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Study Proposes Biological Mechanism for Potential Link Between COVID-19 and Lung Cancer Risk

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Study Suggests Potential Link Between COVID-19 and Increased Lung Cancer Risk

A new study published in the journal Frontiers in Immunology has identified a potential biological mechanism that could link SARS-CoV-2 infection to an increased risk of lung cancer. The research, which integrated clinical data with animal and cellular model studies, suggests a specific protein interaction may alter the lung environment in ways that could promote tumor formation over time.

The authors emphasize that their findings are preliminary and that further research is required to confirm and understand the long-term implications.

Study Overview and Methodology

The research was conducted by teams from the Marshall University Joan C. Edwards School of Medicine and The Hebrew University of Jerusalem. The study combined three investigative approaches:

  • Analysis of human clinical data from the TriNetX Research Network.
  • Research using animal models.
  • Research using cellular models.

The goal was to examine how SARS-CoV-2, the virus that causes COVID-19, may contribute to long-term lung disease beyond the acute phase of illness.

Key Findings and Proposed Mechanism

The study's central finding involves the protein thymidine phosphorylase (TYMP). Researchers propose that TYMP may interact with the spike protein of the SARS-CoV-2 virus.

This interaction is hypothesized to:

  • Promote inflammation and fibrosis (scarring) in the lung.
  • Activate biological pathways associated with cancer growth.
  • Alter the lung's immune environment in ways that could potentially support the formation of tumors.

In the clinical data analysis, researchers observed a higher incidence of lung cancer among patients with a history of COVID-19 compared to those without. This observed higher incidence was noted to be particularly pronounced among current and former smokers.

Researcher Statements

Wei Li, Ph.D., professor of biomedical sciences at the Joan C. Edwards School of Medicine and a co-corresponding author of the study, stated: "Our findings suggest that COVID-19 may do more than cause acute illness—it may also create biological conditions in the lung that could contribute to increased cancer risk over time."

David Gozal, M.D., M.B.A., Ph.D. (Hon), vice president for health affairs and dean of the Joan C. Edwards School of Medicine, who served as a consultant on the study, said: "The collaboration between basic and translational scientists and clinicians enabled the identification of mechanisms underlying epidemiological evidence linking COVID-19 infection to the potential increased risk of lung cancer."

Authorship, Funding, and Next Steps

  • Authors: Cayleigh Wallace of Marshall University and Alex Gileles-Hillel, M.D., of Hebrew University and Hadassah Medical Center served as co-first authors. Co-corresponding authors are Wei Li, Ph.D., and Hong Yue, Ph.D., of Marshall University.
  • Funding: The study received funding from several sources, including National Institutes of Health grants R15HL145573 and R01HL177493, the West Virginia Clinical and Translational Science Institute-Pop-Up COVID-19 Fund, and the Cancer Biology Pilot Grant Program.
  • Future Research: The authors uniformly state that additional research is necessary to better understand the proposed relationship and its long-term implications. This work supports a pending NIH R03 grant application led by Hong Yue, Ph.D. The researchers describe the findings as providing a foundation for future studies focused on understanding long-term cancer risk and identifying potential targets for prevention and treatment.

The full study, "Integrated multi-omics analysis reveals a potential link between SARS-CoV-2 infection and increased lung cancer risk via TYMP-mediated mechanisms," is available online at doi.org/10.3389/fimmu.2026.1798566.