A Guide to RNase L and Chronic Fatigue Syndrome (ME/CFS)

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.

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”


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.

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.

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.

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.

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.

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.

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.

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