A recent study suggests that a prevalent viral infection might be at the root of nearly every case of lupus, presenting some compelling new evidence.
The research, conducted by scientists at Stanford University, proposes that the Epstein-Barr virus (EBV) could be the key factor behind what is often termed the ‘cruel mystery’ of lupus.
Known for causing ‘kissing disease’ (or mononucleosis), the study indicates that EBV can directly invade and alter specific immune cells, possibly triggering the autoimmune disease systemic lupus erythematosus, commonly referred to as lupus.
“This is the most significant finding to come from my lab throughout my entire career,” notes immunologist and lab director William Robinson.
“We believe this applies to all cases of lupus.”
Related: Lupus Tracked to Changes in a Single Gene That Tames The Immune System
Most adults worldwide have been exposed to EBV at some point, with the virus typically remaining inactive within their cells.
In contrast, lupus patients exhibit a more intense infection, possibly due to contracting a more aggressive strain of EBV. Research indicates that roughly 1 in 400 B cells in individuals with lupus is infected by EBV, which is about 25 times more than in healthy people.
In laboratory settings, the infection appeared to activate a mechanism within B cells that heightens their pro-inflammatory genes.
This could “promote systemic disease and provoke autoimmune responses,” argue the authors, led by immunologist Shady Younis at Stanford.
The findings might help unravel the long-standing mystery surrounding lupus triggers and why symptoms can seem to flare and subside unpredictably.
Lupus is characterized by the immune system mistakenly attacking healthy tissues, resulting in widespread inflammation and, in severe cases, life-threatening consequences.
The disease, recognized in historical records as far back as 850 CE, currently lacks a known cause or cure. It wasn’t officially described until the 19th century, with its name stemming from a rash that resembles a wolf’s bite.
The mystery of lupus might stem from its complex nature, possibly influenced by various factors, including nutrient deficiencies, genetics, hormonal changes, or infections.
The recent Stanford findings suggest a potential unifying explanation involving viral origins.
For years, there’s been a suspicion among researchers that EBV is connected to lupus. The virus affects B cells, which also show imbalances in lupus patients. However, measuring EBV during its dormant phase within B cells has proven difficult.
Stanford researchers developed an innovative sequencing technique to determine which B cells were infected. Their results revealed that lupus patients have a significantly higher number of EBV-infected B cells compared to those without lupus, particularly memory B cells, which are essential for rapid immune responses.
In a healthy body, only about 20 percent of B cells are ‘autoreactive’ and capable of producing antibodies and activating immune cells. But EBV’s infection appears to revert some latent B cells to a pro-inflammatory state.
This mechanism aligns with a recent immunotherapy for lupus that targets and replaces faulty B cells, showing substantial benefits in clinical trials and leading to remission-like outcomes.
Virologist Guy Gorochov from Sorbonne University in France, who was not part of this study, mentioned that the research is “impressive.” He added, “It’s not the last word on lupus,” but acknowledged the team’s traction on an intriguing concept.
Looking ahead, these findings could be significant for understanding other autoimmune diseases linked to EBV, such as multiple sclerosis, long COVID, and myalgic encephalomyelitis/chronic fatigue syndrome.
The study was published in Science Translational Medicine.
