Myalgic Encephalomyelitis [ME] is recognized by the WHO as a Neurological disease. Unfortunately, this recognition continues to be thwarted by influential Psychiatric “road blocks” against pure unbiased ME research. This deleterious situation against progress has been augmented by [a] the lack of viral surveillance [“Oh! it’s just another virus” – “Yes, but which one”?] and [b] the opening of Psychiatric led CFS clinics. No one benefits, least of all the patients.


Annotated in the post WW11 medical literature is the term Benign Myalgic Encephalomyelitis [ME]; due to Enteroviral infection. Far from benign, far from current thought.

Enteroviruses Most infections are subclinical or minor - only a few progress to serious illness. Nevertheless they are the major cause of Aseptic Meningitis, Encephalitis, Myelitis, Myositis, Myocarditis, Pancreatitis and Thyroiditis. To the astute clinical mind these are the components of ME syndrome. It is also no surprise that ME pregnancies produce foetal abnormalities of brain and heart. Furthermore, what genetic and environmental factors are involved in host susceptibility to such serious illnesses?


Why does the host’s Immune system fail to clear Enteroviruses from infected cells? Why are infected cells not lysed or ordered to commit apoptosis [suicide]. In a serious multi-organ illness such as ME one answer springs immediately to mind. We the viral host wish to live albeit at a cost. So what are the self-preservation influences? What are the inhibitory factors influencing the activity of NKcells and Cytotoxic Tcells. Is it as simple as T cell exhaustion? How do Enteroviruses, in part, hoodwink our defences and co-exist with our cellular proteins. They do, but at the cost of a sick cell → sick organ → a sick host.

Alas more questions than answers.

That is why this disease should be clearly defined and separated from the comedy sink of CFS


Viral/host co-existence is of benefit only if the host can enjoy a near normal quality of life e.g. Herpes viruses – Epstein-Barr. Varicella-Zoster. However these latent infections are totally different to persistently replicating Enteroviral infections where there is a poor quality of life. All the more reason why this illness should be clearly defined treated and eventually prevented.

Research should involve:- [a] Correctly selected patients. The only validated selection ME score chart is that of the late Dr John Richardson [JRRG score chart]. Validated by * + VP1 antigen test in blood, * +Buspirone challenge test indicating hypothalamic dysfunction [Demitrack 1991.Bakheit 1992. J Richardson. Journal of Chronic Fatigue]. * SPET brain perfusion scans [Duval DeCosta. JRichardson] [b] Thorough clinical examination by a competent physician utilising above investigations. [c] Once co-existence has been established and IgM antibodies disappear it is virtually impossible to identify the virus, its genome or it’s footprint in ME infected tissues. However, advances in immunobiology may hold the key to confirm causality and treatment. Recent advances in T memory cell morphology is promising -TCM expansion in inguinal lymph nodes, in association with cytokine and chemokine levels, upon cognate viral challenge could lead to a viable diagnostic test. Treatment:

The John Richardson Research Group’s clinic continues to combine carefully paced activity and immune modulation [i.m. IgG. see below] which in time reduces patient’s JRRG score. Antiviral agents to date have been ineffective. However, once the viral “switch” which allows hijacking of cellular protein production is discovered then a cure will be possible. Prevention: * Vaccination. Considering the mortality and morbidity caused throughout life by Enteroviruses, vaccination is easily justified; more so than MMR. There will be a significant reduction in death from Myocarditis, DCM and Meningo –encephalomyelitis. There will be a significant reduction in Thyroid failure[PTF] and Type1 Diabetes. Finally, ME will be an illness of the past.


IgG may work via a multi-step model where the injected IgG first forms a type of immune complex in the patient. Once these immune complexes are formed, they interact with activating Fc receptors on dendritic cells which then mediate anti-inflammatory effects helping to reduce the severity of the inflammatory state and potential for autoimmune disease [PTF and Diabetes]

IgG also blocks the antibody receptors on immune cells (macrophages), leading to decreased damage by these cells, or regulation of macrophage phagocytosis.

IgG may also regulate the immune response by reacting with a number of membrane receptors on T cells, B cells, and monocytes that are pertinent to autoreactivity and induction of tolerance to self.

A recent report stated that IgG application to activated T cells leads to their decreased ability to engage microglia. As a result of IgG treatment of T cells, the findings showed reduced levels of tumour necrosis factor-alpha and interleukin-10 in T cell-microglia co-culture. The results add to the understanding of how IgG may affect inflammation of the central nervous system in autoimmune inflammatory diseases.

In conclusion

Sadly, in place of clarity, we continue to muddy the upstream waters of causality. All we achieve is condemnation of future generations to the continuing misery of ME through lack of appropriate prevention and treatment.