Respiratory Viruses and Dormant Cancer Cells: Unveiling the Hidden Threat of Relapse

The emerging intersection between respiratory viruses and cancer progression is posing a hidden threat. A key mechanism is involving the reactivation of dormant cancer cells, with the inflammatory mediator IL-6 playing a crucial role during infection.

Infections by respiratory viruses, such as influenza and COVID-19, are being linked to the activation of dormant cancer cells in specific contexts. This activation is thought to arise from inflammatory responses that disrupt the microenvironmental balance maintaining dormancy.

Preclinical and early clinical observations indicate that infections by respiratory viruses, such as influenza and COVID-19, may precipitate activation of dormant cancer cells, particularly described in breast cancer lung metastasis models.

Signals consistent with reactivation have been observed in murine models and limited translational contexts, without implying population-level frequency.

The inflammatory milieu during respiratory viral infection may also activate dormant cancer cells, linking infection to progression. Evidence suggests that IL-6, a cytokine elevated during these infections, contributes to disruption of cellular dormancy. This shift can move cells from dormancy toward active proliferation. Investigators propose that targeting IL-6 signaling may help prevent such reactivation in research and early clinical settings.

Recent studies support exploring additional strategies for metastasis prevention in the post-infection context. IL-6's role extends beyond general inflammation and appears to contribute to dormancy escape, without implying primacy over the underlying infection.

Alterations in IL-6 signaling may contribute to cancer cell activation and relapse risk. For patients with recent infections, these signals could warrant enhanced vigilance in select high-risk groups, framed as investigational considerations rather than standard of care.

Survivors describe heightened concern after respiratory infections when told that post-infection inflammation is under study as a potential driver of dormancy escape; clinicians often contextualize this as emerging evidence and discuss participation in monitoring or registry studies where appropriate.

Because IL-6 signaling can remain elevated after respiratory infection, clinicians face nuanced decisions about when heightened surveillance is justified versus when reassurance is appropriate, given that the dormancy-escape link is still being established.

Approaches targeting IL-6 signaling are under investigation as potential ways to mitigate post-infection reactivation risk. Understanding and intervening in the virus–cancer interface may eventually influence outcomes for survivors if ongoing studies confirm benefit.

Key Takeaways:

• Respiratory viruses may reactivate dormant cancer cells in certain contexts, potentially heightening metastasis risk.
• Elevated IL-6 during infection appears to contribute to dormancy escape and proliferation.
• Metastasis risk assessment should consider post-infection inflammatory context in research and select clinical scenarios.
• Targeting IL-6 signaling is an emerging research avenue that may mitigate post-infection reactivation risk.