COVID-19: Drug Stops Immune Attacks on Healthy Cells
- A new study from the Hebrew University of Jerusalem reveals a mechanism by which the COVID-19 virus may induce immune-mediated tissue damage.
- the study, published in Cell Reports, highlights the role of the virus's nucleocapsid protein (NP).
- Anti-NP antibodies mistakenly label these cells for destruction, activating the classical complement pathway.
A breakthrough study reveals how the COVID-19 virus can trigger the immune system to attack healthy cells, causing tissue damage and potentially contributing to severe outcomes, including long COVID. Researchers at the Hebrew University of Jerusalem discovered that the SARS-CoV-2 nucleocapsid protein spreads to uninfected cells, prompting an immune response that mistakenly targets healthy cells. Encouragingly, the research highlights enoxaparin, a common blood thinner, may block this harmful protein interaction, potentially preventing the immune system from attacking. news Directory 3 brings you this vital data. This finding offers a potential new strategy for COVID-19 treatment and for managing the immune response. Discover what’s next as researchers explore new therapeutic interventions.
COVID-19: Viral Protein Triggers Errant Immune Response
A new study from the Hebrew University of Jerusalem reveals a mechanism by which the COVID-19 virus may induce immune-mediated tissue damage. The research indicates that the SARS-CoV-2 virus can cause the immune system to target cells it never infected.
the study, published in Cell Reports, highlights the role of the virus’s nucleocapsid protein (NP). While NP is known for packaging viral RNA within infected cells, researchers discovered it can transfer to neighboring, uninfected epithelial cells and attach to their surfaces. This viral protein on otherwise healthy cells is then recognized by the immune system.
Anti-NP antibodies mistakenly label these cells for destruction, activating the classical complement pathway. This process leads to inflammation and cellular damage, potentially contributing to severe COVID-19 outcomes and complications like long COVID. Understanding this mechanism may open doors to new strategies for preventing immune-driven damage in COVID-19 and other viral infections.
Researchers, using lab-grown cells, imaging, and patient samples, found that the nucleocapsid protein attaches to Heparan Sulfate proteoglycans, sugar-like molecules on cell surfaces. This attachment leads to clumps of viral protein forming on healthy cells, prompting the immune system to attack, potentially damaging both infected and healthy cells.
The study also found that enoxaparin, a common blood thinner, can prevent the viral protein from attaching to healthy cells by binding to the same spots. Lab experiments and patient sample tests showed enoxaparin stopped the protein from attaching and prevented the immune system from mistakenly attacking cells. This identifies a potential avenue for COVID-19 treatment and managing immune response.
The study was a collaborative effort involving Dr. Alexander Rouvinski, Prof. Ora Schueler-Furman, Prof. Reuven Wiener, Jamal Fahoum, and Maria Billan from the Faculty of Medicine at the Hebrew University of Jerusalem, along with clinicians Dr.Dan Padawer, Prof. Dana Wolf,and Dr. Orly Zelig from Hebrew university-Hadassah Medical Center. SARS-CoV-2 infection experiments were performed at the barry Skolnick Biosafety Level 3 National Unit.
What’s next
Ongoing studies will explore new strategies for preventing immune-driven damage in COVID-19 and other viral infections, potentially leading to novel therapeutic interventions.