A new study published in the Science Translational Medicine has revealed a connection between the virus called the pstein-Barr virus (EBV), a pathogen silently carried by almost 95% of adults with systemic lupus rythematosus, better known as lupus. This Stanford-led research shows that EBV could highjack a tiny subset of immune cells and push the body into a full-blown autoimmune attack. It uses ultraprecise sequencing technique to do so, which scientists have finally been able to tract down in the infected immune cells and have been able to uncover how just a handful of them could lead to widespread inflammation. As per the researchers, the mechanism could explained virtually all lupus cases. Why Lupus Has Been So Hard to ExplainLupus impact is severe as it affects hundred thousand Americans, and has an estimate of 5 million people being affected with this worldwide. It is a chronic autoimmune disorder in which the immune system mistakenly attacks the nuclei of the body's own cells, and leads to damage across organs. These organs include anywhere from skin, joints, to heart, kidneys, and even the nervous system. A reason that continues to remain mysterious is why 90% of lupus patients are women. While medications can slow the disease and help most people live normal lives, the condition can be life-threatening for about 5% of patients. Despite decades of research, scientists have struggled to pinpoint a single trigger. EBV has always been a suspect, but until now, no one had the tools to prove it.You May Have The Virus That Triggers LupusDespite the devastating truth about lupus, almost everyone has EBV, the virus that could trigger it. It is so common that even one researcher joked that the only way to avoid is be living "in a bubble". How does it spread? EBV usually spreads through saliva, by sharing utensils as kids, or kissing. It can cause mononucleosis, the classic “kissing disease,” which often leaves people with lingering fatigue.What makes this tricky is that once EBV infects you, it never fully leaves. It is like herpes or chickenpox viruses, which could tuck its genetic material into the nuclei of infected cells and lies dormant, sometimes, throughout life. Among its favorite hiding spots are B cells, powerful immune cells responsible for producing antibodies and activating other parts of the immune system.Typically, only a tiny fraction of someone’s B cells carry EBV, making them nearly impossible to detect with older scientific tools.What Does This Breakthrough May Mean For Finding These EBV Inside Rogue B Cells?Using their new high-precision sequencing method, the Stanford team discovered that in a healthy person, fewer than 1 in 10,000 B cells carry EBV. But in patients with lupus, the ratio jumps dramatically to 1 in 400—a 25-fold increase.This matters because EBV-infected B cells occasionally produce an important viral protein called EBNA2. EBNA2 behaves like a genetic on-switch. It activates dormant human genes, many of which are involved in inflammation. Once switched on, these B cells turn into aggressive, hyper-inflammatory antigen-presenting cells. They, in turn, rally other immune cells, especially helper T cells, to join the attack.Those T cells then recruit hundreds of other B cells that mistakenly target the nuclei of healthy cells. The result? A runaway chain reaction that leads to the formation of antinuclear antibodies, the hallmark of lupus.Critically, most of the B cells joining the attack are not EBV-infected. But once the inflammatory cascade begins, EBV need not be present in every cell. It only needs a few instigators.Do Everyone With EBV Get Lupus?While nearly all of us has EBV, only some people develop autoimmune diseases. This could be because certain EBV strains may be more likely to convert B cells into the 'driver cells' that would kick-start autoimmunity. Genetics too plays an important role in how someone's immune system responds to these infected cells. This new finding therefore just does not offers a broader understanding of lupus, but also opens doors for treatment strategies. Many biotech companies are already developing EBV vaccines, though these would need to be given in early infancy because vaccines cannot clear an existing infection.There’s also interest in aggressive therapies like ultradeep B-cell depletion, which aims to wipe out all circulating B cells and allow new, EBV-free cells to grow back.Researchers say the same EBV-triggered mechanism may play a role in other autoimmune conditions, including multiple sclerosis, rheumatoid arthritis, and Crohn’s disease.
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