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Researchers from the Hebrew University of Jerusalem have uncovered a mechanism by which a protein from the SARS-CoV-2 virus—the virus responsible for COVID-19—may cause the immune system to mistakenly target healthy cells. The findings, published in Cell Reports, provide new insight into the causes of severe COVID-19 complications and suggest potential avenues for treatment.

The study focuses on the virus’s nucleocapsid protein (NP), which typically functions to package viral genetic material inside infected cells. Surprisingly, scientists found that this protein can move beyond infected cells and attach itself to nearby, healthy epithelial cells.

Once NP appears on the surface of these uninfected cells, the immune system misidentifies them as infected and deploys anti-NP antibodies. These antibodies mark the healthy cells for destruction, activating the classical complement pathway—a part of the immune system that can cause inflammation and tissue damage. This process may contribute to both severe cases of COVID-19 and the lingering symptoms associated with long COVID.

Using lab-grown cells, patient samples, and high-resolution imaging, the researchers demonstrated that NP binds to specific molecules on cell surfaces, forming clusters that make the immune system’s confusion even worse.

Importantly, the study also highlighted a possible solution. Enoxaparin—a widely used blood thinner and heparin analog—was found to block NP from binding to healthy cells. By occupying the same binding sites that NP targets, enoxaparin prevented immune cells from mistakenly attacking these cells in both laboratory and patient-derived samples.

The researchers believe this discovery could lead to new strategies to prevent immune-related complications not only in COVID-19 but potentially in other viral infections as well.