Case study 6

Scenario

43-year old man with RRMS previously treated with interferon-beta-1a, but had breakthrough disease activity and was found to have high titre neutralizing anti-interferon beta antibodies. Now on DMF and doing well.

Question

As neutralizing anti-interferon-beta antibodies affect antiviral responses will I be at increased risk of Covid-19 infection?

Yes and no!

COVID-19 infection risk is predominantly been driven by exposure to the virus. If you don't get exposed you don't get infected. What we don't know is how many people have asymptomatic infection with the virus. If this is large number then having anti-IFNbeta NABs may blunt antiviral responses and increase your risk of getting symptomatic infection and potentially more severe infection. However, as there is little we can do about NABs at the present time you need to be extra vigilant about hygiene etc. Whether or not you need to self-isolate to prevent being exposed is a difficult question to answer; I would say yes if the risk of COVID-19 virus exposure was only likely to be an issue for 2-3 weeks. However, as it the COVID-19 risk is likely to last months/years I don't this is feasible.

Please be careful and take care of yourself.

You may be interested in the following case study on NABs being linked to herpes virus reactivation.

Fine et al. Do Neutralising Antibodies Against Exogenous Interferon-Beta Inhibit Endogenous Signalling Pathways? Mult Scler Relat Disord, 4 (1), 88-91 Jan 2015

Introduction: Interferon-beta (IFNβ) is currently the most used disease-modifying treatment for relapsing-remitting multiple sclerosis (RRMS), but it can lead to the production of neutralising antibodies (NABs) against IFNβ.

Clinical case: A lady with a past history of genital herpes was diagnosed with RRMS, started IFNβ treatment with a good initial response. Three years later her treatment was interrupted to become pregnant. After delivery she restarted IFNβ; she had more reactivations of genital herpes and experienced intermittent sensory symptoms often coinciding with herpes reactivation. High NABs titres against IFNβ were found. Since the introduction of famciclovir as prophylactic antiviral therapy and a switch from IFNβ to glatiramer acetate, herpes reactivations ceased and she had no further MS relapses.

Conclusion: Exacerbations of genital herpes coinciding with MS relapses suggest a potential link between the development of NABs and inhibition of anti-viral action of endogenous IFNβ. This case highlights that NABs not only decreases exogenous IFNβ treatment efficacy, but may also interfere with anti-viral properties of endogenous IFNβ. Investigating patients who are treated with biological medication will allow us to better understand the biology and signalling pathways in humans.

Date & Disclaimer: 18-March-2020; please note the information and advice in this case study may change with time.