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  • SARS-CoV-2 and viral sepsis: observations and hypotheses #MMPMID32311318
  • Li H; Liu L; Zhang D; Xu J; Dai H; Tang N; Su X; Cao B
  • Lancet 2020[May]; 395 (10235): 1517-1520 PMID32311318show ga
  • Since the outbreak of coronavirus disease 2019 (COVID-19), clinicians have tried every effort to understand the disease, and a brief portrait of its clinical features have been identified. In clinical practice, we noticed that many severe or critically ill COVID-19 patients developed typical clinical manifestations of shock, including cold extremities and weak peripheral pulses, even in the absence of overt hypotension. Understanding the mechanism of viral sepsis in COVID-19 is warranted for exploring better clinical care for these patients. With evidence collected from autopsy studies on COVID-19 and basic science research on severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) and SARS-CoV, we have put forward several hypotheses about SARS-CoV-2 pathogenesis after multiple rounds of discussion among basic science researchers, pathologists, and clinicians working on COVID-19. We hypothesise that a process called viral sepsis is crucial to the disease mechanism of COVID-19. Although these ideas might be proven imperfect or even wrong later, we believe they can provide inputs and guide directions for basic research at this moment.
  • |*Coronavirus Infections/complications[MESH]
  • |*Lung/immunology/pathology[MESH]
  • |*Pandemics[MESH]
  • |*Pneumonia, Viral/complications[MESH]
  • |Autopsy[MESH]
  • |Betacoronavirus/*pathogenicity[MESH]
  • |Blood Coagulation Disorders/virology[MESH]
  • |COVID-19[MESH]
  • |Critical Illness[MESH]
  • |Cytokines/*metabolism[MESH]
  • |Endothelium[MESH]
  • |Epithelium[MESH]
  • |Humans[MESH]
  • |Inflammation[MESH]
  • |Macrophages[MESH]
  • |SARS-CoV-2[MESH]
  • |Sepsis/*virology[MESH]
  • |Severity of Illness Index[MESH]
  • |Shock/etiology[MESH]

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  • suck abstract from ncbi

    1517 10235.395 2020