SARS-CoV-2 protein triggers immune attack on healthy cells, shows study

Researchers discover that a Covid-19 viral protein can latch onto healthy cells, prompting the immune system to mistakenly attack them - a finding that could change treatment strategies

A new study published in peer-reviewed scientific journal Cell Reports has uncovered an unexpected way in which the SARS-CoV-2 virus, which causes Covid-19, might harm healthy tissues. Researchers found that the virus can indirectly trigger immune attacks on cells it never actually infects. 

Scientists from the Hebrew University of Jerusalem discovered that the virus’s nucleocapsid protein (NP) — usually known for packaging viral RNA inside infected cells — can transfer to neighbouring uninfected epithelial cells and stick to their surfaces. Once on these healthy cells, the NP protein is mistakenly recognised by the immune system. 

“This process activates the classical complement pathway, leading to inflammation and cellular damage that might contribute to severe Covid-19 outcomes and complications such as long Covid,” the study explains. 

 

 

 

Viral protein marks healthy cells for attack

The immune system, seeing the NP protein on these healthy cells, mistakenly treats them as infected. Anti-NP antibodies label these cells for destruction, setting off a harmful chain reaction. This immune attack, researchers believe, may worsen disease severity and contribute to long-lasting symptoms seen in some Covid-19 patients. 

“This research uncovers a surprising way in which the SARS-CoV-2 virus can misdirect the immune system, causing the attack of healthy cells, simply because they have been marked by a viral protein,” the authors wrote.

 

Lab findings confirm the mechanism

The team used lab-grown cells, advanced imaging techniques, and samples from Covid-19 patients to understand how the NP protein attaches to healthy cells. They found that NP binds to heparan sulfate proteoglycans — a sugar-like molecule found on many cell surfaces. 

As a result, clusters of NP proteins form on these cells, prompting the immune system to attack them using antibodies. This mistakenly triggers the complement pathway, harming both infected and healthy cells. 

The researchers also found that the commonly used blood thinner enoxaparin can block NP from binding to healthy cells. As a heparin analog, enoxaparin competes for the same binding sites. In laboratory tests using both cell cultures and samples from patients, enoxaparin prevented NP from attaching to cells and helped stop the immune system from attacking them.