Nikhil Prasad Fact checked by:Thailand Medical News Team Feb 01, 2026 1 hour, 22 minutes ago
Medical News: A new scientific study has uncovered an unexpected and troubling way the SARS-CoV-2 virus may be protecting itself from the human immune system, helping to explain why COVID-19 can sometimes become severe and prolonged. The research reveals that a key viral component, known as the nucleocapsid protein, can hijack natural immune regulators in the blood and use them as a shield against immune attack.
Study reveals how a SARS-CoV-2 protein hijacks human immune regulators to shield the virus from destruction
This
Medical News report highlights findings from researchers based at the Laboratory of Biomedical Microbiology and Immunology, University of Veterinary Medicine and Pharmacy in Košice, Slovakia, and the Institute of Neuroimmunology, Slovak Academy of Sciences in Bratislava, Slovakia
Understanding the Immune System Targeted by the Virus
The human body relies on the complement system, a powerful part of innate immunity made up of more than 30 proteins, to quickly identify and destroy invading microbes. When working properly, this system punches holes in viruses, marks them for destruction, and prevents infection from spreading.
To avoid harming healthy cells, the complement system is tightly controlled by special molecules called complement regulatory proteins. These regulators act like brakes, ensuring the immune response does not get out of hand.
The Viral Protein That Plays a Double Role
The SARS-CoV-2 nucleocapsid protein, commonly called the N-protein, is best known for packaging the virus’s genetic material. However, the study found that this protein does much more. Large amounts of N-protein are released into the bloodstream of infected individuals, especially those with severe COVID-19.
The researchers discovered that the N-protein strongly binds to several major complement regulatory proteins, including C1 inhibitor, C4 binding protein, factor H, and vitronectin. These are the very molecules meant to protect human cells from immune damage.
How the Virus Uses Human Defenses Against Us
Crucially, the study showed that while the viral spike protein alone could not attract these immune regulators, the N-protein could act as a bridge. The N-protein binds to the spike protein on the virus surface and simultaneously captures complement regulatory proteins from human blood.
This creates a three-part complex where the virus becomes coated with human immune regulators. As a result, the virus may appear more like a normal human cell to the immune system, allowing it to slip past immune defenses.
Blocking the Body’s Final Line of Attack
One of the most alarming findings was that the N-protein reduced formation of the membrane attack complex, a structure that normally destroys viruses by punching lethal holes in them. When N-protein levels were higher, this destructive immune mechanism was significantly weakened.
This suggests that SARS-CoV-2 may actively dampen immune killing while circulating in the bloodstream, giving it more time to spread and cause damage.
Why This Matters for Severe COVID-19
High levels of N-protein in blood have already been linked to worse disease outcomes. This study provides a clear biological explanation for that link. By recruiting immune regulators, the virus may both avoid destruction and contribute to immune imbalance, which is often seen in severe COVID-19 cases.
Conclusions
The findings reveal a sophisticated immune evasion strategy used by SARS-CoV-2 that goes beyond what was previously known. The nucleocapsid protein appears to function as a molecular adaptor, allowing the virus to cloak itself with human immune regulatory proteins and weaken the complement system. This mechanism may help explain persistent viral presence, immune dysregulation, and severe disease outcomes in some patients. Understanding this interaction opens new possibilities for treatments that block N-protein interactions, restore proper immune function, and reduce severe COVID-19 complications.
The study findings were published in the peer reviewed journal: Scientific Reports.
https://link.springer.com/article/10.1038/s41598-026-37866-4
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