A report published in the December 2025 issue of Aging-US details discussions from the 10th International Cell Senescence Association (ICSA) conference, held in Rome in September 2025. The report, led by Stefanie Deinhardt-Emmer of Jena University Hospital and Marco De Andrea of the University of Piemonte Orientale and the University of Turin, highlights how infections can trigger cellular senescence. Cellular senescence is a process where cells stop dividing and release inflammatory signals, which is significant for its connection to aging, chronic inflammation, and tissue damage.
The conference emphasized that while cellular senescence has been primarily studied in the context of aging and cancer, it is increasingly recognized as important in infection biology. Researchers presented evidence that both viruses and bacteria can induce senescence in infected cells, which can then spread to surrounding tissues. This phenomenon, called infection-driven senescence (IDS), may help restrict pathogen replication but also has drawbacks such as prolonging inflammation and slowing recovery. These effects are especially pronounced among older adults or those with chronic infections.
Several sessions addressed respiratory viruses like influenza and SARS-CoV-2. Findings indicated that these viruses can cause lung cells to become senescent, contributing to ongoing inflammation and delayed healing. Experimental studies showed that reducing the number of senescent cells improved lung repair even after viral clearance, potentially explaining persistent symptoms seen in some patients after infection.
Chronic viral infections were also discussed. For example, human cytomegalovirus and HIV were shown to promote senescence in immune and vascular cells. In people living with HIV, certain viral proteins were linked to changes similar to accelerated aging despite effective antiviral treatment. These findings could help explain why age-related conditions occur earlier and more often among this group.
Research at the meeting also demonstrated that bacterial infections play a role in cellular senescence. The bacterium Mycobacterium abscessus was reported to induce senescence in immune cells during chronic infection. This led to increased inflammation and greater vulnerability to additional infections. Experimental removal of these senescent cells reduced bacterial loads, suggesting possible new treatment options for persistent bacterial diseases.
"Mechanistically, IDS integrates DNA damage responses, inflammatory signaling, and metabolic stress, with consistent activation of p16INK4a, p21, and NF-κB pathways," according to the meeting report.
Conference speakers also discussed therapies aimed at removing senescent cells or limiting their inflammatory effects—strategies known as senolytic or senomorphic approaches—which have shown promise in preclinical models for reducing infection-related tissue damage and chronic inflammation.
Overall, the report frames infection-driven senescence as a concept linking infection biology with immunity and aging research. The ICSA 2025 discussions underscore growing interest in this field as scientists seek better understanding of chronic disease mechanisms and long-term health impacts following infections.
