From the article:

“In summary, older individuals, especially those with hypertension and diabetes, have reduced ACE2 expression and upregulation of angiotensin II proinflammatory signaling; the increase in ACE2 levels with ACEI/ARB treatment is more likely to be corrective to these changes. We hypothesize that with superimposed COVID-19 disease, SARS-CoV-2 binding to ACE2 acutely exaggerates this proinflammatory background, predisposing these subpopulations to greater COVID-19 disease severity and mortality. This hypothesis is in line with the evidence of a protective role of angiotensin II antagonism against sepsis-associated acute lung injury and supports continuing therapy with ACEIs/ARBs and, more so, urgently calls for expanding ongoing trials treating patients with severe COVID-19 with RAS interventions to examine the role of these interventions in preventing lethal lung complications of COVID-19 as cases surge around the world.”