SARS-CoV-2 Envelope Protein Found to Damage Lung Barrier and Fuel Severe Inflammation
Nikhil Prasad Fact checked by:Thailand Medical News Team Jul 12, 2025 4 hours, 44 minutes ago
Medical News: SARS-CoV-2 Uses Hidden Protein Motif to Weaken Lungs and Spark Illness
Researchers from Institut Pasteur and Université Paris Cité in France have uncovered a crucial reason why SARS-CoV-2—the virus that causes COVID-19—can cause such serious illness. Their findings reveal that a small part of the virus called the PDZ-binding motif (PBM), found in its envelope (E) protein, acts as a hidden weapon. This PBM interferes with the cells in our lungs that are meant to keep harmful substances out, making it easier for the virus to spread and cause inflammation.
SARS-CoV-2 Envelope Protein Found to Damage Lung Barrier and Fuel Severe Inflammation
This
Medical News report shows that when researchers created mutant viruses without this PBM, the results were striking. These altered viruses were much less harmful. In both lab cell cultures and live animal studies using hamsters, the PBM-deficient viruses caused less damage, replicated more slowly, and led to milder symptoms. Hamsters infected with the PBM-deficient viruses did not lose weight, showed little to no signs of inflammation, and retained their sense of smell—unlike those infected with the regular virus.
How the Virus Weakens the Lungs
Normally, lung cells are tightly sealed together using special proteins like ZO-1 that keep the lung barrier strong. But the SARS-CoV-2 E protein, using its PBM, disrupts these junctions. The study found that the PBM interacts directly with ZO-1, pulling it away from its normal location. Without this support, lung cells start to break apart. Infections with PBM-deficient viruses, on the other hand, kept ZO-1 intact, preserving the lung's protective lining.
Lab-grown human bronchial tissues confirmed these findings. PBM-deficient viruses had difficulty replicating and spreading, particularly in the deeper layers of lung-like tissue. These mutant viruses were less able to move from the airway’s surface into the bloodstream, reducing the risk of widespread infection.
Real Impact Seen in Animal Tests
In golden Syrian hamsters, animals infected with the normal virus became sick and inflamed. Their lungs were damaged, and the virus was found in high levels. But animals infected with PBM-lacking viruses had much healthier lungs, minimal signs of illness, and lower viral loads.
Interestingly, the PBM did not seem to play a major role in the virus reaching the brain. Even though some virus was found in the brain’s olfactory bulb (connected to smell), no major brain damage or inflammation was seen.
A Target for Future Therapies
At a genetic level, the absence of the PBM led to much weaker activation of inflammatory pathways. In regular SARS-CoV-2 infection, hundreds of genes linked to immune signaling and cell death become overactive. Without the PBM, many of these signals were reduced, especially early in the infection.
These results suggest that thi
s tiny motif—the PBM—could be a valuable target for future COVID-19 treatments. By blocking this viral tool, it may be possible to reduce inflammation, protect the lung barrier, and ease the severity of the disease.
The study findings were published in the peer reviewed journal: Cellular & Molecular Biology Letters
https://link.springer.com/article/10.1186/s11658-025-00758-y
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https://www.thailandmedical.news/news/long-covid-brain-fog-tied-to-dangerous-vascular-and-heart-related-gene-changes
https://www.thailandmedical.news/news/forensic-doctors-find-that-mysterious-deaths-were-actually-caused-by-covid-19-induced-acute-mesenteric-ischemia
https://www.thailandmedical.news/articles/coronavirus
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