Abstract

At the 10th Annual International Cell Senescence Association (ICSA) Conference, held in Rome (Italy) from September 17–19, 2025, “senescence and infection” emerged as a recurring highlight linking diverse sessions across virology, immunology, and aging research. Presentations addressed virus-induced senescence in influenza A virus (IAV), SARS-CoV-2, cytomegalovirus (CMV), and human immunodeficiency virus (HIV), as well as bacterial infections such as Mycobacterium abscessus. Together, these studies have defined infection-driven senescence (IDS) as a critical biological process in both acute disease and long-term sequelae, connecting infectious pathology with mechanisms of aging and chronic inflammation.

Mechanistically, IDS integrates DNA damage responses, inflammatory signaling, and metabolic stress, with consistent activation of p16INK4a, p21, and NF-κB pathways. Evidence across immune, epithelial, and neuronal systems have revealed that senescence contributes to impaired regeneration, persistent inflammation, and altered host–pathogen dynamics. Emerging therapeutic data suggest that senolytic or senomorphic strategies may alleviate infection-associated tissue damage.

Collectively, the conference highlighted IDS as an expanding frontier that bridges infection biology and aging research, emphasizing its potential relevance for prevention and therapy of chronic age-related disease.