Blockade of Chronic Type I Interferon Signaling to Control Persistent LCMV Infection
Elizabeth B. Wilson, Douglas H. Yamada, Heidi Elsaesser, Jonathan Herskovitz, Jane Deng, Genhong Cheng, Bruce J. Aronow, Christopher L. Karp, David G. Brooks
Science·2013·642 citations
<jats:title>INTERFER(ON)ing Persistence</jats:title>
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During persistent viral infections, a dysregulated immune response fails to control the infection.
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Wilson
<jats:italic>et al.</jats:italic>
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(p.
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) and
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Teijaro
<jats:italic>et al.</jats:italic>
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(p.
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; see the Perspective by
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<jats:related-article xmlns:xlink="http://www.w3.org/1999/xlink" ext-link-type="doi" issue="6129" page="155" related-article-type="in-this-issue" vol="340" xlink:href="10.1126/science.1237568">Odorizzi and Wherry</jats:related-article>
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) show this occurs because type I interferons (IFN I), critical for early responses to viral infection, contribute to the altered immunity seen during persistent infection. Antibody blockade of IFN I signaling during chronic lymphocytic choriomeningitis virus (LCMV) in mice resulted in reduced viral titers at later stages of infection, reduced expression of inhibitory immune molecules and prevented the disruptions to secondary lymphoid organs typically observed during persistent infection with LCMV. Whether type I IFNs are also detrimental to persistent viral infection humans, such as HIV and hepatitis C virus, remains to be determined.
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