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Preliminary evidence of mitochondrial dysfunction associated with post-infective fatigue after acute infection with Epstein Barr Virus

Vernon SD , Whistler T, Cameron B, Hickie IB, Reeves WC, Lloyd A
BMC Infectious Diseases 2006;6:15.
The complete electronic version of this article is available at:
http://www.biomedcentral.com/1471-2334/6/15

Summary

This was the first analysis of gene expression profiles to evaluate risk factors for post-infectious fatigue in studies conducted in collaboration with the group from the University of New South Wales. Gene expression profiling was rapidly evolving and this study used microarrays containing 3,8000 genes. The subsequent gene expression analysis of data from this cohort was able to evaluate expression profiles of 30,000 known genes. This manuscript involves 5 persons who did not improve following acute EBV-positive infectious mononucleosis and 5 HLA-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 10 participants. In this study gene expression profiles at the time of acute illness differed between those who recovered and those who developed CFS. Several genes known to be regulated by EBV differed. More importantly several differentially expressed genes affect mitochondrial functions including fatty acid metabolism and the cell cycle.

Abstract

Background : Acute infectious diseases are typically accompanied by non-specific symptoms including fever, malaise, irritability and somnolence that usually resolve on recovery. However, in some individuals these symptoms persist in what is commonly termed post-infective fatigue. The objective of this pilot study was to determine the gene expression correlates of post-infective fatigue following acute Epstein Barr virus (EBV) infection.

Methods : We followed 5 people with acute mononucleosis who developed post-infective fatigue of more than 6 months duration and 5 HLA-matched control subjects who recovered within 3 months. Subjects had peripheral blood mononuclear cell (PBMC) samples collected at varying time points including at diagnosis, then every 2 weeks for 3 months, then every 3 months for a year. Total RNA was extracted from the PBMC samples and hybridized to microarrays spotted with 3,800 oligonucleotides.

Results : Those who developed post-infective fatigue had gene expression profiles indicative of an altered host response during acute mononucleosis compared to those who recovered uneventfully. Several genes including ISG20 (interferon stimulated gene), DNAJB2 (DnaJ [Hsp40] homolog and CD99), CDK8 (cyclin-dependent kinase 8), E2F2 (E2F transcription factor 2), CDK8 (cyclin dependent kinase 8), and ACTN2 (actinin, alpha 2), known to be regulated during EBV infection, were differentially expressed in post-infective fatigue cases. Several of the differentially expressed genes affect mitochondrial functions including fatty acid metabolism and the cell cycle.

Conclusion : These preliminary data provide insights into alterations in gene transcripts associated with the varied clinical outcomes from acute infectious mononucleosis.

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