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Respiratory Viruses Rouse Dormant Breast Cancer Cells, Elevating Metastasis Risk

IL-6–driven inflammation from respiratory infections co-opts helper T cells to shield reactivated cells, heightening the risk of lung metastasis in survivors

An illustration of cancer cells marked with green, and the proliferation of cells marked in magenta.
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Radiation therapist Kristen Sherry-Taylor prepares a medical linear accelerator for a patient at the Rocky Mountain Cancer Centers in Aurora on Thursday, March 17, 2022.

Overview

  • In mouse models, influenza and SARS-CoV-2 infections triggered IL-6–dependent awakening of dormant breast cancer cells in the lungs, leading to rapid proliferation and metastatic lesion formation.
  • Mice engineered to lack IL-6 showed a marked reduction in cancer cell reactivation after viral infection, confirming the cytokine’s central role in disrupting dormancy.
  • Reactivated cancer cells enlisted helper T cells to evade cytotoxic immune responses before returning to dormancy with a 100-fold increase in residual cell numbers.
  • Analysis of UK Biobank data linked COVID-19 infection to a nearly twofold rise in cancer-related death among survivors, especially in the months immediately following infection.
  • Breast cancer survivors in the Flatiron Health cohort faced a 1.44-fold higher risk of developing lung metastases after COVID-19, prompting calls for vaccination guidance and IL-6–targeted therapies.