Infection-induced reactive oxygen species (ROS) accelerate telomere shortening via DNA damage response pathways, including p53 activation and shelterin complex disruption, leading to replicative senescence in immune cells (Correia-Melo et al., 2014; Ahmed and Lingner, 2018; Jose et al., 2017; Johnson et al., 2025). This evidence concerns the gene TP53 and infection.