Journal of IiME Volume 5 Issue 1 (May 2011) International Science Symposium on ME continued C.burnetii antigen persists, and causes immune modulation with gene expression and symptoms. Usually it is continuous from the initial onset, but episodic relapses may occur due to re-infection or inadvertent Q-fever vaccination. IL-6 is elevated and IL-2 is down. The symptoms fit the criteria for a diagnosis of CFS. 3 Q-fever groups were studied and there were differences in the frequency of carriage of HLA-DR B1*11 and of IFN-γ. 35% were positive in the post-Q-fever syndrome group, and the levels were low in the controls and Q-fever recovered group and the Q-fever endocarditis group.. These differences support the concept of different immune states in chronic Q fever, determined by genetic variations in host immune responses, rather than by the properties of C.burnetii. Anne Boullerne (Illinois, USA) discussed the issue of chronic fatigue in relation to CFS and MS. She described MS as a characteristic autoimmune disorder. She outlined the differences in incidence, symptoms, duration of illness etc. She emphasised that while MS is a neuroimmune disease, CFS is an acquired severe complex system dysfunction. In MS there is oligoclonal IgG in the CSF in 95% of cases, and brain lesions with T and B cells are seen on MRI. She asks the question “Is gliosis present in CFS?” In CFS MRI abnormalities maybe found such as small punctate subcortical white matter intensities in the frontal lobes, small ventricular volume, slow blood flow and some atrophy. She had looked at functional MRI in relation to control imagery and visual imagery. Both were found to be slower in CFS compared to controls. Changes associated with finger tapping and auditory monitoring correlated with subjective fatigue and brain response during challenge involving memory. Using M.R.Spectroscopy, there was an increase in choline in the basal ganglia, no significant difference in glutathione, and ventricular lactate was elevated. There was no alteration in levels of GABA and glutamate. Invest in ME (Charity Nr. 1114035) In a rat model for Gulf War Syndrome, using pyridostigmine, there was no gliosis and no increased permeability of the blood brain barrier. A possible auto-immunity including vasoactive neuropeptides is hypothesised. Warren Tate (Dunedin, NZ) and his team have just initiated a study to develop tools that can accurately detect molecular changes within cells in response to double-stranded RNA (dsRNA) relevent to CFS. He explained how recent XMRV findings had stimulated research and a need for a bank of genetic material. Biomarkers need to be established as well as less specific markers to reflect changes in global homeostasis.There needs to be targetting of a vulnerable point in the biology of XMRV viral RNA that determines the ratio of its structural and enzyme proteins. He went on to describe types of biomarkers: 1. Specific such as in a cell undergoing apoptosis: RNaseL, PKR, phosphorylation of PKR etc 2. Specific biomarkers of disturbed homeostasis 3. General biomarkers – marking global disturbed homeostasis of various organs He explained the RNaseL activation pathway. RNaseL cleavage may be specific to CFS. He is currently studying the ratio of the RNaseL terminal fragment to uncleaved protein. He will also be looking at abnormal PKR activation. This is cleaved by caspase to form the 37D fragment. This undergoes phosphorylation which can be measured – the protein-synthesis factor e1F2α. These 2 phosphorylation events will be detected by specific antibodies against the phosphopeptides of the 2 proteins. Douglas Feinstein (Illinois,Chicago) presented study of noradrenergic treatments for neurodegenerative diseases. Glial cells are activated producing neurotoxins, which Continued page 27 www.investinme.org Page 26/58

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