Summary The incidence, severity, and mortality of COVID-19 infection appear to impact the elderly more negatively, especially in those who are frail and have multiple comorbidities. This chapter reviews the epidemiology of the COVID-19 pandemic with a focus on the older age group. The transmission of the virus to humans likely occurs through the consumption of an infected animal as a source of food, followed by human-to-human transmission through close contact. The epidemiology of COVID-19 incidence, severity of illness, and mortality appear to have unfavourable outcomes for older people. Managing older people with COVID-19 infection includes symptomatic therapy that focuses on the direct relief of the typical symptoms of COVID-19, drug therapy that focuses on agents directly treating the viral infection load, and general supportive care, which focuses on the relief of atypical symptoms in the acute setting. Ethical issue is the participation of older people in clinical trials.;Objective While endothelial dysfunction has been implicated in the widespread thrombo-inflammatory complications of coronavirus disease-19 (COVID-19), the upstream mediators of endotheliopathy remain for the most part cryptic. Our aim was to identify circulating factors contributing to endothelial cell activation and dysfunction in COVID-19. Methods Human endothelial cells were cultured in the presence of serum or plasma from 244 patients hospitalized with COVID-19 and plasma from 100 patients with non-COVID sepsis. Cell adhesion molecules (E-selectin, VCAM-1, and ICAM-1) were quantified by in-cell ELISA. Results Serum and plasma from patients with COVID-19 increased surface expression of cell adhesion molecules. Furthermore, levels of soluble ICAM-1 and E-selectin were elevated in patient serum and tracked with disease severity. The presence of circulating antiphospholipid antibodies was a strong marker of the ability of COVID-19 serum to activate endothelium. Depletion of total IgG from antiphospholipid antibody-positive serum markedly restrained upregulation of cell adhesion molecules. Conversely, supplementation of control serum with patient IgG was sufficient to trigger endothelial activation. Conclusion These data are the first to suggest that some patients with COVID-19 have potentially diverse antibodies that drive endotheliopathy, adding important context regarding thrombo-inflammatory effects of autoantibodies in severe COVID-19.
The COVID-19 pandemic in older people