Genome-Epigenome Interactions Associated with Myalgic Encephalomyelitis/Chronic Fatigue Syndrome
Myalgic Encephalomyelitis/Chronic Fatigue Syndrome (ME/CFS) is an example of a complex disease of unknown etiology. Multiple studies point to disruptions in immune functioning in ME/CFS patients as well as with specific genetic polymorphisms and alterations of the DNA methylome in lymphocytes.
However, the association between DNA methylation and genetic background in relation to the ME/CFS is currently unknown. In this study we explored this association by characterizing the genomic (~4.3 million SNPs) and epigenomic (~480 thousand CpG loci) variability between populations of ME/CFS patients and healthy controls.
We found significant associations of methylation states in T-lymphocytes at several CpG loci and regions with ME/CFS phenotype. These methylation anomalies are in close proximity to genes involved with immune function and cellular metabolism. Finally, we found significant correlations of genotypes with methylation phenotypes associated with ME/CFS.
The findings from this study highlight the role of epigenetic and genetic interactions in complex diseases, and suggest several
genetic and epigenetic elements potentially involved in the mechanisms of disease in ME/CFS.
You've done well to find one that seemingly everyone missed. The way to be most helpful to forum members is to make the title of the paper the title of the thread, then to put the abstract AND the link in the first comment.
As for the content of this paper it looks like they went hunting wooly mammoths and came back with some rabbits. No significant SNPs in the whole population and only one in women. They report some differences in methylation but a) it was unclear how statistically significant those are, and b) I actually don't understand methylation anyway so even if the results were huge I probably wouldn't grasp them!