AHMF: 1999 DeMeirleir Presentation

RNase L Dysfunction Disorder (R.E.D.D.) in CFS

K. De Meirleir1, I. Campine*, P. De Becker, E. Van Steenberge1, C. Bisbal2, T. Salehzada2, B. Lebleu2, C.V. Herst1.

1 Dept of Human Physiology, Free University of Brussels, Brussels, Belgium
2 Inst. of Molecular Genetics, Montpellier University, Montpellier, France.
* I. Campine is supported by funds from the Foundation for Scientific Research, Belgium (F.W.0.)

The unknown aetiology and absence of biochemical markers in CFS are a major problem in this disorder. Activation of immune response and infection by several viruses have been suggested in several studies. Recent work by Suhadolnik et al. has demonstrated increased levels of 2'-5' A oligonucleotides, 2'-5' A synthetase and RNase L activity in mononuclear cell pellets from CFS patients, as well as a low molecular form of RNase L in severely disabled CFS patients. This work was designed to explore the specificity and sensitivity of the presence of the LMW RNase L in CFS.

Mononuclear cell pellets (PBMC) of 57 patients and 18 controls were studied. The technique used to detect the RNase L molecular weight is described by Charachon et al. (Biochemistry 29: 2550-2556, 1990). This technique is different from the one described by the one used by Suhadolnik et al. (Clin Inf Dis 18(Suppl 1)8 96-104, 1994). An RLI binding study was also performed.

A low molecular weight (LMW) 2'-5' A binding polypeptide in the PBMC pellets of CFS patients may objectively contribute to distinguish CFS patients fromk healthy individuals. These observations could provide the basis for the development of a biochemical assay from the differential diagnosis of CFS and for follow up of its clinical evolution.

Supported by grants from ARC and the CFIDS Association to Bernard Lebleu.