Blockade of interferon beta, but not interferon alpha, signaling controls persistent viral infection

Cherie T. Ng, Brian M. Sullivan, John R. Teijaro, Andrew M. Lee, Megan Welch, Stephanie Rice, Kathleen C.F. Sheehan, Robert D. Schreiber, Michael B.A. Oldstone

Research output: Contribution to journalArticlepeer-review

130 Scopus citations


Although type I interferon (IFN-I) is thought to be beneficial against microbial infections, persistent viral infections are characterized by high interferon signatures suggesting that IFN-I signaling may promote disease pathogenesis. During persistent lymphocytic choriomeningitis virus (LCMV) infection, IFNα and IFNβ are highly induced early after infection, and blocking IFN-I receptor (IFNAR) signaling promotes virus clearance. We assessed the specific roles of IFNβ versus IFNα in controlling LCMV infection. While blockade of IFNβ alone does not alter early viral dissemination, it is important in determining lymphoid structure, lymphocyte migration, and anti-viral T cell responses that lead to accelerated virus clearance, approximating what occurs during attenuation of IFNAR signaling. Comparatively, blockade of IFNα was not associated with improved viral control, but with early dissemination of virus. Thus, despite their use of the same receptor, IFNβ and IFNα have unique and distinguishable biologic functions, with IFNβ being mainly responsible for promoting viral persistence.

Original languageEnglish
Pages (from-to)653-661
Number of pages9
JournalCell Host and Microbe
Issue number5
StatePublished - May 13 2015


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