More than six years after COVID‑19 first emerged, researchers are still uncovering how the virus may affect health long after the initial infection has passed.
A new study now suggests that COVID‑19 could be linked to a small increase in lung cancer risk, particularly among people who already have known risk factors such as smoking.
The findings do not mean that COVID‑19 causes cancer. Rather, they point to a possible biological pathway through which the virus may create lung conditions that, over time, could make cancer more likely in some individuals.
Doctors have long recognised that some people who recover from COVID‑19 develop lasting lung problems. One of these is interstitial lung fibrosis, a form of scarring that stiffens lung tissue and makes breathing more difficult. Fibrosis is also known to raise the risk of lung cancer, regardless of its cause.
Until now, however, it has been unclear whether the virus itself plays an active role in creating a cancer‑friendly environment in the lungs, or whether these outcomes are indirect consequences of severe illness.
What the new research shows
The new research, published in Frontiers in Immunology, was led by scientists from institutions in the United States. The team combined large‑scale analysis of health records with laboratory and animal studies to explore how SARS‑CoV‑2, the virus that causes COVID‑19, might influence lung cancer risk.
Using the TriNetX global health database, the researchers compared more than 166,000 people who had COVID‑19 with closely matched individuals who did not. After accounting for age, sex and other factors, they found that:
People who had COVID‑19 showed a modest but statistically significant increase in lung cancer risk and the risk increase was most noticeable among current smokers. The relative risk was about 22% higher, corresponding to a hazard ratio of 1.50 but no increased risk was seen for oral or bladder cancers, suggesting the effect was specific to the lungs.
In simple terms, the study suggests that COVID‑19 survivors, especially smokers, may be slightly more likely to develop lung cancer than similar people who were not infected.
Why this happens
To understand why this might happen, the researchers looked more closely at biological changes in lung tissue.
Their experiments focused on the virus’s spike protein, which allows SARS‑CoV‑2 to enter human cells. Even in the absence of whole virus, exposure to the spike protein appeared to trigger lung injury and inflammation.
A key player in this process was an enzyme called thymidine phosphorylase, or TYMP. The study found that increased TYMP activity was linked to: Ongoing inflammation in the lungs, greater scarring and collagen build‑up, activation of STAT3, a signalling protein known to support tumour growth and changes in immune cells that can favour tumour development.
Step by step, the proposed sequence is that spike‑related lung injury activates TYMP, which then drives inflammation, fibrosis and immune changes that may help tumours take hold.
How strong is the evidence?
The evidence is suggestive but not definitive. The human data show an association, not proof of cause and effect. The laboratory and mouse experiments help explain how a connection could exist, but animal models do not fully reflect what happens in people.
Importantly, the absolute risk for any one person remains small. Lung cancer is influenced by many factors, with smoking still by far the dominant cause. COVID‑19, if it plays a role, is likely to be one piece of a much larger picture.
The authors also stress that longer follow‑up is needed, as lung cancer often takes years to develop.
What this means for the public
For most people, these findings should not cause alarm. They do not change current medical advice, and they do not suggest that people who had COVID‑19 are likely to develop cancer.
However, the results do reinforce the importance of known protective measures. Avoiding smoking, attending recommended health checks and seeking medical advice for persistent respiratory symptoms remain the most effective ways to reduce lung cancer risk.
For people with existing lung disease or a history of smoking, the study highlights the need for ongoing clinical awareness after COVID‑19 infection.
Treatment and prevention implications
The identification of TYMP as a potential driver opens up new research avenues. Drugs that affect this pathway already exist for other conditions, raising the possibility that targeted treatments could one day reduce post‑viral lung damage or lower cancer risk.
At present, this is a research finding rather than a clinical option. No treatments are recommended on the basis of this study alone.
What remains unknown
Key questions remain unanswered. Researchers need to know how long any increased risk lasts, whether it applies equally to mild and severe COVID‑19, and how vaccination influences these effects.
It is also unclear how these findings translate across different age groups and underlying health conditions. Further studies in people, with longer follow‑up periods, will be essential.
Pandemic’s long shadow
This research adds to a growing body of work showing that COVID‑19 can have lasting biological effects beyond the acute infection. While the individual risk of lung cancer appears to remain low, the study offers a plausible explanation for how viral injury could contribute to long‑term lung disease in some people.
Understanding these mechanisms matters, not because they point to immediate danger, but because they help guide future prevention, monitoring and treatment strategies as the world continues to reckon with the pandemic’s long shadow.
