Clinical features and multiomics profiles indicate coagulation and platelet dysfunction in COVID-19 viral sepsis
Zhiqing Xiao,
Minggui Lin,
Ning Song,
Xue Wu,
Jingyu Hou,
Lili Wang,
XinLun Tian,
Chunge An,
Charles S. Dela Cruz,
Lokesh Sharma,
De Chang
Affiliations
Zhiqing Xiao
Department of Pulmonary and Critical Care Medicine at The Seventh Medical Center, College of Pulmonary and Critical Care Medicine of The Eighth Medical Center, Chinese PLA General Hospital, Beijing 100853, China; Hebei North University, Zhangjiakou 075000, Hebei, China
Minggui Lin
Beijing Tsinghua Changgung Hospital, Tsinghua University School of Medicine, Beijing 102218, China
Ning Song
Department of Infectious Diseases, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China
Xue Wu
Department of Pulmonary and Critical Care Medicine at The Seventh Medical Center, College of Pulmonary and Critical Care Medicine of The Eighth Medical Center, Chinese PLA General Hospital, Beijing 100853, China
Jingyu Hou
Department of Infectious Diseases, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei 050000, China
Lili Wang
Beijing Tsinghua Changgung Hospital, Tsinghua University School of Medicine, Beijing 102218, China
XinLun Tian
Department of Pulmonary and Critical Care Medicine, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China
Chunge An
Department of Pulmonary and Critical Care Medicine at The Seventh Medical Center, College of Pulmonary and Critical Care Medicine of The Eighth Medical Center, Chinese PLA General Hospital, Beijing 100853, China
Charles S. Dela Cruz
Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA
Lokesh Sharma
Division of Pulmonary, Allergy, Critical Care, and Sleep Medicine, Department of Medicine, University of Pittsburgh School of Medicine, Pittsburgh, PA 15213, USA; Corresponding author
De Chang
Department of Pulmonary and Critical Care Medicine at The Seventh Medical Center, College of Pulmonary and Critical Care Medicine of The Eighth Medical Center, Chinese PLA General Hospital, Beijing 100853, China; Corresponding author
Summary: 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.
