Stanford Study Links Lupus Progress to Common Virus, EBV
STANFORD, CA – Researchers at Stanford medicine have established a compelling link between the Epstein-Barr virus (EBV), which infects approximately 95% of the population, and the development of lupus, an autoimmune disease. The study, published recently, details how a viral protein, EBNA2, triggers a cascade of genetic and immunological events within B cells, ultimately leading to the self-attack characteristic of lupus.
EBV remains latent in B cells after initial infection. The Stanford team discovered that EBNA2 acts as a “transcription factor,” activating genes within the B cell that promote inflammation. This activation includes turning on genes coding for other transcription factors, further amplifying the pro-inflammatory response.
The altered B cells then function as ”professional antigen-presenting cells,” stimulating helper T cells to target cell-nuclear components. Thes T cells,in turn,recruit additional antinuclear B cells and killer T cells,creating a substantial immune response. Critically, the study found that even uninfected B cells can join this autoimmune attack if enough activated cells are present, resulting in lupus symptoms.
“If there are enough of them, the result is a bout of lupus,” researchers state.
The findings suggest EBV may play a role in other autoimmune diseases like multiple sclerosis, rheumatoid arthritis, and Crohn’s disease, where EBNA2 activity has been observed. Researchers are investigating whether specific EBV strains are more likely to initiate this autoimmune cascade.
While EBV vaccines are in development and undergoing clinical trials, they would need to be administered shortly after birth to be effective, as they cannot eliminate the virus in already-infected individuals.
Stanford University’s Office of Technology Licensing has filed a provisional patent submission related to the study’s findings. Researchers involved – Aaron Robinson, Fatima Younis, and Mahesh Pandit – are co-founders and stockholders of EBVio Inc.,a company developing an experimental lupus treatment involving complete B-cell depletion followed by regeneration with EBV-free cells. Robinson is also a director and shareholder of Flatiron bio, LLC.
The study was funded by the National Institutes of Health (grants R01AR078268, R01AI173189-01, PATHO-PH2-SUB_17_23 and R01AI024717), the VA Palo Alto Health care System, the Lupus Research alliance, and the Brennan Family. Contributing institutions included the U.S.Department of Veterans Affairs Medical Center, Cincinnati; the University of Massachusetts School of Medicine; the University of oklahoma Health Sciences Center; and Rockefeller university.
