Journal of IiME Volume 6 Issue 1 (June 2012) physical activity. The highly heterogeneous nature of the CFS population and the lack of uniformity in both diagnostic criteria and exercise testing protocols preclude pooling of data. Still, we conclude that at least a subgroup of CFS patients present with an abnormal response to exercise. Importantly, the exacerbation of symptoms after exercise is seen only in the (ME)CFS population and not in fatigue-associated disorders such as depression. Earlier (studies) revealed that in (ME)CFS patients, irrational fear of movement is not related to exercise performance. The aim of this study was to examine the interactions between several intracellular immune variables and exercise performance in (ME)CFS. These data add to the body of literature showing impairment of intracellular immunity in patients with (ME)CFS. The results provide evidence for an association between intracellular immune dysregulation and exercise performance in patients with (ME)CFS” (J Nijs, N McGregor, K De Meirleir et al. Medicine & Science in Sports & Exercise 2005:Exercise Immunology in CFS:16471654). 2005 “The hypothesis of the present study is that the appearance of cell-specific autoimmune antibodies may define subsets of (ME)CFS. (ME)CFS is clinically similar to several autoimmune disorders that can be diagnosed and characterised by autoantibody profiles. For this reason, we conducted an exhaustive evaluation of 11 ubiquitous nuclear and cellular autoantigens in addition to two neuronal specific antigens. Very few studies have evaluated the presence of autoantibodies in people with (ME)CFS. The findings of this study hint that evaluation of certain autoantibodies may give clues to on-going pathology in subsets of (ME)CFS subjects. Among (ME)CFS subjects, those who had been sick longer had higher rates of autoantibodies” (S Vernon et al. Journal of Autoimmune Diseases May 25th, 2005:2:5). 2006 The CFIDS Association produced a special issue of the Chronicle entitled “The Science and Research of CFS” (2005-2006); it contained a major article by Professor Nancy Klimas entitled “The State of Invest in ME (Charity Nr. 1114035) CFS Research” in which she noted factors that have contributed to the slow progress in unravelling (ME)CFS: these included the troublesome case definition, the need to identify sub-groups and the need to attract good researchers. Professor Anthony Komaroff considered the known abnormalities of the neurological and immune systems, and Dr Susan Levine provided a detailed overview of the immune abnormalities in her article entitled “Immune System Gone Haywire?” in which she focused in the six prominent immune abnormalities consistently shown over the previous 18 years: (i) impaired function of NK cells; (ii) increased number of destructive T cells and increased number of T cells expressing activation markers; (iii) activation of several proinflammatory cytokines; (iv) dysregulation of the 2’5 A RNase L antiviral pathway; (v) predominance of Th-2 cellular immunity and (vi) differential expression of gene markers whose products cause T cell activation. She noted that these findings are important and intriguing, in particular that intracellular perforin, an NK-cell lytic protein, is reduced in (ME)CFS patients. She noted that in (ME)CFS there is often reactivation of latent viruses and she also drew attention to the observation of aberrant cytotoxicity in (ME)CFS subjects who demonstrated a differential gene expression of at least 35 gene sequences compared with matched normal controls that suggest a link with organophosphate exposure. In addition, she noted that stress is known to affect both immune activity and neuroendocrine responses in (ME)CFS. 2006 In an article entitled “Exploring the Gene Scene”, Dr Jonathan Kerr from St George’s University of London said: “In 2001 I became increasingly involved in a collaborative study group concerned about the lack of research attention (ME)CFS has received, particularly in terms of how the disease is actually caused and perpetuated. We also take issue with the trivialisation of (ME)CFS and the labelling of patients as sufferers of a psychiatric or psychological disease. To address the problem, we turned to the study of gene activity……Most genes are expressed in the white blood cells and various groups have shown that the white blood cells of (ME)CFS patients exhibit reproducible www.investinme.org Page 72 of 108
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