ABSTRACT
Background: Patients who have had the disease Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV- 2) COVID-19, mild, moderate or severe, has persisting symptoms weeks to moths after recovery of infection, with the risk of developing long-terms effects. Some alterations are related to damage of the vascular endothelium, generating thrombosis, a direct relation of the endothelial dysfunction. There are not data related on frequency of endothelial colony-forming cells (ECFCs) at 9 months of patients recovered from mild-moderate COVID-19 disease. Aim(s): We analyzed the frequency and morphology of ECFCs from recovered COVID-19 patients at 9 months post-infection. Method(s): Human mononuclear cells (MNCs) were obtained from peripheral blood from 15 recovered COVID-19 patients 9 months after disease, 10 healthy human volunteers with schedule of 2 vaccines (controls 1) and 10 healthy human volunteers without vaccines (controls 2), matched by age. All were men (25-50 years) without a history of major comorbidities. We assayed the frequency, morphological characteristics and proliferation of the ECFCs. The study was approved by the Scientific and Ethical Committee of the IMSS (number IMSS-R- 2020- 785- 167). Informed written consent was obtained from all subjects before enrollment. Result(s): ECFCs were detected in average on day 18 of culture in recovered COVID-19 patients, on day 14 in controls 1 and day 21 in controls 2, respectively. In recovered COVID-19 patients, ECFCs show abnormalities in size with elongations, large cytoplasm with prominent nuclei, similar to senescent state with no proliferative capacity when they were sub-cultured. These findings were different from those observed in controls 1 and 2 respectively. Conclusion(s): We demonstrate for the first time that ECFCs from patients recovered from COVID-19 at 9 months has characteristics of dysfunctional endothelial similar to those observed in patients recovered after 30 days after infection. This finding may support our understanding of the physiology of dysfunctional endothelium from COVID-19 disease at long term.