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Gene expression correlates of postinfective fatigue syndrome after infectious mononucleosis
Cameron B, Galbraith S, Zhang Y, Davenport T, Vollmer-Conna U, Wakefield D, Hickie I, Dunsmuir W, Whistler T, Vernon S, Reeves WC, Lloyd A
Journal of Infectious Diseases 196:56-66, 2007.
Summary
This is another of the post-infectious fatigue studies conducted in collaboration with the group from the University of New South Wales. This manuscript involves 6 persons who did not improve following acute EBV-positive infectious mononucleosis and 8 matched controls that suffered acute infectious mononucleosis but had completely recovered within 6-months. The objective was to determine whether gene expression patterns differed over time in the two groups. In this case we obtained blood specimens at multiple time points (through 1 year) from the 14 participants; 65 blood specimens in all. We then examined activity (expression levels) of 30,000 genes in each specimen and evaluated associations between patterns of gene expression and illness. We found that activity levels of 234 genes were significantly correlated with severity of fatigue and 180 were correlated with musculoskeletal pain. The genes whose activity levels were involved included several that have functional roles in signal transduction, immune response and neuronal metabolic pathways.
Abstract
Background. Infectious mononucleosis (IM) commonly triggers a protracted postinfective fatigue syndrome (PIFS) of unknown pathogenesis.
Methods. Seven subjects with PIFS with 6 or more months of disabling symptoms and 8 matched control subjects who had recovered promptly from documented IM were studied. The expression of 30,000 genes was examined in the peripheral blood by microarray analysis in 65 longitudinally collected samples. Gene expression patterns associated with PIFS were sought by correlation with symptom factor scores.
Results. Differential expression of 733 genes was identified when samples collected early during the illness and at the late (recovered) time point were compared. Of these genes, 234 were found to be significantly correlated with the reported severity of the fatigue symptom factor, and 180 were found to be correlated with the musculoskeletal pain symptom factor. Validation by analysis of the longitudinal expression pattern revealed 35 genes for which changes in expression were consistent with the illness course. These genes included several that are involved in signal transduction pathways, metal ion binding, and ion channel activity.
Conclusions. Gene expression correlates of the cardinal symptoms of PIFS after IM have been identified. Further studies of these gene products may help to elucidate the pathogenesis of PIFS.
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