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.
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
* + 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.
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.
* 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.
THE BENEFITS of IMMUNOGLOBULIN
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
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.