Health
Stanford Study Links Epstein-Barr Virus to Lupus, Revealing Hidden Trigger Behind Autoimmune Disease
New research from Stanford University links the Epstein-Barr virus (EBV) to lupus disease, showing how the virus can push immune cells to attack the body’s own tissues. The findings, published this week in Science Translational Medicine, suggest that the common childhood virus may be the key trigger behind lupus, a chronic autoimmune disorder that affects millions worldwide.
According to the study, EBV — a virus carried by more than 90 percent of adults — appears to manipulate the body’s immune cells in a way that sparks lupus. “This is the single most impactful finding to emerge from my lab in my entire career,” said Dr. William Robinson, professor of immunology and rheumatology at Stanford University and the study’s senior author. “We think it applies to 100 per cent of lupus cases.”
Lupus occurs when the immune system mistakenly attacks healthy tissues, leading to inflammation that can damage the skin, joints, kidneys, heart, and nervous system. The disease affects women far more than men, accounting for roughly 90 percent of cases. While medications such as ibuprofen can manage symptoms, about 5 percent of patients develop life-threatening complications. There is currently no cure.
Epstein-Barr virus is best known for causing mononucleosis, or “mono,” often called the “kissing disease.” Most people contract it during childhood or adolescence through saliva, such as by sharing food, drinks, or through kissing. “Practically the only way to not get EBV is to live in a bubble,” Robinson said, noting that the odds of exposure are nearly 20 to 1.
Once inside the body, EBV hides within B cells — immune cells responsible for making antibodies to fight infection. The virus can hijack these cells, turning them rogue and prompting them to attack the body’s own tissues. Researchers found that in lupus patients, EBV-infected B cells are about 25 times more common than in healthy individuals.
The virus produces a protein known as EBNA2, which activates human genes linked to inflammation. This triggers an immune chain reaction where B cells stimulate other immune cells to attack cell nuclei, a hallmark of lupus. When enough of these overactive cells accumulate, a full autoimmune response develops.
The study also suggests that the same viral mechanism may contribute to other autoimmune conditions such as multiple sclerosis, rheumatoid arthritis, and Crohn’s disease. Researchers believe that genetics, variations in viral strains, and environmental factors may determine why some individuals develop autoimmune disorders after infection.
Several biotechnology firms are developing vaccines to prevent EBV infection, with early-stage clinical trials already underway. However, experts say such vaccines would only be effective if administered before initial exposure — meaning protection would need to start early in life.
If confirmed, Stanford’s discovery could reshape the understanding of autoimmune diseases and pave the way for preventive strategies against one of the world’s most persistent viruses.
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