Abstract
Severe COVID-19 shares pathophysiological, immunological, metabolic, and clinical features with classic bacterial sepsis. Patients with severe COVID-19 have sepsis-like manifestations, such as acute respiratory distress syndrome and multiple organ failure. However, research indicates that COVID-19 leads to acute respiratory distress syndrome and that septic syndrome is more fatal than septic syndrome of other etiologies. SARS-CoV-2 initially infects the lungs; however, in COVID-19-associated sepsis, the majority of deaths are caused by the subsequent involvement of multiple organs. Many patients who died because of COVID-19 died from sepsis, a life-threatening dysfunctional response to infection that is accompanied by respiratory and multiple organ failure.
Overlapping molecular characteristics are found in patients with severe COVID-19 and sepsis from all causes. Endotypes that reflect different etiologies of sepsis have been identified in patients with severe COVID-19. Whole-blood proteomics and transcriptomics are useful in identifying the pathogenetic mechanisms and multimolecular signatures of COVID-associated sepsis and other sepsis, which allow for the development of more specific criteria for early diagnosis, patient classification, and therapeutic choices.
The detection of sepsis endotypes in patients with COVID-19 implies that sepsis endotypes may be useful for clinical risk stratification in COVID-associated sepsis and the potential opportunity to treat these patients with targeted immunomodulatory therapies that can correct endotype-specific dysfunctional immune processes.