Vascular underpinning of COVID-19

Open Biology
Vanessa WaznyChristine Cheung

Abstract

COVID-19 management guidelines have largely attributed critically ill patients who develop acute respiratory distress syndrome, to a systemic overproduction of pro-inflammatory cytokines. Cardiovascular dysfunction may also represent a primary phenomenon, with increasing data suggesting that severe COVID-19 reflects a confluence of vascular dysfunction, thrombosis and dysregulated inflammation. Here, we first consolidate the information on localized microvascular inflammation and disordered cytokine release, triggering vessel permeability and prothrombotic conditions that play a central role in perpetuating the pathogenic COVID-19 cascade. Secondly, we seek to clarify the gateways which SARS-CoV-2, the causative COVID-19 virus, uses to enter host vascular cells. Post-mortem examinations of patients' tissues have confirmed direct viral endothelial infection within several organs. While there have been advances in single-cell RNA sequencing, endothelial cells across various vascular beds express low or undetectable levels of those touted SARS-CoV-2 entry factors. Emerging studies postulate alternative pathways and the apicobasal distribution of host cell surface factors could influence endothelial SARS-CoV-2 entry and replication...Continue Reading

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Citations

Mar 16, 2021·Frontiers in Cardiovascular Medicine·Johanna Hol FosseReidunn Edelmann
Apr 13, 2021·Emergent Materials·Thibault ColombaniSidi A Bencherif
Apr 23, 2021·Modern Pathology : an Official Journal of the United States and Canadian Academy of Pathology, Inc·Marco ChilosiClaudio Doglioni
May 29, 2021·Pulmonary Circulation·Kurt R StenmarkThomas E Morrison

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Methods Mentioned

BETA
ELISA
surface plasmon resonance
electron microscopy

Clinical Trials Mentioned

NCT04381936
NCT04275245

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