You can’t have ME/CFS without knowing a little something about the Ebstein-Barr Virus. PWCs have heard EBV throughout their illness probably about as much as they have heard the words Chronic Fatigue Syndrome. The Epstein-Barr Virus was discovered in 1964 by Michael Epstein & Yvonne Barr.
For the majority of the population, exposure to the Ebstein-Barr Virus is usually harmless and over 90% of the population have been infected with EBV during their childhood. It seems though that when Epstein-Barr Virus infects someone when they are adolescents and adults it is more likely to cause problems and disease for the person (IM – infectious mono).
According to the CFIDS Association:
While EBV infection hasnt been causally linked to CFS, we know that about 5 to 10 percent of people with IM following EBV infection will not recover after six months and will develop CFS. We also know that the severity of the IM during the initial stages of the EBV infection is the greatest predictor for developing CFS. Unfortunately, we dont yet know what it is about the severity of the acute EBV infection that puts a person at risk for CFS.
A recent paper published in the Journal of Affective Disorders identifies pathways and biomarkers that correlate with fatigue and symptoms of chronic active EBV infection. Because of the known connections between EBV, IM and CFS, chronic active EBV infection (CAEBV) may be a useful model for understanding the chronic immune activation and the pathophysiology of CFS.
When a person develops infectious mono (IM), an EBV specific immunity develops. But there are another group of peole with IM who develop what is known as CAEBV – chronic or recurrent IM, unusual patterns of antibodies to the virus, severe fatigue and impaired quality of life:
Chronic immune activation features similar characteristics, and the authors proposed that tryptophan metabolisma process necessary for serotonin production and proper immune functionmight be involved.
In the study investigation, 20 people with chronic active EBV infection and 10 healthy age-matched controls were studied. Those with chronic active EBV infection were examined at four and eight months.
Tryptophan metabolism was measured in each person. Investigators also measured EBV viral DNA and serum neopterin, which is a marker of cellular immune system activation.
The investigators found that the CAEBV patients with detectable EBV viral DNA had significantly higher serum neopterin and lower tryptophan levels than CAEBV patients without EBV viral DNA. Healthy controls did not show this relationship between neopterin and tryptophan. In addition, tryptophan degradation was aggravated in CAEBV patients with severe fatigue.
Tryptophan is one of the least abundant essential amino acids, yet its involved in a number of biological functions, including the immune response. The results of this study show that increased tryptophan degradation is associated with cell-mediated immune activation. This disturbance in tryptophan metabolism may explain the fatigue experienced by people with CAEBV, making CAEBV a useful model for understanding the chronic immune activation and pathophysiology of CFS.