Chronic Fatigue Syndrome: Inflammation, Immune Function, and Neuroendocrine Part 2

Antiviral treatments

At the 2007 International Association of Chronic Fatigue Syndrome meeting, investigators presented two phase 1 studies of valganciclovir in CFS patients with evidence of HHV-6 or EBV infection. Kogelnik et al. [31*] found evidence of clinical improvement in 20 of 23 subjects with acute onset CFS and high EBV and/or HHV-6 antibody titers. Lerner et al. [32*] presented data from an open-label phase 1 trial supporting EBV reactivation affecting cardiac function in profoundly ill CFS patients. The study, which was a follow-up to his previously published study of 19 CFS patients with cardiac wall motility abnormalities, showed a favorable clinical response from most of the 60 patients to 6 months of oral valganciclovir. Both investigators cautioned that the drug had a significant risk of bone marrow suppression and renal toxicity, and phase 2 placebo control studies are underway.

In an open-label study of folinic acid, authors reported a high incidence of chronic reactivated EBV infection accompanied by B-cell immunodeficiency in patients with CFS. A significant proportion of these patients experienced a marked improvement in symptoms after treatment with folinic acid [33].

A retrospective study measuring the response of patients with CFS to azithromycin found that 58 of the 99 participants reported a decrease in symptom severity [34]. The responders improved to an estimated maximum of 80% of their premorbid level. Those patients who responded to the treatment had lower levels of plasma acetylcarnitine. The investigators theorize that the efficacy of the azithromycin could be attributed to the modulating effect on the chronically primed immune glia-cells in the brain or in the activated immune system of the patients with CFS.

Conclusions

The preponderance of available research confirms that immune dysregulation is a primary characteristic of CFS. New research has further elucidated our understanding of the genomics of the illness and the role of viral infection and reactivation in the pathogenesis. Advances in the field should result in targeted therapies to impact immune function, HPA axis regulation, and persistent viral reactivation in CFS patients. Future research investigating these important areas may lead to promising new discoveries and options for treating CFS.

Tags: CFS, immune function, inflammation, neuroendocrine, virus, therapy