A Guide to RNase L
and Chronic Fatigue Syndrome (ME/CFS) by Cort Johnson
RNase L
is an enzyme found in all cells that is activated when a cell is under
attack by viruses, some bacteria and at least some toxins. Upon
activation it destroys both pathogenic and/or host mRNA thus putting the
cell into an 'antiviral state'. Recent studies have shown that RNase L also
plays a role in apoptosis (cell suicide), muscle cell differentiation, cell
migration and a host of other activities. In most CFS patients thus far
studied the RNase L enzyme is broken up into pieces. An RNase L fragment
commonly seen in CFS patients is the closest thing to a biomarker yet found
for this disease.
I
invite you to explore the fascinating and multifaceted world of RNase L
deregulation in CFS. I suggest you start by reading the chapter by
chapter synopses of a book Chronic Fatigue Syndrome A Biological Approach
published in 2002 that views CFS through the prism of RNase L
dysfunction. If your interest is piqued you can keep up to date on research
into RNase L deregulation in CFS by reading synopses of recent papers
devoted to that topic.
*Updates
- To check out a
great powerpoint presentation by Dr. De Meirleir on the multivarious world
of RNase L dysfunction in CFS at the new U.S Redlabs website,
click here. This will help you wend your
way through the complex and interesting world of RNase and CFS.
The medical advisor for the Alison
Hunter Foundation in Sydney, Australia, Dr. Michael Barratt, has done an
overview of a series of talks by Dr. De Meirleir in 2005 that
incorporate biology and treatment. Dr. De Meirleir claims to have identified
three coherent subsets of CFS patients.
Synopses of "CHRONIC FATIGUE SYNDROME A BIOLOGICAL
APPROACH"
Introduction to CFS ABA
- CFS
ABA Chapters I, II:
RNase L and the retroviral state, how RNase L is produced
and activated and how RNase L is fragmented in CFS patients.
CFS
ABA Chapters III, IV:
Further documentation of RNase L dysfunction in CFS, RNase L
fragmentation is correlated with CFS symptoms, RNase L's inhibitor is
fragmented. RNase L fragmentation in CFS may lead to a channelopathy.
CFS
ABA Chapter V:
The interferon signaling system and RNase L. A major signaling protein and a
protein involved in apoptosis (cell suicide) are fragmented in CFS. An
possible explanation for the hypothyroid clinical state in CFS.
CFS ABA Chapter VI:
A strange pattern of apoptosis (cell suicide) in CFS. Three proteins
involved in immune defense (eif-2a, p53, G-actin) are fragmented.
Activity levels of IFN regulated dsRNA activated enzyme, PKR, are
upregulated in CFS.
CFS
ABA Chapter VII:
Explaining symptom grouping
and symptoms in CFS: RNase L, infectious events and cytokine activity are
major factors in CFS. Increased free radical activity, nitric oxide; amino
acid dysregulation and protein breakdown.
CFS
ABA Chapter VIII:
Triggering CFS - pathogens take advantage of a window of opportunity
caused by poor cellular immunity. Risk factors for CFS. Poor cellular
immunity and RNase L deregulation - a recipe for disaster.
CFS ABA Chapter X:
Putting it all together. The cause of RNase L fragmentation? Viral elements
in the gene pool? RNase L fragmentation in multiple sclerosis.
RNase L, PKR and nitric oxide - a new disease scenario.
To Overviews of Papers on RNase L
Dysregulation in ME/CFS