Impairments of the 2-5A synthetase/RNase L pathway in chronic fatigue syndrome

In Vivo. Nov-Dec 2005;19(6):1013-21.

Abstract

This paper provides an overview of the evidence addressing the impairments of the 2'-5' oligoadenylate (2-5 A) synthetase/RNase L pathway in Chronic Fatigue Syndrome (CFS) patients. The 2-5A synthetase/RNase L pathway in CFS patients appears to be both up-regulated (i.e. increased levels of bioactive 2-5A synthetase and increased activity of the RNase L enzyme) and deregulated (elastase and calpain initiate 83 kDa RNase L proteolysis, generating two major fragments with molecular masses of 37 and 30 kDa, respectively). The deregulation of the 2-5A synthetase/RNase L pathway in CFS accompanies decreased NK-function and deregulation of apoptotic pathways. Since various components of the pathway appear to be related to performance during a graded exercise stress test, some evidence supportive of the clinical importance of the impaired pathway in CFS patients has been provided. Studies addressing the treatment of the deregulation of the 2-5A synthetase/RNase L pathway in CFS are warranted.

Publication types

  • Comparative Study
  • Review

MeSH terms

  • Adenine Nucleotides / metabolism*
  • Adolescent
  • Adult
  • Apoptosis
  • Endoribonucleases / genetics
  • Endoribonucleases / metabolism*
  • Exercise Test
  • Fatigue Syndrome, Chronic / enzymology*
  • Fatigue Syndrome, Chronic / metabolism*
  • Female
  • Forecasting
  • Humans
  • Hydrolysis
  • Isoenzymes / genetics
  • Isoenzymes / metabolism
  • Killer Cells, Natural / enzymology
  • Killer Cells, Natural / metabolism
  • Male
  • Middle Aged
  • Models, Biological
  • Molecular Weight
  • Oligoribonucleotides / metabolism*
  • Up-Regulation

Substances

  • Adenine Nucleotides
  • Isoenzymes
  • Oligoribonucleotides
  • 2',5'-oligoadenylate
  • Endoribonucleases
  • 2-5A-dependent ribonuclease