1998 Clinical and Scientific Meeting

Neil R. McGregor, R. Hugh Dunstan , Mark Donohoe [1], Timothy K. Roberts, Henry L. Butt [2], Jennifer A. Watkins, Raymond N. Murdoch

Collaborative Pain Research Unit: Department of Biological Sciences
The University of Newcastle, Callaghan
NSW 2308, Australia.
Neurobiology Research Unit
Centre for Oral Health Research
University of Sydney
Westmead Hospital
NSW 2084, Australia.
1 Environmental Medical Centre
NSW 2088, Australia.
2 Division of Microbiology and Infectious Diseases
Hunter Area Pathology Service
John Hunter Hospital
NSW 2305, Australia.

Assessment of Plasma Lipid Homeostasis in Relationship to Epstein Barr Virus Antibody Titres in Patients Reporting Sudden Onset Chronic Fatigue

A study was undertaken in 20 chronic fatigue syndrome (CFS) patients who reported a sudden viral-like onset and 39 age and sex-matched control subjects. Plasma saponified lipid products were assessed using capillary gas chromatography - mass spectrometry (GC-MS) to measure qualitative changes in plasma lipid profiles. Epstein Barr virus (EBV) IgM, IgG, early antigen (EBEA) and nuclear antigen (EBNA) were measured in the CFS patients.

Eighteen of the 20 sudden-CFS patients had evidence of a past EBV infection. No patients had EBV IgM, 14 (70%) had positive EBV IgG titres, 14 (70%) were EBV nuclear antigen (EBNA) positive and 5 (25%) were EBV early antigen (EBEA) positive. EBEA was associated with changes in cis-5,8,11,14-eicosatetraenoate, cholesterol, 5a-cholest-7-en-3b-ol and the 5a-cholest-7-en-3b-ol:cholesterol ratio supportive of alterations in phospholipid hydrolysis and cholesterol metabolism consistent with a cytokine response.

These cytokine associated lipid changes, as well as changes associated with EBNA and EBV IgG, were not associated with the lipid alterations differentiating CFS patients from control subjects reported previously. The lipid changes differentiating CFS patients from control subjects may be related to combinations of genetic, dietary, immunological, environmental or pathogen altered responses.


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