Preprint Hypothesis Version 1 This version is not peer-reviewed

SARS-CoV2 at the Alveolar Epithelial-Endothelial Interface – A Hypothesis for the Pathogenesis of COVID-19

Version 1 : Received: 29 May 2020 / Approved: 31 May 2020 / Online: 31 May 2020 (16:28:19 CEST)

How to cite: Acosta Saltos, A.; Carolina Acosta Saltos, F. SARS-CoV2 at the Alveolar Epithelial-Endothelial Interface – A Hypothesis for the Pathogenesis of COVID-19. Preprints 2020, 2020050480 (doi: 10.20944/preprints202005.0480.v1). Acosta Saltos, A.; Carolina Acosta Saltos, F. SARS-CoV2 at the Alveolar Epithelial-Endothelial Interface – A Hypothesis for the Pathogenesis of COVID-19. Preprints 2020, 2020050480 (doi: 10.20944/preprints202005.0480.v1).

Abstract

Severe COVID-19 is associated with viraemia and multiple organ disease. Similar clinicopathological features have been previously seen in SARS and MERS. Clinically, the severity of SARS, MERS and COVID-19 has been associated with the presence of SARS-CoV, MERS-CoV or SARS-CoV2 viraemia in affected patients. In vitro work has looked at the pattern of viral entry and release from polarised epithelial cells infected by coronaviruses. This work has demonstrated a correlation between the severity of a coronavirus infection and the ability of the virus to reach and infect the basal surface of host cells. It has been postulated that this ability helps the virus invade the bloodstream of the host, resulting in a systemic infection with multiple organ involvement. Here we propose that basal surface release and entry of COVID-19 into and out of cells at epithelial-endothelial interface plays a key pathogenic role in severe COVID-19 disease.

Subject Areas

endothelial; infection; basement membrane; fibroblast; fibrosis; nsp7; hypothesis; pathogenesis; COVID-19; SARS-CoV2

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