Fig. 1

SARS-CoV-2 sites of infection and complications in diabetic patients. As is the case for SARS-CoV, SARS-CoV-2 uses the ectopeptidase ACE2 as an entry site in human host cells. ACE2 is part of the renin-angiotensin system, responsible for the termination of the angiotensin signal, promoting conversion of angiotensin II (Ang II) into angiotensin 1–7 (Ang 1–7). Ang II acts through the angiotensin receptor 1 (AT1), which results in vasoconstriction and sympathetic nervous stimulation. Ang 1–7, on the other hand, acts on angiotensin receptor 2 (AT2), and has opposite effects, inducing vasodilation. ACE2 is expressed throughout the respiratory epithelium, from the nasal and oral mucosa to the epithelium in alveoli. Diabetic patients are at higher risk of infection and complications from COVID-19 as a result of several factors. Dampened anti-viral response with reduced interferon production is a common feature seen in persons with diabetes. Additionally, diabetic patients may be more vulnerable to SARS-CoV-2 infection due to elevated ACE2 expression. Finally, diabetes-related subclinical pulmonary dysfunction and microvascular disease may be aggravating factors that contribute to the severity of the respiratory symptoms associated with COVID-19