA sensors and robust IFN-stimulated genes expression but a repressed type I IFN production. SARS-CoV-2 infection activated T and B cell responses during the early onset but resulted in transient adaptive immunosuppression during severe disease state. Activation of apoptotic pathways and functional exhaustion may contribute to the reduction of lymphocytes and dysfunction of adaptive immunity, whereas increase in IL2, IL7, and IL15 may facilitate the recovery of the number and function of lymphocytes. Our study provides comprehensive transcriptional signatures of peripheral blood response in patients with moderate COVID-19.
| Medienart: |
E-Artikel |
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| Erscheinungsjahr: |
2021 |
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| Erschienen: |
2021 |
| Enthalten in: |
Zur Gesamtaufnahme - volume:206 |
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| Enthalten in: |
Journal of immunology (Baltimore, Md. : 1950) - 206(2021), 9 vom: 01. Mai, Seite 2146-2159 |
| Sprache: |
Englisch |
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| Beteiligte Personen: |
Yan, Qihong [VerfasserIn] |
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| Links: |
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| Themen: |
Clinical Trial |
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| Anmerkungen: |
Date Completed 03.05.2021 Date Revised 03.05.2021 published: Print-Electronic Citation Status MEDLINE |
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| doi: |
10.4049/jimmunol.2001325 |
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| funding: |
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| Förderinstitution / Projekttitel: |
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| PPN (Katalog-ID): |
NLM324012403 |
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| 520 | |a Copyright © 2021 by The American Association of Immunologists, Inc. | ||
| 520 | |a Coronavirus disease 2019 (COVID-19) is caused by a novel coronavirus named severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), with some patients developing severe illness or even death. Disease severity has been associated with increased levels of proinflammatory cytokines and lymphopenia. To elucidate the atlas of peripheral immune response and pathways that might lead to immunopathology during COVID-19 disease course, we performed a peripheral blood RNA sequencing analysis of the same patient's samples collected from symptom onset to full recovery. We found that PBMCs at different disease stages exhibited unique transcriptome characteristics. We observed that SARS-CoV-2 infection caused excessive release of inflammatory cytokines and lipid mediators as well as an aberrant increase of low-density neutrophils. Further analysis revealed an increased expression of RNA sensors and robust IFN-stimulated genes expression but a repressed type I IFN production. SARS-CoV-2 infection activated T and B cell responses during the early onset but resulted in transient adaptive immunosuppression during severe disease state. Activation of apoptotic pathways and functional exhaustion may contribute to the reduction of lymphocytes and dysfunction of adaptive immunity, whereas increase in IL2, IL7, and IL15 may facilitate the recovery of the number and function of lymphocytes. Our study provides comprehensive transcriptional signatures of peripheral blood response in patients with moderate COVID-19 | ||
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| 650 | 4 | |a Research Support, Non-U.S. Gov't | |
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| 650 | 7 | |a Inflammation Mediators |2 NLM | |
| 700 | 1 | |a Li, Pingchao |e verfasserin |4 aut | |
| 700 | 1 | |a Ye, Xianmiao |e verfasserin |4 aut | |
| 700 | 1 | |a Huang, Xiaohan |e verfasserin |4 aut | |
| 700 | 1 | |a Feng, Bo |e verfasserin |4 aut | |
| 700 | 1 | |a Ji, Tianxing |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Zhilong |e verfasserin |4 aut | |
| 700 | 1 | |a Li, Feng |e verfasserin |4 aut | |
| 700 | 1 | |a Zhang, Yudi |e verfasserin |4 aut | |
| 700 | 1 | |a Luo, Kun |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Fengjuan |e verfasserin |4 aut | |
| 700 | 1 | |a Mo, Xiaoneng |e verfasserin |4 aut | |
| 700 | 1 | |a Wang, Jianhua |e verfasserin |4 aut | |
| 700 | 1 | |a Feng, Liqiang |e verfasserin |4 aut | |
| 700 | 1 | |a Hu, Fengyu |e verfasserin |4 aut | |
| 700 | 1 | |a Lei, Chunliang |e verfasserin |4 aut | |
| 700 | 1 | |a Qu, Linbing |e verfasserin |4 aut | |
| 700 | 1 | |a Chen, Ling |e verfasserin |4 aut | |
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