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Interferon-induced proteins are elevated in blood samples of patients with chemically or virally induced Chronic Fatigue Syndrome (CFS)

  [ 28 votes ]   [ Discuss This Article ] • May 4, 1999

Overlapping symptomatologies between Chronic Fatigue Syndrome
(CFS) and Chemical Sensitivity have been observed by different
investigators. Therefore, it is of great importance to develop
biomarker(s) for possible differentiation between viral
induced CFS (without sensitivity to chemicals) versus
chemically induced CFS. Since interferon induced proteins 2-5A
Synthetase and Protein Kinase RNA (PKR) have been implicated
in the viral induction of CFS, the objective of this study was
to utilize 2-5A and PKR activity for differentiation between
CFS induced by either viruses or chemicals.

Based on the CDC definition and criteria, twenty CFS patients who were positive for viral genome(s) (mainly HHV6; HTLVII, EBV, and CMV) and
did not have any history of exposure to toxic chemicals were
included in this study. As a comparison, the second group of
patients consisted of twenty individuals from the same
geographical area who were negative for viral genomes but had
been exposed to methyl tertiary-butyl ether concentration of
up to 70 ppb and benzene concentration up to 14 ppb. All
patients complained of fatigue and other symptoms overlapping
between the two groups. From all 40 patients, blood was drawn,
leukocyte extract was prepared and assayed for 2-5A Synthetase
and PKR activity. Clinical specimens which were positive for
viral genomes showed from 2.2-38.7 fold increase in 2-5A
activity and 1.3-13.5 fold increase in PKR activities over the
background of the healthy controls. Similarly, the second
group (negative for viral genomes, but exposed to chemicals)
showed a 1.1-29.2 fold increase for 2-5A Synthetase and a
1.3-11.6 fold increase for PKR when they were compared to
healthy subjects.

To elucidate mechanisms involved in viral
versus chemical induction of 2-5A Synthetase and PKR, MDBK
cell lines were cultured either in the presence or absence of
HHV6, MTBE, or Benzene, heat shock proteins and
interferon-beta. 2-5A and PKR activities were measured in all
the above conditions. A clear induction of 2-5A and PKR was
observed when MDBK cells were exposed to HHV6, MTBE, and
Benzene. This induction was more significant with HSP90,
HSP70, and IFN-beta indicating their involvement in the
mechanism of action. However, when MDBK cells were incubated
either with MTBE + Benzene or HHV6 in the presence or absence
of anti IFN-beta or anti-HSP-70, the activities of both 2-5A
and PKR in HHV6 infected cells were inhibited by more than 90%
due to addition of anti IFN-beta, and only 20% by addition of
anti-HSP70. While in MTBE + Benzene exposed cells anti
IFN-beta reduced the activity of these enzymes by 40% and
anti-HSP70 by more than 90%. This variation in the induction
of 2-5A and PKR by anti-HSP70 or IFN-beta indicates
involvement of IFN-beta in viral induction 2-5A and PKR, and
HSP involvement in chemical induction of these enzymes.

We conclude that 2-5A and PKR are not only biomarkers for viral
induction of CFS, but biomarkers to other stressors that
include MTBE and Benzene.

Vojdani A, Lapp CW

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