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The Role of Host-Cellular Responses in COVID-19 Endothelial Dysfunction.

SARS-CoV2, Severe acute respiratory syndrome coronavirus 2, is a novel member of the human 30 coronavirus family that has recently emerged worldwide to cause COVID-19 disease. COVID-19 disease has been declared a worldwide pandemic with over 270 million total cases, and >5 million deaths as of this writing. Although co-morbidities and preexisting conditions have played a significant role in the severity of COVID-19, the hallmark feature of severe disease associated with SARS-CoV2 is respiratory failure. Recent findings have demonstrated a key role for 35 endothelial dysfunction caused by SARS-CoV2 in these clinical outcomes, characterized by endothelial inflammation, the persistence of a pro-coagulative state, and major recruitment of leukocytes and other immune cells to localized areas of endothelial dysfunction. Though it is generally recognized that endothelial impairment is a major contributor to COVID-19 disease, studies to examine in greater detail the initial cellular events involved in triggering endothelial 40 dysfunction are needed. In this article, we review the general strategy of pathogens to exploit endothelial cells and the endothelium to cause disease. We discuss the role of the endothelium in COVID-19 disease and highlight very recent findings that identify key signaling and cellular events that are associated with the initiation of SARS-CoV2 infection. These studies may reveal specific molecular pathways that can serve as potential means of therapeutic development against 45 COVID-19 disease.