期刊
JOURNAL OF CELL COMMUNICATION AND SIGNALING
卷 14, 期 4, 页码 469-470出版社
SPRINGER
DOI: 10.1007/s12079-020-00574-3
关键词
Interferon regulator factors (IRFs); SARS-CoV-2; Tocilizumab
类别
资金
- American Heart Association National Scientist Development Grant [09SDG2260957]
- National Institutes of Health National Heart, Lung, and Blood Institute [R01 HL-105932]
- Joy McCann Culverhouse endowment
In the past two decades, two beta-coronaviruses, severe acute respiratory syndrome-related coronavirus (SARS-CoV-1) and the Middle East respiratory syndrome-related coronavirus (MERS-CoV), have infected approximately 8000 and 2500 across the globe, respectively (de Wit et al.2016; Amanat and Krammer2020). The current viral pandemic, caused by SARS-CoV-2, has already affected 4.23 M in less than a year. Of greater concern, the disease caused by SARS-CoV-2, COVID-19, still has a rapidly increasing global burden (Wu et al.2020; Zhu et al.2020). To better understand the biology of COVID-19, an initial barrage of studies compared SARS-CoV-2 to other respiratory viruses: MERS-CoV, SARS-CoV-1, human parainfluenza virus 3 (HPIV3), respiratory syncytial virus (RSV), and Influenza A Virus (IAV). These studies indicate that SARS-CoV-2 infected individuals have a consistent chemokine signature comprising cytokines and monocyte-associated chemokines (CCL2 and CCL8). Therefore, it appears that monocyte cytokine production, particularly in those with a diminished innate immunity, is a driving feature of COVID-19 infection.
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