Interferon-λ cures persistent murine norovirus infection in the absence of adaptive immunity

Author:

Nice Timothy J.1,Baldridge Megan T.1,McCune Broc T.1,Norman Jason M.1,Lazear Helen M.2,Artyomov Maxim1,Diamond Michael S.123,Virgin Herbert W.1

Affiliation:

1. Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.

2. Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA.

3. Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA.

Abstract

Turning viral persistence on and off Norovirus causes >90% of the world's gastroenteritis. Norovirus can establish persistent infections, which may contribute to its spread. How does norovirus establish itself as a permanentw resident of the gut and how can such persistent infections be cured (see the Perspective by Wilks and Golovkina)? Baldridge et al. studied mice persistently infected with norovirus and found that viral persistence required the gut microbiota: resident bacteria in the gastrointestinal tract. Antibiotics prevented persistent mouse norovirus infection in a way that depended on the secreted antiviral protein interferon λ (IFN-λ). Nice et al. report that IFN-λ can cure mice persistently infected with norovirus, independent of the adaptive immune system. Science , this issue p. 266 , p. 269 ; see also p. 233

Funder

NIH

American Cancer Society

Cancer Research Institute

W. M. Keck Fellowship

Broad Foundation

Crohn's and Colitis Foundation

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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