Journal
SCIENCE
Volume 347, Issue 6219, Pages 269-273Publisher
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1258100
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Funding
- NIH [R01 AI084887, U19 AI109725, U19 AI083019, U19 AI106772, 5T32A100716334, 5T32CA009547, F31CA177194-01, 5T32AI007163]
- Crohn's and Colitis Foundation Genetics Initiative [274415]
- Broad Foundation [IBD-0357]
- Cancer Research Institute and American Cancer Society
- Washington University
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Norovirus gastroenteritis is a major public health burden worldwide. Although fecal shedding is important for transmission of enteric viruses, little is known about the immune factors that restrict persistent enteric infection. We report here that although the cytokines interferon-alpha (IFN-alpha) and IFN-beta prevented the systemic spread of murine norovirus (MNoV), only IFN-lambda controlled persistent enteric infection. Infection-dependent induction of IFN-lambda was governed by the MNoV capsid protein and correlated with diminished enteric persistence. Treatment of established infection with IFN-lambda cured mice in a manner requiring nonhematopoietic cell expression of the IFN-lambda receptor, Ifnlr1, and independent of adaptive immunity. These results suggest the therapeutic potential of IFN-lambda for curing virus infections in the gastrointestinal tract.
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