SARS-CoV-2 and viral sepsis: observations and hypotheses

SARS-CoV-2 and viral sepsis: observations and hypotheses

2020-05-09 | Hui Li, Liang Liu, Dingyu Zhang, Jiyang Xu, Huaping Dai, Nan Tang, Xiao Su, Bin Cao
The COVID-19 Resource Centre, established by Elsevier in January 2020, provides free information in English and Mandarin on the novel coronavirus. Elsevier grants permission to make all COVID-19-related research available in PubMed Central and other public repositories, with unrestricted reuse and analysis rights, as long as the resource centre remains active. The article discusses the clinical features of severe or critically ill COVID-19 patients, noting that many developed typical shock symptoms, including cold extremities and weak peripheral pulses, even without overt hypotension. These patients often exhibited severe metabolic acidosis and organ dysfunction, meeting the criteria for sepsis and septic shock. The authors hypothesize that viral sepsis is a crucial mechanism in the pathogenesis of COVID-19, and they propose several hypotheses based on autopsy studies and basic science research. The introduction highlights the global impact of the SARS-CoV-2 outbreak, with over 200,000 confirmed cases by March 19, 2020. The disease affects about 5% of patients, leading to severe lung injury and multiorgan dysfunction. The article details the pathological changes in various organs, including the lungs, spleen, kidneys, liver, and brain, and suggests that SARS-CoV-2 can directly attack multiple organs, particularly those with high expression of ACE2 or L-SIGN. The immune response to SARS-CoV-2 is discussed, emphasizing the role of proinflammatory cytokines and chemokines. The authors highlight the importance of identifying the primary source of the cytokine storm and understanding the kinetics of cytokine activation. They also explore the dysregulated immune response, including lymphopenia, and its potential mechanisms. The article further examines the abnormal coagulation observed in COVID-19 patients, with a significant association between coagulopathy and poor prognosis. The authors suggest that SARS-CoV-2 may directly attack vascular endothelial cells, leading to abnormal coagulation and sepsis. In conclusion, the authors hypothesize that in mild cases, the immune system can contain the virus, but in severe cases, the epithelial–endothelial barrier is disrupted, leading to uncontrolled inflammation and viral sepsis. Effective antiviral therapy and measures to modulate the immune response are essential for improving patient outcomes. The article calls for further research to explore the mechanisms of viral sepsis and the impact of various treatments.The COVID-19 Resource Centre, established by Elsevier in January 2020, provides free information in English and Mandarin on the novel coronavirus. Elsevier grants permission to make all COVID-19-related research available in PubMed Central and other public repositories, with unrestricted reuse and analysis rights, as long as the resource centre remains active. The article discusses the clinical features of severe or critically ill COVID-19 patients, noting that many developed typical shock symptoms, including cold extremities and weak peripheral pulses, even without overt hypotension. These patients often exhibited severe metabolic acidosis and organ dysfunction, meeting the criteria for sepsis and septic shock. The authors hypothesize that viral sepsis is a crucial mechanism in the pathogenesis of COVID-19, and they propose several hypotheses based on autopsy studies and basic science research. The introduction highlights the global impact of the SARS-CoV-2 outbreak, with over 200,000 confirmed cases by March 19, 2020. The disease affects about 5% of patients, leading to severe lung injury and multiorgan dysfunction. The article details the pathological changes in various organs, including the lungs, spleen, kidneys, liver, and brain, and suggests that SARS-CoV-2 can directly attack multiple organs, particularly those with high expression of ACE2 or L-SIGN. The immune response to SARS-CoV-2 is discussed, emphasizing the role of proinflammatory cytokines and chemokines. The authors highlight the importance of identifying the primary source of the cytokine storm and understanding the kinetics of cytokine activation. They also explore the dysregulated immune response, including lymphopenia, and its potential mechanisms. The article further examines the abnormal coagulation observed in COVID-19 patients, with a significant association between coagulopathy and poor prognosis. The authors suggest that SARS-CoV-2 may directly attack vascular endothelial cells, leading to abnormal coagulation and sepsis. In conclusion, the authors hypothesize that in mild cases, the immune system can contain the virus, but in severe cases, the epithelial–endothelial barrier is disrupted, leading to uncontrolled inflammation and viral sepsis. Effective antiviral therapy and measures to modulate the immune response are essential for improving patient outcomes. The article calls for further research to explore the mechanisms of viral sepsis and the impact of various treatments.
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