COVID-19 Triggers Chronic Gastritis, Alters Stomach Cell Functions and Push Gastric Cells Toward Cancer Like States!
Nikhil Prasad Fact checked by:Thailand Medical News Team Mar 28, 2025 3 weeks, 2 days, 14 hours, 45 minutes ago
Medical News: New research has revealed that the SARS-CoV-2 virus can drastically worsen chronic stomach inflammation and push gastric cells toward cancer like states even long after the initial infection has cleared.
A new collaborative study by scientists from Yonsei University College of Medicine, Seoul National University, Gyeongsang National University College of Medicine-South Korea, and Vanderbilt University School of Medicine-USA has uncovered shocking findings that suggest the SARS-CoV-2 virus could silently damage the stomach in ways never seen before. Even after the respiratory infection appears to have resolved, the virus leaves behind serious changes in the stomach's cellular and molecular makeup - especially when another common bacterium, Helicobacter pylori, is present.
COVID-19 Triggers Chronic Gastritis, Alters Stomach Cell Functions and Push Gastric Cells Toward
Cancer Like States!
This
Medical News report explores how the COVID-19 virus, although not directly infecting the stomach, significantly alters its gene expression and immune environment. The implications are enormous, especially considering that more than half of the world’s population is infected with H. pylori and millions have contracted COVID-19.
Post COVID Alters the Stomach Without Direct Infection
In the study, researchers used K18-hACE2 genetically engineered mice, a well-established model for studying COVID-19, to investigate how the virus affects the stomach. The mice were infected with a non-lethal dose of SARS-CoV-2 and their stomach tissues were analyzed over a 4-week period. Surprisingly, even though the virus was undetectable in the stomach and no structural damage was seen under the microscope, the stomach tissue showed over 1,100 changes in gene activity.
Many of these altered genes were linked to metaplasia - a condition where stomach cells start transforming into intestinal-like cells, a known precursor to stomach cancer. Markers such as CDX2 and CLDN4 were strongly expressed, both of which are considered early indicators of gastric carcinogenesis.
Even more alarming was the observation that immune cells like macrophages and mast cells, which usually increase in response to infections, remained elevated in the stomach for weeks after the virus had been cleared from the lungs. Cytokine tests also showed spikes in molecules like CXCL13, associated with immune cell recruitment and chronic inflammation.
COVID Makes H Pylori Infections Worse
To understand the real-world implications, the researchers then explored what would happen when SARS-CoV-2 infection was combined with a prior or subsequent infection with Helicobacter pylori, the well-known bacterium that causes ulcers and is strongly linked to gastric cancer. The mice were divided into groups that received the viral infection before or after being infected with H. pylori.
The results were troubling. Both groups - the ones infected with SARS-CoV-2 before and after H. pylori exposur
e - developed far more severe chronic gastritis than mice infected with H. pylori alone. However, the worst outcomes were seen in mice that contracted the virus after the bacterial infection (the post-COVID group). These animals showed intense immune cell infiltration, thickening of the stomach lining, significant parietal cell loss (responsible for producing stomach acid), and an expansion of metaplastic and proliferative cells.
Strikingly, SARS-CoV-2 did not increase the amount of H. pylori in the stomach, suggesting that it wasn’t helping the bacteria grow. Instead, the virus appeared to be altering the stomach environment, making it more prone to inflammation and cellular transformation.
Gene Pathways Leading Toward Cancer Activation
The team performed additional transcriptomic analyses (RNA sequencing) on the stomach tissue and found that the post-COVID mice had significant activation of dangerous molecular pathways. These included IL6/JAK-STAT3 and KRAS signaling - pathways known to be involved in cancer development. The gene WFDC2, which is a prognostic marker and potential therapeutic target in gastric cancer, was also dramatically upregulated.
Protein studies further confirmed that phosphorylated forms of ERK and STAT3 - proteins that help drive cells toward unchecked growth and transformation - were elevated in the co-infected mice. These molecular changes mirrored the histological signs of pre-cancerous development seen under the microscope.
Implications for Human Health and Long COVID
Although the study was conducted in mice, the implications for human health are deeply concerning. Many people who had COVID-19 and also carry H. pylori may now be at heightened risk for long-term stomach problems, including chronic gastritis and even gastric cancer. These findings add to the growing body of evidence that long COVID is not just a temporary inconvenience but a condition that can lead to chronic organ damage.
The researchers also noted that even though SARS-CoV-2 was no longer present in the stomach after a few weeks, the immune system and gene expression patterns it triggered remained disrupted. This suggests that the virus can cause lasting damage to tissues it never even directly infects.
Study Limitations and Future Directions
While the research provides strong evidence of a link between SARS-CoV-2 infection and worsened gastric disease, it is not without limitations. The study used only male mice and did not directly demonstrate cancer development - though many precancerous markers and processes were clearly activated. The research team emphasized the need for more studies using human stomach tissues, especially from individuals who experienced long COVID symptoms involving the digestive tract.
Another key limitation is the absence of a direct infection of gastric cells by the virus. This points to a need to further investigate how immune responses and inflammatory signals generated elsewhere in the body - such as the lungs - can affect distant organs like the stomach.
Conclusion
This groundbreaking study has unveiled a disturbing connection between COVID-19 and long-term stomach health. Even after the virus has left the body, it leaves behind a ticking time bomb in the stomach. The fact that the virus can dramatically worsen the effects of H. pylori infection - already a leading cause of ulcers and gastric cancer - adds urgency to the situation.
These findings suggest that individuals who have recovered from COVID-19, especially those with known H. pylori infections or unexplained gastrointestinal symptoms, may require long-term medical monitoring. The emergence of metaplasia, chronic inflammation, and preneoplastic cellular changes are signs that something serious could be brewing below the surface. As millions around the world continue to suffer from long COVID symptoms, this study provides a powerful reminder that the virus’s damage may not be limited to the lungs or immune system - it could be quietly laying the groundwork for much more severe diseases in the years to come.
The study findings were published in the peer reviewed journal: Cellular and Molecular Gastroenterology and Hepatology
https://www.sciencedirect.com/science/article/pii/S2352345X25000529
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