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Immune responsiveness in chronic fatigue syndrome
J D Milton1, G B Clements, R H Edwards
1Department of Medicine, University of Liverpool, UK.
Insights
This study found no evidence of chronic viral infections or altered immune responses to viruses in patients with chronic fatigue syndrome (myalgic encephalomyelitis). Immune markers did not significantly differ from control groups, suggesting viruses are not a primary cause.
Area of Science:
- Immunology
- Virology
- Infectious Diseases
Background:
- Chronic fatigue syndrome (CFS), also known as myalgic encephalomyelitis (ME), is a complex condition with debated etiology.
- Investigating potential viral triggers and immune system dysregulation is crucial for understanding CFS/ME.
Purpose of the Study:
- To identify immunological evidence of chronic viral infections in CFS/ME patients.
- To compare immune responsiveness to viruses in CFS/ME patients versus healthy and muscular dystrophy control groups.
Main Methods:
- Assessed circulating immune complexes (IgM, IgG).
- Measured lymphocyte proliferation responses to concanavalin A and Coxsackie B virus antigen.
- Quantified IgM antibodies and neutralizing antibodies to Coxsackie B viruses and other respiratory viruses.
Main Results:
- Elevated IgM immune complexes were found in 17% of CFS/ME patients, not significantly different from controls.
- No significant differences in lymphocyte proliferation responses to mitogens or viral antigens were observed.
- Antibody titres to Coxsackie B and other respiratory viruses did not reveal notable differences between CFS/ME patients and controls.
Conclusions:
- The study found no evidence supporting a viral etiology for chronic fatigue syndrome (myalgic encephalomyelitis).
- Neither persistent viral infection nor altered immune response to viruses could be identified as a cause of CFS/ME.
Abstract:
We have endeavoured to find immunological indications of chronic virus infection in patients with chronic fatigue syndrome (myalgic encephalomyelitis) and to investigate immune responsiveness to viruses in such patients in comparison with normal subjects and patients with muscular dystrophy. Levels of circulating IgM immune complexes were elevated (above the 95% normal control range) in 10 (17%) of 58 patients with chronic fatigue syndrome, which was not significantly different from the normal controls or from dystrophy controls (by Mann Whitney U test). Levels of IgG complexes were only increased in 10% of patients. Lymphocyte proliferation in response to concanavalin A (Con A), assessed by increase in 3H-thymidine incorporation, did not differ between 14 patients and 18 normal subjects. The proliferative response to Coxsackie B virus antigen did not differ between chronic fatigue patients and normal subjects when expressed either as an increase in counts or as a stimulation index. Adjustment of the counts in relation to the proliferation response to Con A, as an indication of the overall proliferative response of the cell preparation, did not reveal any hidden difference. IgM antibodies to Coxsackie B viruses were not found in any of 20 patients and in 1 of 20 dystrophy controls. Significant levels of neutralizing antibodies to Coxsackie B viruses 1-5 were found in 6 out of 19 (32%) patients compared with 4 out of 17 (24%) dystrophy controls, which does not differ from currently expected normal incidence. Antibody titres to other respiratory viruses were also not notably different between the patient and control groups. In conclusion we can find no evidence for a definable viral aetiology for the chronic fatigue syndrome, neither in terms of a persistent infection nor an altered ability to respond to virus.