Background: Natalizumab-associated progressive multifocal leukoencephalopathy (PML) in MS occurred in two individuals also treated with interferon β1a, raising concerns about the interaction of these disease-modifying agents and leading to the recommendation to avoid their concomitant administration. However, type I interferons are antiviral.
Epub: Miller et al. Disease-modifying drugs for multiple sclerosis and JC virus expression. J Neurovirol. 2012 May 15.
Methods: Using a technique called real-time quantitative PCR for the detection and quantification of the John Cunningham virus (JCV), DNA in peripheral cells (PBMCs), and urine in MSers, we tested the hypothesis that MS disease-modifying drugs (DMD) qualitatively and quantitatively alter JCV prevalence and viral copy numbers.
Results: 239 MSers were enrolled in a cross-sectional study in which blood and urine specimens were collected at a single time and 37 newly diagnosed, treatment-naïve MSers were enrolled in a longitudinal study in which specimens were obtained at diagnosis and 6 months after treatment initiation. JCV DNA was detected in PBMCs of only two MSers (0.07 %), but was commonly detected in the urine (46.8 %) in this population. There was no effect of DMDs on blood or urinary JCV prevalence or viral copy numbers with either glatiramer acetate (Copaxone®) or interferon-β therapy (Avonex®, Betaseron®, or Rebif®). The small number of MSers on other therapies precluded meaningful comment about their effects.
Conclusions: No obvious effect of the platform DMDs on JCV prevalence rates was observed even for the interferon-βs, which are anti-viral drugs.
“Nice hypothesis, negative study. IFNbeta which is an anti-viral drug did not alter the shedding of the JC virus in the urine of MSers. PML is there for unlikely to respond to IFNbeta a treatment that has been proposed for other viral infections.”
“For those of you who are interested. Interferon beta was originally tried in MS as MS was considered to be a viral infection. Some of us, including me, still think that MS is due to a viral infection, which is why we have launched the Charcot Project. The question that occupies my thoughts most of time is: “Is the viral infection simply a trigger that sets off an autoimmune disease or is the virus actively involved in the disease process?” This distinction is very important for both prevention and treatment strategies targeting viruses. More on this over the next few years.”