COVID-19 Spike Protein Causes Elevation of Thymidine Phosphorylase That Increases Risk of Lung Cancer
Nikhil Prasad Fact checked by:Thailand Medical News Team Jul 18, 2026 59 minutes ago
Medical News: Researchers from the Department of Biomedical Sciences and the Department of Pediatrics at the Joan C. Edwards School of Medicine, Marshall University, Huntington, West Virginia, USA, together with scientists from the Department of Pediatrics, Hadassah Medical Center and the Faculty of Medicine, The Hebrew University of Jerusalem, Israel, have uncovered concerning new evidence that the SARS-CoV-2 spike protein triggers biological changes that significantly increase the risk of lung cancer. Their findings point to a protein called thymidine phosphorylase (TYMP) as a key driver that links COVID-19-related lung injury to long-term cancer development.
New research shows the SARS-CoV-2 spike protein raises TYMP levels, driving lung inflammation, fibrosis
and a significantly higher risk of lung cancer
COVID-19 Leaves Behind More Than Lung Damage
While COVID-19 is primarily known as a respiratory disease, scientists have increasingly recognized that many survivors continue to experience long-term lung complications. One of the most serious is pulmonary fibrosis, a condition in which excessive scar tissue develops in the lungs. Since lung fibrosis is already a well-established risk factor for lung cancer, researchers wanted to determine exactly how SARS-CoV-2 might trigger this dangerous progression.
To investigate, the team combined a large-scale analysis of patient data from the TriNetX Research Network with laboratory studies using genetically engineered mice. The human data showed that people who had previously been infected with COVID-19 faced a significantly higher risk of developing lung cancer than those who had not been infected. The increase was greatest among current smokers, followed by former smokers, although even individuals who had never smoked showed a measurable increase in risk. Interestingly, the same pattern was not observed for oral or bladder cancers, suggesting the harmful effects are largely confined to the lungs.
TYMP Emerges as a Major Driver of Disease
The researchers focused on TYMP because previous studies had shown that its levels rise sharply during COVID-19 infection. Their experiments demonstrated that exposure to the SARS-CoV-2 spike protein alone was enough to increase lung injury, inflammation and tiny blood clots inside the lungs.
The spike protein attracted large numbers of neutrophils, immune cells that normally fight infection but can also damage healthy tissue when activated excessively. At the same time, it altered the normal processing of the ACE2 receptor, which is used by SARS-CoV-2 to enter human cells. These combined effects produced extensive tissue injury that eventually developed into lung fibrosis.
Remarkably, mice that lacked TYMP experienced much milder lung damage. They developed fewer inflammatory changes, fewer microthrombi, reduced collagen deposition and significantly less fibrosis, demonstrating that TYMP plays a central role in amplifying the harmful effects of the spike protein.
Why Lung Cancer Risk Rises
This
>Medical News report highlights how the risk for lung cancer increases due to COVID-19. Perhaps the most striking finding was the dramatic increase in lung tumor formation following exposure to the spike protein. Half of the lung lobes examined in normal mice developed tumors after spike protein exposure, whereas only 18 percent of lung lobes developed tumors in mice lacking TYMP.
The tumors that formed after spike protein exposure were also considerably larger and more aggressive. Surprisingly, many displayed features resembling squamous cell carcinoma, a type of lung cancer not normally seen in this experimental model.
Further investigation showed that TYMP activated the STAT3 signaling pathway, which is known to promote chronic inflammation, tissue scarring and cancer growth. The researchers also found that TYMP reshaped the immune environment by increasing inflammatory molecules such as G-CSF, CCL2, CXCL1, TIMP-1 and CXCL13 that favor tumor development, while reducing protective immune signals that normally help the body eliminate abnormal cells. This shift created an environment that allowed cancer cells to grow more easily.
Potential New Targets for Prevention
The findings identify TYMP as a promising therapeutic target for reducing the long-term complications of COVID-19. The researchers note that tipiracil, an FDA-approved TYMP inhibitor currently used in cancer treatment, could potentially be investigated as a way to reduce post-COVID lung fibrosis and lower future lung cancer risk. They also suggest that therapies targeting the STAT3 pathway may help limit persistent lung injury after SARS-CoV-2 infection.
Conclusion
The study provides compelling evidence that the SARS-CoV-2 spike protein is not merely involved in viral entry but can actively drive biological processes that promote lung injury, chronic inflammation, fibrosis and eventually lung cancer through elevation of thymidine phosphorylase. While additional human studies are needed to confirm these long-term risks, the combined clinical and laboratory findings strongly suggest that COVID-19 survivors, particularly smokers and former smokers, may benefit from continued monitoring of their lung health and that therapies targeting TYMP could represent an important strategy for preventing serious long-term complications.
The study findings were published in the peer reviewed journal: Frontiers in Immunology.
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2026.1798566/full
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Read Also:
https://www.thailandmedical.news/articles/coronavirus
https://www.thailandmedical.news/articles/long-covid
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