Journal of IiME Volume 5 Issue 1 (May 2011) International Science Symposium on ME continued the presence of auto-antibodies, with antibodies directed at thyroid peroxidase and parietal cells. Up to 30% of patients may respond to antiviral medication. Ekua Brenu (Queensland, Australia) had looked at innate and adaptive immunity in CFS. It was postulated that her study could assist in developing biomarkers. The study involved 253 patients and 100 controls. Studies were undertaken at zero and 6 months. Cytotoxic activity of NK cells and CD8+T cells was significantly reduced. Perforin and granzyme activity was reduced. When looking at NK cell phenotypes, CD56 bright cells were significantly diminished. Cytokine secretion from CD4+T cells showed significant elevation of IL-10, IFN-γ and TNF-α. FOXP3 expression was also heightened in the CFS group. Vasoactive intestinal peptide (VIP) receptors were also investigated and found to be significantly elevated. Kenny de Meirlier (Brussels, Belgium): Because chronic activation of the immune system is present in progressive HIV and is a better predictor of disease outcome than viral load, it is important to test the hypothesis that a similar pattern may be observed in XMRV positive CFS patients. 16 XMRV positive patients (using culture assay) had a large number of tests performed. These patients were found to have reduced lymphocyte numbers and CD57+lymphocytes reduced, as observed in HIV. There was evidence of an activated innate immune system (increased elastase activity and C4a). sCD14 was significantly higher than expected, and this correlated with plasma lipopolysaccharide (LPS) a proinflammatory component of the gram-negative bacterial envelope. Low stool IgA indicated dysfunctional mucosa-associated lymphomal tissue in XMRV positive patients. Serum IL-8,IL10,MCP-1 and MIP-1β are increased and might constitute a biological signature for viral infection. This all provides supportive evidence for Invest in ME (Charity Nr. 1114035) microbial translocation being part of the pathology of XMRV +ve patients. He described a Norwegian study of severely disabled CFS patients in which the plasma LPS was elevated in those with a low Karnofsky score. This suggests a leaky gut syndrome. Stool analysis in CFS patients has indicated overgrowth of enterococci, streptococci and fungi with diminished E.Coli count. This can lead to overproduction of hydrogen sulphide which is toxic to mitochondria and affects ATP. Richard Kwiatek (Adelaide, Australia) is a rheumatologist with a particular interest in neuro-imaging. MRI was performed to look for brainstem dysfunction in CFS. Whole-brain optimised voxel-based volumetry and novel quantification of T1-weighted and T-2 weighted signal levels in structural MRI were used. Voxels build a 3-D map of the brain. In the CFS patients seated pulse pressure was reduced, and seated heart rate and asleep heart rate were increased, compared to controls. This was then correlated with brain change, other symptoms and fatigue. Prefrontal white matter volume reduced with increasing sleeping heart rate in CFS with the opposite in controls. Midbrain white matter volume reduced with increasing fatigue. There was a strong correlation between total brainstem grey matter volume and seated pulse pressure in the CFS patients. Brainstem grey matter changes suggest a failure of cerebrovascular auto-regulation, potentially mediated by astrocytes. Astrocyte dysfunction may therefore be central to CFS pathogenesis. There seems to be disrupted autonomic nervous system homeostasis. He does not feel it is reduced blood volume that will be causing this. Barrie Marmion (Adelaide, Australia) has studied Q-fever and its aftermath for many years. There were 11 suffering from post Qfever fatigue syndrome out of 39 who had had the acute illness in one study cited. The Continued page 26 www.investinme.org Page 25/58
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