Revisiting the antiviral theory to explain interferon-beta's effectiveness for relapsing multiple sclerosis

Abstract

Treatments with interferon-beta (IFN beta) - a cytokine with established antiviral effects - were initially considered for multiple sclerosis (MS), as epidemiological data pointed towards a viral etiological agent for it. Later, when no specific agent was found for MS, theories explaining IFN beta's mechanism of action (MOA) relied on anti-inflammatory mechanisms, which did not explain its ineffectiveness for disease progression independent of relapse activity (PIRA) in progressive forms of MS. Now, with new evidence backing the Epstein-Barr virus (EBV) as a conditional agent in MS etiopathogenesis as well as linking the reactivation of a wide range of other Her-pesviridae with MS onset/relapse, it may be time to revisit the antiviral theory to explain IFN beta's MOA, look at the evidence from the past two decades from that perspective, and address the paucity of knowledge with new direct studies and discussions.