Jonathan Kerr of St George’s, University of London, and his team used two techniques to look at differences in the expression of 47,000 genes and their variants in people with CFS and a group of unaffected people.
They used a DNA microarray chip to examine gene expression in 27 people with CFS and 54 controls. They also used “massive parallel signature sequencing” to assess gene activity in 20 people with CFS and 20 without by measuring the amount of mRNA each gene produces. The team ended up with about 100 genes where differences in expression between CFS patients and controls were most striking.
“Most of the abnormally expressed genes are involved in the immune system,” says Kerr, although he points out that the exact pattern of gene expression varies between sufferers. Both over and underactive immune expression have been blamed for the symptoms of CFS in the past, but the lack of a single marker has hampered diagnosis. Kerr’s work, though preliminary, could herald two breakthroughs: a treatment for the illness based on immune therapy, and a diagnostic test based on a broad spectrum of proteins.
Kerr is in the process of setting up clinical trials using beta interferon, a treatment for multiple sclerosis. It boosts the immune system by enhancing the activity of natural killer cells, which fight viruses. Since viruses are believed to play a role in triggering CFS in many people, beta interferon might clear the infection and help them to shake off CFS.
A test for a disease as misunderstood as CFS would also be invaluable. Kerr’s team has developed one that uses mass spectrometry to find proteins that are present in people with CFS but not healthy controls. Yet one of the biggest challenges facing those involved in CFS research is that the underlying causes may vary from person to person and one solution is unlikely to fit them all.
MEDICA.de; Source: New Scientist