SARS-CoV-2 Protein NSP6 Disrupts Brain, Heart and Lung Functions While Raising Cancer Risks
Nikhil Prasad Fact checked by:Thailand Medical News Team Oct 24, 2025 4 hours, 39 minutes ago
Medical News: Hidden Viral Protein Could Trigger Long Term Damage
Scientists from the Department of Biotechnology at Delhi University, the School of Life Sciences at Jawaharlal Nehru University, and the Indian Institute of Technology Delhi have uncovered alarming evidence that a little-known SARS-CoV-2 protein called NSP6 could be silently damaging the brain, heart, and lungs, potentially increasing long-term cancer risk. Their detailed computer-based (in silico) study explored how this viral protein interacts with key human genes and biological pathways, revealing new clues to long COVID and recurring infections.
SARS-CoV-2 Protein NSP6 Disrupts Brain, Heart and Lung Functions While Raising Cancer Risks
Unlike the more familiar spike protein, NSP6 operates inside human cells where it helps the virus replicate and evade the immune system. The researchers found that this protein hijacks normal cellular processes linked to inflammation, oxidative stress, and cell division — factors that can eventually trigger tumor formation. According to this
Medical News report, NSP6 interferes with genes that regulate how cells grow, recycle waste, and repair DNA damage, and these disruptions are most severe in the brain, heart, and lung tissues.
How the Study Was Conducted
Using advanced bioinformatics tools, the scientists mapped thousands of interactions between NSP6 and human proteins in three major organs. They identified hub genes — key control points — that become overactive or suppressed during infection.
In the brain, the affected genes included CCND1, CDK2, and CDC6, which are linked to the cell cycle and certain cancers such as small-cell lung cancer and prostate cancer. In the heart, crucial genes like TGFB1, RAB7A, and LGALS3 were disturbed, all known to influence inflammation, fibrosis, and heart failure. The lungs showed disruptions in genes responsible for oxygen transport, immune signaling, and tissue regeneration, such as EGF and TGFBR2.
The researchers also examined how microRNAs — small molecules that regulate gene activity — were altered by SARS-CoV-2 infection. Some of these viral-regulated microRNAs, such as hsa-mir-124-3p and hsa-mir-155-5p in the brain and hsa-mir-1-3p in the lungs, were found to control genes involved in cell proliferation and immune response. Disturbances in these regulators may lead to chronic inflammation and increased cancer susceptibility over time.
Potential Drug Targets Identified
The study also identified several existing drugs that might counteract the damaging effects of NSP6. In the brain, cancer drugs like palbociclib and methotrexate, as well as acetaminophen, were shown to target some of the affected genes. In the heart, inositol could potentially help stabilize TGFB1 and APP pathways, while in the lungs, drugs like irinotecan and cetuximab could interfere with EGF and TGFBR2 signaling — both of which are linked to tumor growth and fibrosis.
Why the Findings Matter
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The discovery of NSP6’s far-reaching influence adds new urgency to studying long COVID. By hijacking cellular machinery across multiple organs, the protein might leave behind a biological “footprint” that predisposes survivors to chronic inflammation, cardiovascular disease, and even cancer. The research team stressed that Galectin-3 (LGALS3) — one of the affected genes found in both the heart and brain — is known to promote all ten hallmarks of cancer, highlighting how COVID-19 infection could have hidden oncogenic potential.
Conclusion
This groundbreaking analysis sheds light on how a single SARS-CoV-2 protein may create long-term molecular chaos in vital organs, paving the way for serious post-infection complications. It underscores the need for ongoing monitoring of COVID-19 survivors and deeper investigation into viral proteins beyond the spike. The findings also open the door to repurposing existing cancer and anti-inflammatory drugs to mitigate these hidden effects.
The study findings were published in the peer-reviewed journal: Cardio-Oncology.
https://link.springer.com/article/10.1186/s40959-025-00387-6
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