This review examines whether acute infection-driven inflammation can promote cancer progression. While chronic infections have well-established epidemiological associations with cancer incidence and progression, less is known about the potential tumor-promoting effects of transient, acute infections. The authors summarize recent experimental data implicating common respiratory viruses—specifically influenza and SARS-CoV-2—and discuss how infection-driven immune responses may create conditions that favor tumor expansion and dissemination.
Human epidemiology robustly links chronic infections to cancer risk, but the relationship between acute infections and cancer progression is comparatively underexplored. The review highlights emerging experimental findings that acute respiratory viral infections can be associated with accelerated tumor growth and spread in model systems. These data provide initial evidence that the inflammatory and immune consequences of an acute infectious episode can influence tumor biology, although the review emphasizes that the precise extent and generalizability of these effects in humans require further definition.
Acute infections trigger a rapid inflammatory cascade at the site of infection and systemically. This cascade involves proinflammatory mediators and cellular responses that can remodel local tissues. According to the review, such remodeling can alter the tumor microenvironment in ways that may favor cancer cell survival and growth. Key processes described include changes in cytokine and chemokine profiles, alterations to stromal and vascular components, and shifts in the balance of immune cell populations within tissues. The authors argue that these rapid tissue-level changes can create permissive niches for tumor cells to survive, proliferate, or disseminate.
A central theme of the review is the dynamic reprogramming of immune cells during acute infection. Infection-induced signals can change the activation states, trafficking behavior, and effector functions of innate and adaptive immune cells. These reprogrammed immune cells can, in some contexts, reduce effective anti-tumor surveillance or produce factors that directly support tumor cell survival. The review underscores that such rapid immune reprogramming is a plausible mechanism by which an otherwise transient infection could exert lasting effects on tumor progression in experimental settings.
Importantly, the authors note that acute infections do not uniformly promote tumor growth. Acute immune responses can also generate potent anti-tumor effects by activating cytotoxic pathways or enhancing antigen presentation. The review stresses the dual nature of infection-driven immunity: the same infection-induced processes may either restrain or facilitate cancer progression depending on context. Identifying the factors that determine this balance—such as infection type, timing relative to tumor development, tissue context, and host immune status—is presented as essential for understanding clinical implications.
The review concludes that defining how acute infections skew immune programs toward protumor or antitumor outcomes is critical for future strategies to manage cancer. Improved mechanistic understanding could guide interventions to mitigate infection-associated tumor promotion while preserving beneficial anti-tumor immunity. The authors call for continued experimental and translational research to clarify causal pathways and to inform clinical guidance on infection management in patients at risk for cancer progression. Specific translational or clinical recommendations are not detailed in the abstract; the review frames these directions as priorities for ongoing study.
The article is a review published in PLoS Biology in 2026 (PMID: 42743107, DOI: 10.1371/journal.pbio.3003962). Conflict of interest disclosures state that two authors (M.R. and J.D.) serve on the scientific advisory board for Mitotherapeutix, and J.D. has additional advisory roles and editorial responsibilities; other authors declare no competing interests. The work is distributed under a Creative Commons Attribution License. The abstract and metadata note MeSH terms including SARS-CoV-2, influenza, inflammation, tumor microenvironment, and disease progression, reflecting the review’s focus.