Abstract
Purpose: To determine whether sudden - and gradual - onset groups of chronic fatigue syndrome (CFS) patients had characteristic lipid profiles which may be indicative of specific viruses or cytokine responses. Design: Laboratory-based survey. Materials and methods: A study was undertaken in 60 CFS patients and 39 age and sex-matched non-CFS control subjects. Plasma saponified lipid products were assessed using capillary gas chromatography-mass spectrometry (GC-MS) to measure qualitative changes in plasma lipid profiles. Results: Twenty of the CFS patients reported an acute viral-like infection at onset and were assessed for antibodies to Epstein-Barr virus (EBV) and Cytomegalovirus (CMV) whereas the remaining 40 CFS patients reported a gradual onset (G-CFS). None of the sudden-onset patients (S-CFS) had immunological evidence of a current common viral infection. The S-CFS, G-CFS and control groups were well resolved by discriminant function analysis of their lipid profiles (p < 0.0001), where trans-9-octadecenoic acid (elaidic acid) and octadecanoic acid (stearic acid) were the primary discriminating factors. The differences between the S-CFS and G-CFS groups did not include the primary differential features observed between CFS and control subjects but were consistent with some post-viral modification of lipid homeostasis. Conclusions: These data suggest that viral infections may influence the development of CFS in certain patients, but not necessarily represent the causal agents. The changes in lipid homeostasis observed in CFS patients from this study may reflect common long-term sequelae to single or multiple pathogen-induced modifications of lipid homeostasis and may represent the culmination of several infectious challenges and environmental influences. The differences in lipid homeostasis characterized for the sudden - and gradual - onset groups provide a molecular basis for the heterogeneity observed in the CFS patients which may have arisen from combinations of underlying genetic, dietary, immunological, environmental or pathogen-altered responses.