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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Eur J Immunol. 2016 Feb;46(2):300–302. doi: 10.1002/eji.201546224

Figure 1.

Figure 1

Sustained IFN-I signaling during persistent viral infection limits enforced viral replication during secondary viral infection. (A) VSV infection in naïve animals induces low levels of IFN-I, which allow for virus replication in CD169+ macrophages. This virus replication in turn promotes the generation of viral antigen, priming of antigen-specific B cells, and production of antiviral antibodies to help control infection. (B) During persistent viral infection, sustained IFN-I signaling prevents virus replication in CD169+ macrophages, preventing the generation of viral antigen and induction of antigen-specific B-cell responses and antiviral antibodies. The inhibition of antiviral B-cell responses prevents efficient control of secondary VSV infection.**