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

Blockade of interferon Beta, but not interferon alpha, signaling controls persistent viral infection.
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DOI:
10.1016/j.chom.2015.04.005
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发表时间:
2015-05-13
影响因子:
30.3
通讯作者:
Oldstone MB
Oldstone MB
中科院分区:
医学1区
文献类型:
--
作者:
Ng CT;Sullivan BM;Teijaro JR;Lee AM;Welch M;Rice S;Sheehan KC;Schreiber RD;Oldstone MB

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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.
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