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

By Hui Li, Liang Liu, Dingyu Zhang, Jiuyang Xu, H. Dai, Nan Tang, Xiaodong Su, B. Cao. The Lancet, 2020

1,052 citations recorded by the source corpus.

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.

Subfields: Infectious Diseases, Neurology

View Paper: https://www.semanticscholar.org/paper/14f8d9c6de3afc3ac628ed4bbbbf800e633e9775

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Citations in the corpus

Autopsy Findings and Venous Thromboembolism in Patients With COVID-19 (2020, background): “In a subgroup of patients with severe COVID19, high plasma levels of proinflammatory cytokines were observed (23).”
Elevated Calprotectin and Abnormal Myeloid Cell Subsets Discriminate Severe from Mild COVID-19 (2020, neutral): “, 2020a); however, the primary source of the cytokine storm and of the mechanisms behind lymphocytopenia remains elusive (Li et al., 2020).”
The cytokine storm and COVID‐19 (2020, background): “25‐28 Electron microscopy has revealed the presence of SARS‐CoV‐2 virus particles in bronchial and alveolar type II epithelial cells, but not in other tissues.(26,27) Therefore, although a”