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:
Abstract/conclusion:
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:
https://academic.oup.com/cid/article/33/12/2080/366051/Antiviral-Pathway-Activation-in-Patients-with
Dr Charles Shepherd
Hon Medical Adviser, MEA