Summary
This study elucidates mechanisms by which respiratory viral infections—influenza and SARS-CoV-2—awaken dormant breast cancer cells in the lung, driving rapid metastatic progression through interleukin-6-dependent pathways and impaired T cell immunity. Experimental findings in mice are corroborated by human observational data showing that SARS-CoV-2 infection substantially elevates cancer mortality and metastasis risk. The work reveals a critical intersection between infectious disease and cancer relapse, with implications for understanding post-infection cancer outcomes.
UK applicability
These findings are directly applicable to UK cancer survivors and public health strategy. The use of UK Biobank data in the validation cohort ensures relevance to the UK population; NHS oncology services should consider counselling cancer survivors on respiratory infection risk mitigation, whilst public health policies may need to account for enhanced disease severity in this vulnerable population during future respiratory pandemics.
Key measures
DCC proliferation and phenotype transition; expansion of carcinoma cells into metastatic lesions; T cell activation and CD8+ cytotoxicity; cancer-related mortality risk; lung metastasis incidence in SARS-CoV-2 infected versus uninfected cancer survivors
Outcomes reported
The study demonstrated in mice that influenza and SARS-CoV-2 infections cause dormant disseminated cancer cells in the lung to lose their quiescent phenotype and proliferate into metastatic lesions within two weeks, with mechanisms dependent on interleukin-6. Human observational data from UK Biobank and Flatiron Health databases confirmed that SARS-CoV-2 infection substantially increases cancer-related mortality and lung metastasis risk in cancer survivors.
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