SARS-CoV-2 and Cancer Biology: Exploring the Mechanistic Links

Abstract

Background

Five years after the emergence of SARS-CoV-2 and the declaration of the COVID-19 pandemic, the long-term implications of COVID-19 for cancer biology remain incompletely understood. Beyond the major disruptions in cancer screening, diagnosis, and treatment observed worldwide, increasing attention has focused on whether SARS-CoV-2 infection and post-acute sequelae of COVID-19 (Long COVID) may induce persistent biological alterations relevant to tumor progression or recurrence.

Recent Findings

Current evidence does not support SARS-CoV-2 as a classical oncogenic virus or demonstrate direct viral carcinogenesis. However, experimental, transcriptomic, and clinical studies suggest that SARS-CoV-2 infection can induce persistent inflammatory and immune alterations that overlap with pathways implicated in cancer biology. Among the most consistently reported findings are chronic activation of IL-6/STAT3 and NF-κB signaling, immune dysregulation, T-cell exhaustion, oxidative stress, mitochondrial dysfunction, and senescence-associated inflammatory programs. Additional proposed mechanisms include perturbation of tumor suppressor pathways, epigenetic remodeling, and microRNA alterations involving the let-7/LIN28B/STAT3 axis. Experimental models have further suggested that inflammatory remodeling induced by respiratory viral infection may influence dormant tumor cell behavior and tissue microenvironments under defined conditions. However, many of these observations derive from in vitro systems, animal models, or association studies, and their long-term relevance to human oncogenesis remains uncertain.

Conclusion

Collectively, current evidence supports the existence of convergent biological mechanisms between SARS-CoV-2–induced inflammatory stress responses and pathways involved in cancer progression, rather than direct oncogenic transformation. Future longitudinal studies integrating immune profiling, inflammatory biomarkers, transcriptomic and epigenetic analyses, and clinical cancer outcomes will be essential to determine whether persistent post-infectious alterations contribute to tumor progression, recurrence, or susceptibility in selected patient populations.