Interferon Beta for Multiple Sclerosis

The next issue of The Medical Letter (May 11, 2015) will include an article on a new pegylated formulation of interferon beta-1a (Plegridy) recently marketed for treatment of multiple sclerosis (MS). Interferon beta or glatiramer acetate (Copaxone) is generally used first to treat patients with relapsing-remitting MS, but both must be injected: daily with Copaxone and 1-3 times a week with interferon. So the pegylated interferon, which only needs to be injected once every 2 weeks because of its longer half-life, might find some buyers.

One of the references we cite (V Annibali et al. Cytokine Growth Factor Rev 2015; 26:221) makes an interesting case for a viral etiology of the disease and antiviral activity as interferon’s mechanism of action in treating it. The virus these investigators favor as the etiologic agent in MS is the Epstein-Barr virus (EBV), a herpesvirus that infects most adults and persists in infected B cells. Both EBV and MS are found only in humans. Increases in EBV titers have been shown to precede the first symptoms of the disease, and a history of infectious mononucleosis is strongly associated with MS.

Interferons were first tried in MS in the late 1980s because of their ability to interfere with viral replication. Interferon beta was shown to reduce the activity of the disease without causing intolerable side effects, and was first approved by the FDA in 1993. It clearly reduces the number of relapses and new brain lesions visible on MRIs, especially in the early inflammatory stages of the disease. Clinical studies with drugs that have more specific activity against herpesviruses, such as acyclovir, have not produced significant evidence of benefit, possibly because of EBV-induced interference with antiviral immune responses. Interferon beta seems to be able to restore some of these responses. Whether the longer half-life of Plegridy conveys any advantage in antiviral or immunomodulatory activity remains to be seen.

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