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Downregulation of RNase L inhibitor correlates with upregulation of interferon-induced proteins (2-5A synthetase & RNase L) in patients with Chronic Fatigue and Immune Dysfunction Syndrome (CFIDS)

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By Vojdani A, Choppa PC, Lapp CW • • April 11, 1998

Chronic Fatigue Immune Dysfunction Syndrome (CFIDS) is a disorder
characterized by debilitating fatigue associated with
immunological abnormalities and cognitive impairments. The
recently cloned RNase L Inhibitor (RLI) gene encodes a
specific protein which is believed to regulate 2-5A synthetase
and RNase L activity via the formation of a latent
heterodimeric protein complex. In the present study, we
investigated the levels of 2-5A synthetase, RNase L and RLI in
patients with CFIDS as compared to healthy controls.

Quantitative Competitive PCR (Q/C PCR) analysis showed a
statistically significant decrease in RLI mRNA present in the
peripheral blood lymphocytes (PBL) of patients with CFIDS (n =
25, mean = 569, S.E = 154) as compared to RLI mRNA level
present in peripheral blood lymphocytes (PBL) of healthy
controls (n = 15, mean = 2296, S.E = 506; p < 0.0001). The
decrease in RLI mRNA in CFIDS individuals correlated directly
with RLI and RLI: RNase L protein ratio while showing an
inverse relationship to the 2-5A synthetase and RNase L
activity. This RLI mRNA and protein deficiency in CFIDS
patients may explain the increase in activity of RNase L found
in CFIDS patients. The unidirectional decrease in RLI message
and protein levels in CFIDS individuals may contribute to the
destabilization of the latent RLI:RNase L heterodimeric
protein complex, resulting in the excessive activation of
RNase L shown in this study. The increased activation of RNase
L may result in an increased cellular RNA turnover and
subsequent inhibition of protein synthesis; thus resulting in
general fatigue, myalgia muscle weakness and other
symptomatologies shown in CFIDS patients. Furthermore, this
data supports the hypothesis that the antiviral 2-5
oligoadenylate synthetase (2-5OAS) overexpression in
individuals with CFIDS correlates with an increase in RNase L
activity and with a decrease in RNase L inhibitor.

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