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New Research: Chronic Fatigue Gene Signs Found

  [ 1374 votes ]   [ Discuss This Article ]
www.ProHealth.com • August 1, 2005


Scientists believe they have pinpointed biological markers of chronic fatigue syndrome which could help develop a test and treatment for the condition. CFS, or ME, makes people feel extremely tired, and can cause weakness, headaches, and disrupted sleep. Scientists, now based at St George's Hospital, London, found differences in the way genes are expressed in white blood cells of people with CFS/ME. But others say the New Scientist findings may not explain all cases. It is also due to be published in the Journal of Clinical Pathology. The scientists say their findings fit with the understanding that a virus, such as Epstein-Barr, may trigger CFS/ME, because that illness might alter how genes are expressed. CFS/ME often first appears as a flu-like illness, but does not then go away. 'Hijacked' The researchers compared levels of gene expression in the white blood cells of 25 healthy people and 25 who had CFS using DNA chip technology. They found differences in the behaviour of 35 of the 9,522 genes they analysed. Further genetic testing showed 15 of the genes were up to four times more active in people with CFS, while one gene was less active. Several genes the team pinpointed play important roles in mitochondria, the "powerhouse" of cells. One of the products of these genes is EIF4G1, which is involved in the protein production in mitochondria. EIF4G1 is hijacked by some viruses, so cells may compensate by increasing gene expression. The genetic differences lead to changes in how blood proteins behave which could allow the development of a blood test for CFS, the team say. Other genes are involved in regulating the immune system or playing important roles in nerve cells. The team will now carry out further research on 1,000 CFS patients and healthy people. Not 'made-up' Dr Jonathan Kerr who led the research team, which is currently in the process of moving to St George's, said: "The involvement of such genes does seem to fit with the fact that these patients lack energy and suffer from fatigue." He added the work could also potentially lead to a treatment for the condition. "We have shown that a significant part of the pathogenesis resides in the white blood cells and in their activity. It will open the door to development of pharmacological interventions." Dr Russell Lane, a neurologist at Charing Cross Hospital, in London, said: "This exciting new work shows that some aspects of this complex illness may be understandable in molecular terms, and that CFS is not a 'made-up' illness." Chris Clark, chief executive of Action on ME, told the BBC News website: "The prospect of having a diagnostic test is very encouraging because many people with ME can currently take well over a year to find out what is wrong with them." Dr Neil Abbot of Merge, a charity which funds research into CFS/ME, said: "CFS/ME can have very different effects on patients. "We're not looking at just one condition with a definitive patient group. "So it might be hard to get a gene signature which works for everyone with CFS/ME." But he added: "This research probably won't be the answer for everyone, but it is still very interesting."



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