New research provides compelling evidence that the Epstein-Barr virus (EBV), common culprit behind glandular fever or “kissing disease,” plays a direct role in triggering lupus, an autoimmune disorder affecting millions worldwide.
While EBV infects a staggering 95% of adults globally with typically mild or no symptoms, about 90% of people diagnosed with lupus exhibit elevated antibodies against the virus. This long-standing observation has fueled speculation about a potential link between these two conditions. Scientists have finally begun to uncover the “how” behind this connection.
How EBV Hijacks the Immune System
William Robinson and his team at Stanford University developed a groundbreaking technology called EBV-seq to meticulously examine individual B-cells – the immune system’s antibody factories – in people with lupus. Their findings revealed that infected memory B-cells, responsible for remembering past pathogens, were significantly more prevalent in lupus patients compared to healthy individuals.
These infected cells weren’t merely harboring the virus; EBV was actively reprogramming them. The virus produces a protein called EBNA2, which binds to specific genes (ZEB2 and TBX21) within these memory B-cells, essentially turning up their activity. This leads to a cascade effect:
- T-cell Activation: Infected memory B-cells trigger the activation of helper T-cells, another type of immune cell.
- Uncontrolled Immune Response: These activated T-cells then recruit and activate uninfected B-cells, creating an escalating cycle of immune system activity.
This runaway response ultimately leads to the immune system attacking healthy tissues – a hallmark of lupus.
Genetic Predisposition: While EBV infection appears to be a critical trigger, it’s unlikely the sole cause. Robinson suggests that genetic factors likely play a role in making some individuals more susceptible. People with specific genetic predispositions may possess B-cells that are more prone to mistakenly targeting healthy tissues when exposed to EBV.
Implications for Treatment and Prevention:
These groundbreaking findings shed light on the potential effectiveness of certain CAR T-cell therapies currently being tested for lupus. These therapies involve genetically engineering a patient’s own T-cells to target specific immune cells, including potentially those infected with EBV. Early clinical trials have shown promising results, leading some experts to suggest that they might even offer a cure for lupus by eliminating these problematic B-cells.
Further research is needed to confirm the long-term efficacy and safety of CAR T-cell therapy in treating lupus. This discovery also strengthens the argument for developing an EBV vaccine, which could potentially prevent a significant number of lupus cases in the future.
While challenges remain regarding cost-effectiveness and ensuring widespread accessibility, this research offers hope for more targeted and effective treatments for lupus – and possibly other autoimmune diseases driven by similar mechanisms.
