A meeting report published on 23 December 2025 in Aging-US (Volume 17, Issue 12) brings together the main scientific discussions from the 10th International Cell Senescence Association conference, held in Rome in September 2025. Led by Stefanie Deinhardt-Emmer of Jena University Hospital and Marco De Andrea of the University of Piemonte Orientale and the University of Turin, the report, titled “Cellular senescence meets infection”, reflects a growing shift in how researchers understand the long-term biological consequences of infectious disease.
At the centre of the report is cellular senescence, a state in which cells permanently stop dividing and begin releasing inflammatory and tissue-altering signals. Traditionally associated with ageing and cancer, senescence is now gaining attention for its role in infection biology. The authors emphasise that this link is vital because it connects acute and chronic infections with long-lasting inflammation, tissue damage, and age-related decline, helping to explain why some infections have effects that persist long after pathogens are cleared.
A key concept discussed throughout the meeting was infection-driven senescence (IDS). Researchers described how viruses and bacteria can trigger senescence in infected cells and spread their effects to neighbouring tissues through inflammatory signalling. While this response may initially help limit pathogen replication, it can also prolong inflammation and impair recovery. These outcomes are particularly relevant in older adults and in individuals experiencing chronic or recurrent infections.
Respiratory infections were a major focus of the conference. Several sessions explored how influenza viruses and SARS-CoV-2 induce senescence in lung epithelial cells, contributing to sustained inflammation and reduced tissue repair. Experimental models showed that lowering the number of senescent cells improved lung healing even after viral clearance, offering a potential explanation for persistent respiratory symptoms observed in some patients following viral infection.
Chronic viral infections were also highlighted as important drivers of senescence. Evidence was presented showing that human cytomegalovirus and HIV promote senescence in immune and vascular cells. In people living with HIV, viral proteins were linked to biological changes resembling accelerated ageing, despite effective antiviral therapy. These findings help clarify why age-related conditions often appear earlier and more frequently in this population.
Notably, the report shows that infection-induced senescence is not limited to viruses. Researchers described how the bacterium Mycobacterium abscessus induces senescence in immune cells during chronic infection, increasing inflammation and susceptibility to further disease. Across the conference, speakers discussed emerging therapies aimed at removing senescent cells or reducing their harmful inflammatory signals. Together, these discussions present IDS as a unifying framework linking infection, immunity, and ageing, with significant implications for understanding chronic disease and long-term health after infection.
More information: Stefanie Deinhardt-Emmer et al, Cellular senescence meets infection: highlights from the 10th annual International Cell Senescence Association (ICSA) conference, Rome 2025, Aging-US. DOI: 10.18632/aging.206349
Journal information: Aging-US Provided by Impact Journals LLC
