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Nikhil Prasad  Fact checked by:Thailand Medical News Team Jul 03, 2025  5 days, 9 hours, 33 minutes ago

BREAKING! SARS-CoV-2 Virus Produces MicroRNA That Causes Lung Scarring by Disabling Key Immune Protein

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BREAKING! SARS-CoV-2 Virus Produces MicroRNA That Causes Lung Scarring by Disabling Key Immune Protein
Nikhil Prasad  Fact checked by:Thailand Medical News Team Jul 03, 2025  5 days, 9 hours, 33 minutes ago
Medical News: New Viral Trick Discovered That Can Cause Severe Lung Damage Even After Infection Clears
In an alarming scientific breakthrough, researchers from the Institute of Laboratory Medicine and the School of Life Sciences at Nanjing University, along with collaborators from the State Key Laboratory of Analytical Chemistry for Life Science and Southern Medical University in China, have discovered that the SARS-CoV-2 virus—responsible for the COVID-19 pandemic—can produce a special type of molecule called a microRNA that directly causes lung scarring or fibrosis.


SARS-CoV-2 Virus Produces MicroRNA That Causes Lung Scarring by Disabling Key Immune Protein

This Medical News report sheds light on how this viral microRNA, identified as miR-nsp3-3p, leads to severe and long-lasting lung damage by disabling a vital protein in human lung tissue called ALCAM (Activated Leukocyte Cell Adhesion Molecule). ALCAM normally helps protect and maintain the structure and function of lung cells.
 
How the Viral Molecule Triggers Lung Fibrosis
The team found that miR-nsp3-3p was present at high levels in the respiratory samples of patients with severe or critical COVID-19. Surprisingly, it was not significantly detectable in blood samples, suggesting it mostly stays in the lungs and airways. The microRNA works by attaching itself to ALCAM's genetic message and blocking its production.
 
Without enough ALCAM, lung cells begin a process called epithelial-mesenchymal transition (EMT)—a transformation where healthy lung cells change into scar-forming cells. This change makes the lung tissue stiff and less functional, leading to difficulty in breathing and other complications associated with pulmonary fibrosis.
 
To prove this, the scientists conducted experiments on mice by introducing miR-nsp3-3p through a viral vector. Mice showed clear signs of lung scarring, but when treated with a compound that blocked miR-nsp3-3p, the damage was partially reversed. The lungs had less inflammation, less collagen buildup (a marker of fibrosis), and lower levels of fibrosis-related genes.
 
Cellular Evidence Confirms the Threat
In laboratory-grown lung cells (A549 and Beas-2B), miR-nsp3-3p was shown to reduce ALCAM levels and cause cells to exhibit features of EMT: a drop in E-cadherin (an epithelial marker) and a rise in vimentin and α-SMA (markers of fibrotic change). This effect was reversible—when researchers artificially boosted ALCAM in these cells, the fibrotic changes were undone.
 
The same pattern was seen again in mice, confirming the harmful role of miR-nsp3-3p in both lab and living systems. Lung tissues showed signs of fibrotic damage, which was notably improved when the microRNA was blocked.
 
Implications for Long COVID and Future Research
Pulmonary fibrosis is one of the most worrying long-term effects of COVID-19, and this study reveals a specific mechanism by which the vir us might cause such damage—independent of the initial infection or immune response. This also opens a path for future treatments that target miR-nsp3-3p or protect ALCAM function.
 
The researchers emphasize that miR-nsp3-3p might also affect other genes and tissues, potentially explaining various lingering effects of COVID-19. More studies are needed to find out whether this microRNA remains in the body after recovery and how it may contribute to long COVID symptoms.
 
Conclusion
The study reveals that SARS-CoV-2 can produce a viral microRNA, miR-nsp3-3p, that directly contributes to lung fibrosis by blocking a protective protein called ALCAM and triggering cellular changes that lead to scarring. This discovery provides a crucial piece of the puzzle in understanding why some COVID-19 survivors suffer from lasting lung damage and opens the door to developing treatments that can target this microRNA to prevent or reduce post-infection complications. Understanding and blocking these viral microRNAs could be key to preventing long-term harm in future pandemics or viral outbreaks.
 
The study findings were published in the peer reviewed journal: Virologica Sinica
https://www.sciencedirect.com/science/article/pii/S1995820X25000914
 
For the latest COVID-19 News, keep on logging to Thailand Medical News.
 
Read Also:
https://www.thailandmedical.news/news/hidden-lung-damage-in-millions-post-covid-may-be-permanent-and-irreversible
 
https://www.thailandmedical.news/news/favipiravir-that-was-used-to-treat-covid-19-actually-causes-lung-inflammation-lung-damage-and-lung-fibrosis
 
https://www.thailandmedical.news/news/breaking-covid-19-news-australian-scientists-discover-a-microrna-called-cov2-mir-o8-that-is-encoded-by-sars-cov-2-and-is-possibly-pathogenetic

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