From H1N1 to 2019-nCoV, what do we learn?
10.1016/j.cjtee.2020.06.005
- Author:
Gui-E LIU
1
;
Yuan TIAN
1
;
Wen-Jun ZHAO
1
;
Shuang-Ming SONG
1
;
Lei LI
2
Author Information
1. State Key Laboratory of Trauma, Burns and Combined Injury, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China.
2. State Key Laboratory of Trauma, Burns and Combined Injury, Research Institute of Surgery, Daping Hospital, Army Medical University, Chongqing 400042, China. Electronic address: leili@cjtrauma.com.
- Publication Type:Editorial
- Keywords:
COVID-19;
Excessive inflammatory response;
Immunosuppression;
Sepsis
- MeSH:
Betacoronavirus;
Coronavirus Infections;
complications;
epidemiology;
immunology;
Humans;
Immune Tolerance;
Inflammation;
complications;
Influenza A Virus, H1N1 Subtype;
Influenza, Human;
complications;
epidemiology;
immunology;
Pandemics;
Pneumonia, Viral;
complications;
epidemiology;
immunology;
Sepsis;
etiology
- From:
Chinese Journal of Traumatology
2020;23(4):187-189
- CountryChina
- Language:English
-
Abstract:
The COVID-19 pandemic is still raging across the world. Everyday thousands of infected people lost their lives. What is worse, there is no specific medicine and we do not know when the end of the pandemic will come. The nearest global pandemic is the 1918 influenza, which caused about 50 million deaths and partly terminate the World War Ⅰ. We believe that no matter the virus H1N1 for the 1918 influenza or 2019-nCoV for COVID-19, they are essentially the same and the final cause of death is sepsis. The definition and diagnostic/management criteria of sepsis have been modified several times but the mortality rate has not been improved until date. Over decades, researchers focus either on the immunosuppression or on the excessive inflammatory response following trauma or body exposure to harmful stimuli. But the immune response is very complex with various regulating factors involved in, such as neurotransmitter, endocrine hormone, etc. Sepsis is not a kind of disease, instead a misbalance of the body following infection, trauma or other harmful stimulation. Therefore we should re-think sepsis comprehensively with the concept of systemic biology, i.e. inflammationomics.
