Blockade of Chronic Type I Interferon Signaling to Control Persistent LCMV Infection

Author:

Wilson Elizabeth B.1,Yamada Douglas H.1,Elsaesser Heidi1,Herskovitz Jonathan1,Deng Jane2,Cheng Genhong1,Aronow Bruce J.3,Karp Christopher L.4,Brooks David G.1

Affiliation:

1. Department of Microbiology, Immunology and Molecular Genetics and the UCLA AIDS Institute, David Geffen School of Medicine, University of California, Los Angeles (UCLA), Los Angeles, CA 90095, USA.

2. Division of Pulmonary and Critical Care Medicine, David Geffen School of Medicine, UCLA, Los Angeles, CA 90095, USA.

3. Division of Biomedical Informatics and Division of Developmental Biology, Cincinnati Children’s Hospital Research Foundation and the University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.

4. Division of Molecular Immunology, Cincinnati Children’s Hospital Research Foundation and the University of Cincinnati College of Medicine, Cincinnati, OH 45267, USA.

Abstract

INTERFER(ON)ing Persistence During persistent viral infections, a dysregulated immune response fails to control the infection. Wilson et al. (p. 202 ) and Teijaro et al. (p. 207 ; see the Perspective by Odorizzi and Wherry ) 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.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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