"Here we propose the concept of infection-driven senescence (IDS) to describe the phenomenon in which microbial agents, beyond viruses, can trigger cellular senescence in host cells."
BUFFALO, NY — January 7, 2026 — A new meeting report was published in Volume 17, Issue 12 of Aging-US on December 23, 2025, titled " Cellular senescence meets infection: highlights from the 10th annual International Cell Senescence Association (ICSA) conference, Rome 2025 ."
Led by Stefanie Deinhardt-Emmer from Jena University Hospital and Marco De Andrea from the University of Piemonte Orientale and the University of Turin , the report summarizes key discussions from the 10th International Cell Senescence Association conference held in Rome in September 2025. It focuses on how infections can trigger cellular senescence, a state in which cells stop dividing and release inflammatory signals. This link is important since it connects infectious diseases with aging, chronic inflammation, and lasting tissue damage.
Although cellular senescence is best known for its role in aging and cancer, the meeting highlighted its emerging importance in infection biology. Researchers described how viruses and bacteria can induce senescence in infected cells and spread its effects to nearby tissues. This process, known as infection-driven senescence (IDS), can help limit pathogen replication but may also prolong inflammation and slow recovery, particularly in older adults and during chronic infections.
Several sessions focused on respiratory viruses like influenza and SARS-CoV-2. Researchers showed that these viruses can promote senescence in lung cells, contributing to persistent inflammation and reduced healing. Experimental models suggested that decreasing the amount of senescent cells improved lung repair, even after the virus was cleared, offering insight into why some patients experience long-lasting respiratory symptoms.
Chronic viral infections were another major theme. Human cytomegalovirus and HIV were shown to drive senescence in immune and vascular cells. In people with HIV, viral proteins were associated with biological changes resembling accelerated aging, despite effective antiviral therapy. These findings help explain why age-related conditions occur earlier and more frequently in this population.
In the meeting, it was also demonstrated that senescence is not limited to viral infections. Researchers reported that the bacterium Mycobacterium abscessus induces senescence in immune cells during chronic infection. These senescent cells increased inflammation and susceptibility to further infection. Removing them reduced bacterial levels in experimental models, suggesting new directions for treating persistent bacterial disease.
"Mechanistically, IDS integrates DNA damage responses, inflammatory signaling, and metabolic stress, with consistent activation of p16INK4a, p21, and NF-κB pathways."
Across the conference, speakers discussed therapies that either remove senescent cells or reduce their harmful inflammatory signals. These approaches, known as senolytic and senomorphic strategies, showed promise in preclinical studies as potential tools to limit infection-related tissue damage and chronic inflammation.
Overall, the meeting report presents infection-driven senescence as a unifying concept linking infection, immunity, and aging. The discussions at ICSA 2025 highlight a growing field with important implications for understanding chronic disease and the long-term health effects of infections.
Paper DOI: https://doi.org/10.18632/aging.206349
