ABSTRACT
Earlier chapters in this book have described in detail the structure and biochemical mechanisms leading to the activation and actions of the 2,5A-synthetase RNase-L system. This chapter will concentrate on the results or effects of activation or deregulation of this system within the chronic fatigue syndrome (CFS) patient and also try to assess some of the co-morbidity factors involved in the disease complexity. The major actions of the 2,5A-synthetase/RNase-L system are for antiviral defense
and controlled cellular degeneration or apoptosis. Deregulation of these actions via the removal or reduction of messenger RNA and the inhibition of protein synthesis, along with effects of the RNase-L fragments and other enzyme or receptor systems initiated by the deregulators of the RNase-L system, will have very large influences upon host homeostatic mechanisms and hence symptom expression. The reduced ability to produce proteins such as receptors, membrane pumps, and many other intracellular proteins and enzymes will alter control of cellular homeostasis. These biochemical changes are also influenced by the biochemical deregulating effects of the sporadic reactivation of persistent viruses or influences of bacterial pathogens. These alterations will significantly influence brain, immune, and other functions and hence symptom expression.
