RNase L, Chronic Fatigue Syndrome (ME/CFS) and Mycoplasma

Nijs, J., Nicolson, G. L., De Becker, P., Coomans, D. and K. De MeirLeir. 2002 High Prevalence of Myplasma infections among European chronic fatigue syndrome patients. Examination of four Mycoplasma species in blood of chronic fatigue syndrome patients. FEMS Immunology and Medical Microbiology 34 209-14

Mycoplasma are very primitive bacteria that contain circular (not helical) DNA and some ribosomes (protein producing factories) but lack a cell wall and other organelles. They are usually restricted to the mucousal tissues in the mouth, genitals and digestive tract but are able, if the endothelium is damaged, to invade the body and cause systemic damage.

The immune activation seen in CFS has spurred research which indicated people with CFS have much higher rates of mycoplasma infections than controls. Because mycoplasma infections have been shown to activate T and B cells and thus probably macrophages as well, the authors speculated that increased macrophage activation in CFS patients would result in increased elastase production and therefore increased RNase L fragmentation.

Elastase is one of the two enzymes believed to fragment RNase L in CFS. The question asked in this study was whether mycoplasma infected CFS patients displayed more RNase L fragmentation than non-mycoplasma infected CFS patients.

This study found CFS patients infected with mycoplasmas had significantly higher (p<.016) rates of RNase L fragmentation that uninfected CFS patients. The authors suggested RNase L fragmentation in CFS results in a highly impaired innate cellular defense system that leaves them CFS vulnerable to pathogens such as mycoplasmas.

They note CFS patients initially appear to exhibit high rates of apoptotic activity but if the disease progresses they end up exhibiting low rates of apoptotic activity. They speculate CFS patients with the highest rates of RNase L fragmentation are unable to muster a sufficient apoptotic response towards pathogens and thus exhibit increased rates of intracellular infections. (Apoptosis occurs when the cell, because of a pathogen, or toxin, etc. triggers a suicide program. Cell suicide is an important means of killing intracellular pathogens.)

They suggest that a similar pattern will be displayed in CFS patients with other pathogens such cytomegalovirus, Chlamydia or adenovirus. (As an aside this paper also buttressed the theory of increased RNase L fragmentation in CFS patients. Approximately 80% of CFS patients had over twice as much fragmented as whole RNase L.)

This page last modified on July 10, 2004

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