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Study: Unique Immune Dysfunction Useful in Understanding CFS


(12-07-04 Science is a small step closer to understanding the underlying mechanisms behind CFS, according to a new study by immunologists at Temple University. Researchers there are examining the Rnase L pathway, an antiviral defense system that appears to function differently in people with CFS. According to the authors of the study in the October issue of Journal of Chronic Fatigue Syndrome, “the present study is the first to report a detailed examination of the relationship between the clinical and functional characteristics, immune abnormalities and the status of the RNase L pathway in CFS.”

A global network of researchers has studied the antiviral pathway since the discovery that Rnase L is unregulated in patients with CFS. In 1993, researchers also found that CFS patients have an atypical molecule of Rnase L. Normal Rnase L weighs 80 kDa. CFS patients have both this normal molecule and an abnormal molecule weighing 37 kDa, later dubbed “low molecular weight Rnase L”. Subsequent research has since established that higher amounts of low molecular weight Rnase L correlate to various levels of disability seen in CFS. Independent researchers have also found the molecule is useful in distinguishing CFS from depression and healthy controls.

The recent study found differences in the Rnase L pathway comparing CFS subjects, depression subjects, and healthy controls. The researchers found that depression controls “have an overall functional status much higher than CFS patients, which underscores the severity of functional impairment experienced by this cohort of CFS patients.” The CFS subjects also exhibited a host of immune abnormalities, such as low NK cell function and higher levels of circulating cytokines

The Temple team also found more subtle differences in those who had previous contact with CFS patients. According to the author, Rnase L activity was “more pronounced in the contact controls than in the non-contact controls”. Researchers feel this finding may someday help explain why CFS has occurred in clusters, spouses, and among families, although they do not feel CFS is a transmissible illness. They add, “…the results of the present study are consistent with the immune activation model of CFS, but also add the possibility of additional biochemical changes not of obvious immune or cytokine-mediated origin… these abnormalities may be indicative of a persistent viral infection or a toxic state. ”

The current CDC definition encourages many differing fatiguing illnesses to be integrated within CFS research studies. Yet, many feel the definition is too broad to obtain reliable research results and can be easily manipulated. The authors caution that they restricted their CFS samples by using a “less heterogeneous” group of patients who were “significantly impaired by their illness”. The authors promise that further study will determine the “degree to which the clinical, functional and biochemical abnormalities observed in the CFS study group can be extrapolated to the larger group of patients who meet the criteria for CFS” They say their results highlight “the need to underscore the importance of documentation of clinical and functional parameters using standardized instruments alongside biochemical and immune parameters in research studies on CFS.”