Scientists Discover How SARS-CoV-2 Hijacks G3BP1 Triggering Dangerous Fat Metabolism Changes
Nikhil Prasad Fact checked by:Thailand Medical News Team Oct 31, 2025 6 hours, 39 minutes ago
Medical News: A Hidden Viral Strategy Finally Exposed
A groundbreaking study from Capital Medical University and Hubei University of Medicine in China has uncovered a disturbing mechanism behind how SARS-CoV-2 manipulates human cells. The virus’s nucleocapsid (N) protein directly attacks a vital cellular regulator known as G3BP1, throwing the body’s stress response and fat metabolism into chaos. According to this
Medical News report, the discovery sheds new light on why COVID-19 can cause severe inflammation, fatigue, and organ damage — and why certain variants are deadlier than others.
Scientists Discover How SARS-CoV-2 Hijacks G3BP1 Triggering Dangerous Fat Metabolism
Changes
The Crucial Role of G3BP1 in Cellular Defense
G3BP1 acts like a control tower inside every cell, orchestrating responses to stress and infection. It helps form stress granules that protect essential molecules during viral invasion. But the new research shows that SARS-CoV-2 hijacks this system. Using advanced RNA sequencing, scientists found that the virus’s N protein rewires G3BP1’s RNA interactions — particularly silencing genes that regulate fatty acid metabolism, including ACOT12, PLIN4, GPX1, and ACADS. The result is a total breakdown in lipid balance, forcing the body into a metabolic state that benefits the virus.
Why the Original Wuhan Strain Was More Dangerous
The study also uncovered why early COVID-19 infections were often more severe. The N protein from the Wuhan strain showed a much stronger grip on G3BP1 compared to that of the Omicron variant. This tighter binding likely explains why the first wave of infections triggered stronger inflammation and higher death rates. The research also linked certain blood molecules to disease severity: high levels of dihomolinoleate (20:2n6), a healthy omega-6 fatty acid, appear protective, while 4-androsten-3beta,17beta-diol disulfate, a steroid hormone byproduct, worsens disease progression.
The Virus’s Masterplan to Reprogram Human Metabolism
When G3BP1 is compromised, the cell’s normal energy and fat-processing pathways collapse. This forces the body into metabolic reprogramming — a viral survival tactic that fuels replication while draining host resources. Patients suffer inflammation, fatigue, and tissue damage as their bodies attempt to compensate. Scientists also observed an abnormal rise in genes linked to dihomolinoleate metabolism, suggesting the body’s desperate effort to restore balance.
A New Target for Future COVID-19 Therapies
This breakthrough points to G3BP1 as a critical target for future antiviral treatments. If scientists can block the virus’s ability to bind or damage this protein, it could prevent the cascade of metabolic chaos that leads to severe symptoms. Given G3BP1’s role in cancer and neurodegenerative diseases, this discovery could reshape multiple fields of medicine.
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The study findings were published in the peer reviewed journal: Archives of Virology
https://link.springer.com/article/10.1007/s00705-025-06447-7
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