PDF(Pubmed)
Abstract：
Increased cases of sepsis during COVID-19 in the absence of known bacterial pathogens highlighted role of viruses as causative agents of sepsis. In this study, we investigated clinical, laboratory, proteomic, and metabolomic characteristics of viral sepsis patients (n = 45) and compared them to non-sepsis patients with COVID-19 (n = 186) to identify molecular mechanisms underlying the pathology of viral sepsis in COVID-19. We identified unique metabolomic and proteomic signatures that suggest a substantial perturbation in the coagulation, complement, and platelet activation pathways in viral sepsis. Our proteomic data indicated elevated coagulation pathway protein (fibrinogen), whereas a decrease in many of the complement proteins was observed. These alterations were associated with the functional consequences such as susceptibility to secondary bacterial infections and potentially contributing to both local and systemic disease phenotypes. Our data provide novel aspect of COVID-19 pathology that is centered around presence of sepsis phenotype in COVID-19.
摘要：
在没有已知细菌病原体的情况下，COVID-19期间脓毒症病例的增加强调了病毒作为脓毒症病原体的作用。在这项研究中,我们调查了临床，实验室,蛋白质组学，和病毒性脓毒症患者（n=45）的代谢组学特征，并将其与COVID-19的非脓毒症患者（n=186）进行比较，以确定COVID-19中病毒性脓毒症病理的分子机制。我们确定了独特的代谢组学和蛋白质组学特征，这些特征表明凝血功能存在实质性扰动，补语,和病毒性脓毒症的血小板活化途径。我们的蛋白质组数据表明凝血途径蛋白（纤维蛋白原）升高，而观察到许多补体蛋白的减少。这些改变与功能后果有关，例如对继发细菌感染的易感性，并可能导致局部和全身性疾病表型。我们的数据提供了COVID-19病理学的新方面，该病理学围绕COVID-19中败血症表型的存在。
