Authors

Garcia L, Kerr J, Fletcher MA, Sol C, Klimas N.

Institution

University of Miami Miller School of Medicine and Miami VA Medical Center, Miami, Florida, USA, and St George’s University of London, London, UK

Funding

The study was funded by a research grant ME Research UK awarded to St George’s University, London.

Publication

Bulletin of the IACFS/ME. Abstracts from General Session, Sunday, September 25, 2011, IACFS/ME Biennial International Conference Ottawa, Ontario, Canada

Abstract

There have been a number of studies utilizing genomics to better understand and define CFS/ME. Jonathan Kerr’s group published a series of studies that defined 79 genes associated with this illness, then used the same method to develop biologically defined subgroups (Kerr JR, et al. J Infect Dis 2008). The Miami group has been studying both GWI and CFS/ME using gene activation patterns and proteomics, before during and after an exercise challenge to better understand the mediators of persistence and relapse. In this study we collaborated with Dr Kerr, comparing CFS/ME (n=25), control (n=53) and GWI samples (n=25), the GWI samples studied were drawn prior to the exercise challenge.

The data from the CFS/ME cohort confirmed the findings from Dr. Kerr’s earlier studies. There were significant differences when compared to controls in expression of genes that regulate intracellular pathways mitochondrial function, cell wall and signaling pathways. Genes which regulate cytokine regulation were also significantly different than controls, particularly the pro-inflammatory cytokines TNFa and IL6; antiviral pathways Interferon alpha, beta and omega, and the anti-inflammatory cytokine IL10.

When compared to Gulf War Illness there are some important overlaps: EB12, an EBV induction gene is 6 fold higher than controls in CFS/ME, 2 fold higher in GWI, both significant differences (p<.005). ETS1, a viral oncogene was also upregulated in both groups (p<.-0005). Transcription factor 3, which regulates immunoglobulin production, was markedly elevated in GWI, less so though significantly elevated in CFS/ME (p<.005). Apoptosis genes were markedly upregulated in both groups though GWI saw elevations were 400 fold higher than CFS/ME (p<.0005).

However, the overall trend was that most of the gene regulation abnormalities that are associated with CFS in the Kerr platform were not significantly different in GWI than in controls, and often moved in the opposite direction down regulating intracellular processes in GWI that were upregulated in CFS (73 of 87 genes studied). Using a comprehensive platform, additional genes specific for GWI have been identified by the Miami group (presented separately).