Italian Researchers Discover That Aspirin Disrupts COVID-19 Spike Protein Before It Harms the Body
Nikhil Prasad Fact checked by:Thailand Medical News Team Jan 08, 2026 1 day, 1 hour, 54 minutes ago
Medical News: Aspirin’s Surprising New Ability Revealed
Researchers from Istituto di Ricerche Farmacologiche Mario Negri IRCCS in Bergamo Italy have made an unexpected discovery about aspirin. Long known for easing pain and reducing inflammation, aspirin also appears to directly interfere with the SARS-CoV-2 spike protein’s ability to attach to the human ACE2 receptor. This brand-new finding suggests aspirin may weaken the very first step of viral attack, offering a potential new role for one of the world’s most common medicines.
Aspirin appears to strip key sugars from the COVID spike protein, reducing its ability to bind ACE2 and damage tissues
How the virus normally gains entry
The SARS-CoV-2 coronavirus spike protein uses its S1 portion to latch onto ACE2, a receptor found throughout the lungs, heart, blood vessels, kidneys and brain. This attachment opens the door for infection and can trigger inflammation, clotting, tissue injury and long-term symptoms. Even in patients no longer carrying active virus, circulating spike fragments can still cause harm.
Aspirin weakens spike binding in the lab
In the new study, scientists mixed purified spike S1 protein with different concentrations of aspirin before introducing it to living cells. They found that aspirin-treated spike bound far less successfully to ACE2. The effect strengthened with higher aspirin levels, showing a clear dose-dependent pattern. The same treatment using paracetamol showed no benefit, confirming that aspirin’s effect was unique.
Animal testing strengthens the evidence
To see whether this effect mattered in living tissue, the team tested aspirin-treated spike protein in mice engineered to express human ACE2. Animals exposed to untreated spike developed swollen lung tissue, heavy inflammatory cell infiltration and early fibrotic scarring. In contrast, mice that received spike pre-treated with aspirin showed dramatically reduced lung injury, little collagen buildup and far fewer immune cells.
Importantly, giving aspirin after the spike exposure offered no protection. This proves that aspirin must interact with the spike protein itself before it reaches the body, rather than acting through its usual anti-inflammatory pathways.
The key breakthrough: aspirin alters spike sugar structures
The study’s most important discovery was that aspirin changes the spike protein’s glycosylation—the sugary coating that helps the virus bind ACE2 and avoid the immune system. Aspirin removed or altered sugars at several locations, especially at N61 and S325. When researchers created spike proteins lacking those exact sugar sites, the mutants behaved just like aspirin-modified spike: they barely attached to ACE2 and caused only mild lung abnormalities in mice.
This shows that disrupting spike glycosylation is the major reason aspirin reduces its harmful activity.
Why this matters
This
Medical News report highlights a potential
new use for a cheap, globally available medication. If further research confirms these results in humans, aspirin could become part of an early intervention strategy to weaken the spike protein before it drives tissue damage or long COVID-related complications. Although more clinical research is needed, this discovery provides a promising new angle for reducing the severity of SARS-CoV-2 infection using a familiar and low-cost drug.
The study findings were published in the peer reviewed journal: Frontiers in Immunology.
https://www.frontiersin.org/journals/immunology/articles/10.3389/fimmu.2025.1706997/full
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