Infection-Driven Senescence Explored at ICSA 2025 Conference

A significant advancement in understanding the interplay between infections and aging emerged from the 10th annual International Cell Senescence Association (ICSA) conference held in Rome in September 2025. A new report published in Aging-US on December 23, 2025, highlights critical discussions 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 emphasizes the role infections play in cellular senescence, a condition where cells cease to divide and release inflammatory signals.

The implications of this research are profound, linking infectious diseases with aging, chronic inflammation, and lasting tissue damage. While cellular senescence has long been associated with aging and cancer, the conference underscored its growing relevance in infection biology. Researchers discussed how both viruses and bacteria can induce senescence in infected cells, leading to a phenomenon known as infection-driven senescence (IDS). This response may help contain pathogen replication but can also prolong inflammation and hinder recovery, particularly in older adults and during chronic infections.

Key Findings on Viral Infections and Senescence

The conference sessions extensively covered the impact of respiratory viruses, including influenza and SARS-CoV-2. Studies presented indicated that these viruses can induce senescence in lung cells, contributing to persistent inflammation and impaired healing processes. Experimental models suggested that reducing the number of senescent cells could enhance lung repair, even after viral clearance. This finding provides insight into why some individuals experience prolonged respiratory symptoms following infection.

Chronic viral infections were another focal point of the conference. Researchers revealed that human cytomegalovirus and HIV can drive senescence in immune and vascular cells. In HIV-positive individuals, viral proteins were linked to biological changes resembling accelerated aging, even in the presence of effective antiviral therapy. This highlights the increased prevalence of age-related conditions in this population.

In addition to viral infections, the meeting highlighted findings regarding bacterial infections. Researchers reported that the bacterium Mycobacterium abscessus can also trigger senescence in immune cells during chronic infections. Senescent cells were shown to elevate inflammation and increase susceptibility to subsequent infections. In experimental models, the removal of these cells resulted in decreased bacterial levels, suggesting potential new therapeutic approaches for persistent bacterial diseases.

Future Directions in Senescence Research

Mechanistically, IDS integrates various biological responses, including DNA damage responses, inflammatory signaling, and metabolic stress. Key pathways like p16INK4a, p21, and NF-κB are consistently activated during this process. Throughout the conference, experts discussed innovative therapies aimed at either eliminating senescent cells or mitigating their harmful inflammatory signals. These strategies, termed senolytic and senomorphic approaches, have shown promise in preclinical studies, potentially serving as tools to reduce infection-related tissue damage and chronic inflammation.

The report from ICSA 2025 positions infection-driven senescence as a critical concept linking infection, immunity, and aging. The discussions at the conference reveal a burgeoning field of research with significant implications for understanding chronic diseases and the long-term health effects of infections on aging populations. As this area of study advances, it may pave the way for new therapeutic interventions and better management strategies for infectious diseases and their sequelae.