MAGICAL MEDICINE: HOW TO MAKE AN ILLNESS ... - Invest in ME

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a genetic predisposition to an immunomodulatory response of an inflammatory nature probably secondary
to one or more environmental insults” (N Carlo‐Stella et al. Clin Exp Rhuematol 2006:24(2):179‐182).
2007
Kerr et al reported in detail the genomic and phenotypic differences in 7 genomically‐defined subtypes of
CFS: “In this study, for each CFS/ME subtype, we determined those genes whose expression differed significantly from
that of normal blood donors. Genomic analysis was then related to clinical data for each CFS/ME subtype. Genomic
analysis revealed some common (neurological, haematological, cancer) and some distinct (metabolic,
endocrine, cardiovascular, immunological, inflammatory) disease associations among the subtypes.
Subtypes 1,2 and 7 were the most severe, and subtype 3 was the mildest…It is particularly interesting that in
these genomically derived subtypes, there were distinct clinical syndromes… as would be expected in a
disease with a biological basis…It has long been recognised that subtypes of CFS/ME exist (but Professor
Anthony Pinching, Chairman of the Investment Steering Group that devised the process and criteria for
setting up the CFS Clinics and who oversaw the assessment of bids and who allocated funds ‐‐ and who is
lead advisor on “CFS/ME” to the Department of Health ‐‐ is on record in the CMO’s Working Group 2002
Report (Annex 4: section 3) as asserting that subgrouping “may be considered a matter of semantics and personal
philosophy”)…It is intriguing that within our 88 gene signature, there are several genes with links to various
aetiological triggering factors. For example, virus infection (EIF4G1, EB12) and organophosphate exposure
(NTE). EIF4G1 is an eukaryotic translation initiation factor which is bound and cleaved by a range of
viruses, including enteroviruses which both trigger and persistently infect CFS patients….We have previously
documented upregulation of NTE in (ME)CFS. NTE is the primary site of action of organophosphate (OP)
compounds….Exposure to OP compounds may trigger CFS/ME and Gulf War illness” (Jonathan Kerr et al. J
Clin Pathol 2007: doi:10.1136/jcp.2007.053553).
Commenting on this paper, Dr Neil Abbot, Director of Operations at the charity ME Research UK, said:
“These genes can be subdivided into categories by diseases and disorders or by molecular and cellular functions. The
research team says that three of the genes identified are directly linked with mitochondrial function, and a further ten
have indirect links with mitochondrial metabolism…
Important disorders and functions associated with some of the genes in the putative ME/CFS gene ‘signature’
(include):
“Diseases: Haematological (22 genes); Immunological (14 genes); Cancer (31 genes); Dermatological (3 genes);
Endocrine system (9 genes)
“Molecular and cellular function: Cellular development (26 genes): Cell death (33 genes); gene expression (31 genes);
Cellular growth and proliferation (31 genes); Cellular assembly and organisation (15 genes)
“Physiological system development and function: Haematological system (22 genes); Nervous, immune and lymphatic
system (18 genes); Tissue morphology (18 genes); Survival (17 genes); Immunity (20 genes)” (Breakthrough, Spring
2008:3).
2008
“We have reported the differential expression of 88 human genes in patients with CFS; 85 of these genes were
upregulated and 3 downregulated. Highly represented functions were haematological disease and function,
immunological disease and function, cancer, cell death, immune response and infection…Research studies
have identified various features relevant to the pathogenesis of CFS/ME such as viral infection, immune
abnormalities and immune activation, exposure to toxins, chemicals and pesticides….Various studies have