The 12th Invest in ME Research Conference June, 2017, Part 2
MEMum presents the second article in a series of three about the recent 12th Invest In ME International Conference (IIMEC12) in London.
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RNAaseL test--any labs doing this?

Discussion in 'Diagnostic Guidelines and Laboratory Testing' started by fireflymd, Sep 1, 2017.

  1. fireflymd

    fireflymd Senior Member

    Are there any labs doing this test? Can't seem to find any by searching online.
  2. Hip

    Hip Senior Member

    Do you mean a test for ribonuclease L fragmentation?

    Ribonuclease L which is part of the intracellular immune response, is known to be fragmented in some ME/CFS patients (and in multiple sclerosis too). But is there any benefit in getting tested (assuming there is a commercial test available)? Or is just to help confirm an ME/CFS diagnosis?
  3. notmyself

    notmyself Senior Member

    hey..a stupid question this the same as RNA polimerase III?
  4. Daffodil

    Daffodil Senior Member

    Hi. They stopped doing this test quite a while ago. I think they found it was not useful for diagnosing anything
  5. charles shepherd

    charles shepherd Senior Member

    This test is not available in the UK and the study carried out by John Gow et al concluded that there was no point in testing for antiviral pathway activation in ME/CFS:


    In studies published elsewhere, the 3 research groups that have examined these pathways in CFS only compared patients with healthy control subjects or with patients who had nonspecific syndromes (fibromyalgia and multiple chemical sensitivity syndrome), but not with patients who had infections. Because these pathways are known to be activated during routine infection, patients with known infection are a very important control group. It was reported that 2,5A levels and RNase L activity were significantly elevated in patients with CFS, and both levels returned to normal after treatment with poly(I)-poly(C12U) [4]. Gene expression for 2,5A synthetase, RNase L, and RL1 were investigated, and a significant decrease in RL1 mRNA was found [5]. This work culminated in the report that a breakdown product, a 37-kDa 2,5A binding polypeptide, was present in a significant proportion of patients with CFS (88% vs. 28% in healthy control subjects), with the proposal that this formed the basis of a diagnostic test [6].

    We conclude from our results, however, that patients with CFS showed no significant activation of either pathway. These cascades can remain up-regulated to a degree for months after normal endemic infection, and residual nonspecific increases may account for the results reported elsewhere. Therefore, assay of antiviral pathway activation is unlikely to form a rational basis for a diagnostic test for CFS.

    Full paper:

    Dr Charles Shepherd
    Hon Medical Adviser, MEA

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