Predisposing and Precipitating Factors in Epstein–Barr Virus-Caused Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) following infectious mononucleosis (IM) (due to Epstein Barr Virus) is the classic example of post-viral syndrome. Actually it was the most famous cause, until SARS-CoV-2 disrupted everything and became the most famous agent of post viral syndromes (long covid).
The majority of patients with ME/CFS report infectious illnesses before the onset of ME/CFS, with 30% of cases of ME/CFS due to IM caused by the Epstein–Barr virus. After developing IM, one study found 11% of adults had ME/CFS at 6 months and 9% had ME/CFS at 1 year. Another study of adolescents found 13% and 7% with ME/CFS at 6 and 12 months following IM, respectively.
However, which children are at higher risk of developing ME/CFS following EBV infection?
A very interesting new paper provides an overview of a study that included pre-illness predictors of ME/CFS development following IM in a diverse group of college students who were enrolled before the onset of IM. The authors were able to longitudinally follow youths over time to better understand the risk factors associated with the pathophysiology of ME/CFS. General screens of health and psychological well-being, as well as blood samples, were obtained at three stages of the study (Stage 1—Baseline—when the students were well, at least 6 weeks before the student developed IM; Stage 2—within 6 weeks following the diagnosis of IM, and Stage 3—six months after IM, when they had either developed ME/CFS or recovered).
Briefly, Patients with stomach pain, bloating, and symptoms of an irritable bowel at pre-illness baseline, low levels of IL-13 and/or IL-5 at pre-illness baseline (previously discussed), and severe gastrointestinal symptoms at the time they contracted mononucleosis had a nearly 80% chance of developing severe ME/CFS six months following IM.
In addition, using metabolomic data, the authors identified potentially dysregulated pre-illness pathways that are essential for proliferating cells, particularly during a pro-inflammatory immune response, and are thus consistent with the irregularities in cytokines seen in prior studies.
What does it mean:
IL-5 enhances the production of B1 cells which are anti-inflammatory (impaired B1 cells have been found in multiple sclerosis, systemic lupus erythematosus, and rheumatoid arthritis), and IL-13 has anti-inflammatory properties. Deficiencies in these cytokines before contracting IM may cause the immune system to lack the breadth or suppleness needed to cope successfully with primary EBV infection.
What can we do?