01/24/2026
EBV is the virus that causes mononucleosis, common in teens and young adults but most of us have positive IgG (old, long-term) antibodies to this virus.
For decades medicine has recognized the link between infections and the onset of an autoimmune condition. With better ability to study extremely tiny viruses, we are seeing new research trying to figure out the “why”. Often, these infections are viral but bacteria, protozoa, and tick-borne infections have been known to also trigger the immune system into imbalance of T helper and T regulatory cells.
Treating the infection, unfortunately, does not turn off the dysregulation. We must look at factors that were going on in the host prior to infection that put this person in a position to develop autoimmunity in order to have hope of non-pharmacological remission which is not always possible without the help of medications.
If I am an expert in any area of functional medicine, it is autoimmunity because it’s personal as I have autoimmune thyroid disease and several family members with AI conditions I hope to avoid.
This is one of the clearest mechanistic links yet between Epstein-Barr virus (EBV) and systemic lupus erythematosus (SLE).
In this Science Translational Medicine study, researchers show that EBV doesn’t just coexist with autoimmunity; it can reprogram autoreactive B cells to behave as highly active antigen-presenting cells, amplifying immune dysfunction in lupus.
Using advanced single-cell sequencing, the team demonstrated that EBV infects nuclear antigen–reactive B cells, alters their epigenetic and transcriptional programs, and drives downstream activation of pathogenic T and B cell responses. In other words: a virus reshaping immune “terrain,” not just triggering flares.
This work adds important depth to a long-standing clinical observation: EBV exposure is nearly universal, yet autoimmune disease is not. The difference may lie in how the immune system is reprogrammed under specific conditions.
Important context:
🔬 This is mechanistic, translational research, not a clinical intervention
🧠 Findings help explain disease biology—not guide treatment decisions (yet)
Still, studies like this move us closer to understanding autoimmunity as a systems-level process shaped by infection, immune tolerance, and epigenetic regulation.
PMID: 41223250
Research funding was provided by academic and institutional sources as disclosed by the authors. No industry sponsorship or relevant conflicts of interest were reported.
