Interferon-beta anyone?


Am I wasting everyone’s time and online space writing about interferon-beta? The fact of life is that some of you still use it. In some parts of the world it may be the only disease-modifying therapy that is readily available. However, having said this, there needs to be a method to the madness of picking first line treatments for MS, and this at least for the interferon’s is relatively straight forward.

When you inject interferon’s (IFN), a cascade of physiological changes take place in your body that are measurable and predict response to treatment (the so-called interferon inducible proteins: viperin, myxovirus resistance protein(MxA), anti-IFN antibodies, cytokines to name a few). If the mojo is not happening within you, the chances are that you’re in the medium – long term going to experience treatment failure.

In this study from Poland, the researchers studied 4 interferon-inducible proteins (see Table below) in 45 RRMS participants with follow up.

Table: IFN-B inducible proteins in MS

Disappointingly as you would with a treatment that is ~30% efficacious in terms of relapse rate reduction, the proportion with no evidence of disease activity drops over the years (see Figure below). But, all is not lost as a fair number also remain free of disease progression and just below half relapse free and MRI activity free.

Figure: Proportion of RRMS with no evidence of disease activity

So, what are the factors that determine response to IFN-B?

Based on this study, those with no disease activity at follow up tended to have higher levels of USP18, viperin and MxA at baseline and at 24 months of treatment.

The question then begs why are we not using these biomarkers to predict efficacy and switching those that show negligible response?


Adv Clin Exp Med. 2020 Jun 5. doi: 10.17219/acem/121063. Online ahead of print.

A Long-Term Follow-Up Study on Biochemical and Clinical Biomarkers of Response to Interferon beta-1b Treatment in Relapsing-Remitting Multiple Sclerosis

Anna PietrzakAlicja Kalinowska-ŁyszczarzKrystyna OsztynowiczAlima KhamidullaWojciech KozubskiSławomir Michalak

Background: While interferon beta-1b (IFN-β-1b) is still a commonly used disease-modifying drug in the treatment of multiple sclerosis (MS), therapeutic possibilities are expanding, and treatment failure should be identified early. Markers to predict response to IFN-β-1b, either clinical or biochemical, are therefore urgently needed. Interferon-induced proteins, including viperin, suppressor of cytokine signaling 3 (SOCS3), ubiquitin specific peptidase-18 (USP18), and myxovirus resistance protein A (MxA), are possible markers of IFN-β-1b bioavailability and treatment response.

Objectives: To evaluate viperin, SOCS3, USP18 and MxA as markers of treatment response in Polish IFN-β-1btreated patients with MS.

Material and methods: In 45 IFN-β-1b-treated Polish patients with MS, serum concentrations of viperin, SOCS3, USP18, and MxA were assessed before and after 24 months of IFN-β-1b treatment. The patients were followed clinically and with magnetic resonance imaging (MRI) for a median of 6.8 years.

Results: Low viperin, USP18 and MxA at baseline and 24 months and high SOCS3 at 24 months correlated with higher disease activity up to the 6th year of observation, but only baseline MxA and USP18 were independently related to outcome, with higher concentrations predicting less disease activity in the first 3 years and after the 1st year, respectively.

Conclusions: We confirm the predictive value of MxA and propose USP18 as a possible new prognostic biomarker in IFN-β-1btreated MS patients.

About the author

Neuro Doc Gnanapavan


  • Very happy to see this article! I can take it along to my 2021 appt with the hopes that I can engage with my neurologist about getting on a higher efficacy MS treatment. Diagnosed 14 years ago at 46 (likely had since my 20’s) and have tried Copaxone, Betaseron and Tysabri. Back then the fallback was Avonex. So here I am and there is definitely progression in spinal cord. Brain is still the same. Dr has been dismissive of anything else. My father died 20 years ago as a result of MS so I’m particularly keen on still minimizing any damage to my body with strongest possible treatment available!

  • I was diagnosed 6 months ago with RRMS. Age 46 – I was offered beta interferon or glatiramer (I was told my symptoms so far are mild). I’ve had 17 weeks of Avonex and I now feel worse and have stopped it. I’m hoping to transition back to where I was. I was marathon training so was keen on a once a week treatment. Now I feel tired all the time, I can’t run (a luxury I know), my MS symptoms feel worse … I’m confused that I was offered them as I get the impression these drugs aren’t really used any more.

      • In my case it’s Canada! With one of the highest incidences in the world, we would hope our specialists would be more proactive at treating. I’m now being told that with age comes less inflammation so I fear my treatment options will be limited.

        • Please check out our posts on NEDA (no evidence of disease activity), neurofilaments. The management of MS is a shared process between the physician and the patient, ask the right questions armed with the knowledge.

    • Claire, I used Copaxone at first 14 years ago and loved it. I kept doing everything I was originally able to do after steroids for my « first « official relapse which presented with loss of feeling of both legs below the waist. After relapse recovery, I went back to all my regular activities, including running (not marathons), skiing , and Skating until I couldn’t do those. I’m still ambulatory, ride a bicycle but i developed hives and couldn’t stay on it. This was at a time when you had to inject 7 days a week. I think the newest treatment is only 3x week.

      • Julie – thanks for your advice. I might consider the copaxone .. I’ve stopped the avonex and am waiting/hoping to start feeling like myself again soon!



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