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

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.

Automated summary

Treatment with interferon-beta (IFN beta) was initially considered for multiple sclerosis (MS) due to epidemiological data suggesting a viral etiology. However, the mechanism of action of IFN beta, which relies on anti-inflammatory mechanisms, does not explain its ineffectiveness for disease progression in progressive forms of MS. New evidence linking the Epstein-Barr virus (EBV) and other herpesviruses to MS onset/relapse may call for a reconsideration of the antiviral theory behind IFN beta's mechanism of action.