20 people (10, really – so it’s a really small study). 5 CFIDS with primary EBV, 5 CFIDS with non-EBV, 10 non-CFIDS who had recovered from EBV.
EBV, HHV and CMV detected with PCR.
Levels of all 3 virusses were similar in controls and they concluded that their data did not support the hypothesis of ongoing or reactivated EBV, HHV-6, or CMV infection in the pathogenesis of CFS.
Detection of Herpesviruses and Parvovirus B19 in Gastric and Intestinal Mucosa of Chronic Fatigue Syndrome Patients
They tested 48 CFIDS patients and 35 healthy controls.
For EBV, HHV6, HHV7 there were no big differences between patients and controls .
These virusses are probably not relevant for CFS.
Parvovirus B19 DNA was detected in 40% of the patients, and in less than 15% of the controls.
Parvovirus B19 may be involved in the pathogenesis of CFS, at least for a subset of patients.
HHV-6 and HHV-7 may be involved in the pathogenesis of CFS and reactivation of both viruses may provoke changes in the phenotype of circulating lymphocytes. Dual infection rate was significantly higher in CFS patients. Active HHV-6 and dual (HHV-6 + HHV-7) infections were detected in CFS patients only, and frequency of HHV-7 reactivation was also significantly higher in these patients. HHV-6 variant B was predominant in CFS patients (12/13). The changes of immunological parameters in CFS patients with active dual infection were characterized by significant decrease of CD3+ and CD4+ T cells, significant increase of CD95+ cells and decrease of CD4+/CD8+ ratio.