Editors' ChoiceHost-Microbe Interactions

Turning viral persistence on and off

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Science Signaling  20 Jan 2015:
Vol. 8, Issue 360, pp. ec17
DOI: 10.1126/scisignal.aaa6999

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 permanent 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.

M. T. Baldridge, T. J. Nice, B. T. McCune, C. C. Yokoyama, A. Kambal, M. Wheadon, M. S. Diamond, Y. Ivanova, M. Artyomov, H. W. Virgin, Commensal microbes and interferon-λ determine persistence of enteric murine norovirus infection. Science 347, 266–269 (2015). [Abstract] [Full Text]

T. J. Nice, M. T. Baldridge, B. T. McCune, J. M. Norman, H. M. Lazear, M. Artyomov, M. S. Diamond, H. W. Virgin, Interferon-λ cures persistent murine norovirus infection in the absence of adaptive immunity. Science 347, 269–273 (2015). [Abstract] [Full Text]

J. Wilks, T. Golovkina, Interfering with interferons. Science 347, 233–234 (2015). [Summary] [Full Text]

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