Introduction
Telomeres shorten progressively during an individual's lifetime, being proposed as the primary molecular cause of aging. In COVID-19 the incidence of severe manifestations increases with age, showing higher mortality, suggesting that age-related molecular pathways contribute to the severity of COVID-19. The study aim is to determine if SARS-COV-2 infection is capable of producing alterations in telomere length, and whether these alterations are related to the appearance of fibrotic changes.

Methods
Prospective observational multicenter study of patients admitted with bilateral COVID-19 pneumonia, excluding patients with previous ILD or COPD. Clinical, radiological and pulmonary function variables were collected and telomere length of the patients was determined and compared with a cohort of controls of the same age and sex.

Results

Data were collected from 132 patients (61.4% men, mean age 60±12.3 years). During admission, 18.18% required ETI and IMV. At 12 months after discharge, pulmonary function tests, high-resolution chest computed tomography (HRCT) and blood samples were obtained. 5.3% had an FVC<80%, 38.9% had a DLCO<80% and 28% had fibrotic changes on HRCT. In samples obtained at 12 months, we found telomere length to be shorter compared to their controls. Finally, the relationship between telomeric shortening and the appearance of fibrotic changes at one year was determined, being statistically significant for the group of patients under 60 years of age (p=0.0156). 

Conclusions
COVID-19 produces telomeric shortening that can be determined one year after infection. This shortening could induce the appearance of fibrotic changes especially in younger patients.