The importance of telomeres as special structures at the ends of chromosomes is gradually gaining prominence. They are composed of short, multi-repeated non-transcribed sequences (TTAGGG) and binding proteins, and their main role is to protect chromosome ends from degradation. Recent studies have shown that the length of telomeres may affect the outcome of COVID-19 infection, and the severity of COVID-19 is associated with shortened or dysfunctional telomeres, which may be an important factor contributing to the deterioration of the patient’s condition. In conjunction with this, COVID-19 patients with longer telomeres tended to have better outcomes compared to those with shorter telomeres. This suggests that telomere length can be used as a potential marker to predict the progress of COVID-19 patients’ recovery, highlighting the potential role of telomeres in the immune system. The involvement of telomeres in the recovery and virological processes of COVID-19 patients demonstrates that telomeres contribute to the maintenance of chromosome stability and promote the normal restoration of cellular functions during the recovery process, thereby improving patient outcomes. This review examines the complex relationship between telomere length and COVID-19 disease. Telomere abnormalities may exacerbate lung injury and fibrosis in COVID-19 patients, while COVID-19 infection accelerates telomere shortening, leading to premature cellular senescence. The aim of this review is to gain a deeper understanding of how telomere length affects disease severity and how COVID-19 in turn affects telomere structure and function. In addition, the impact of COVID-19 on the aging process is explored to provide scientific rationale and insights for the development of targeted therapeutic interventions in the future.
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