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The N^pro product of classical swine fever virus and bovine viral diarrhea virus uses a conserved mechanism to target interferon regulatory factor-3

John McCauley^3,

¹ Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Surrey GU24 0NF, UK
² Division of Basic Medical Sciences, St George's, University of London, London SW17 0RE, UK
³ Institute for Animal Health, Compton Laboratory, Compton, Newbury, Berkshire RG20 7NN, UK

Correspondence
Stephen Goodbourn
s.goodbourn{at}sgul.ac.uk

Classical swine fever virus (CSFV) is a member of the genus Pestivirus in the family Flaviviridae. The N^pro product of CSFV targets the host's innate immune response and can prevent the production of type I interferon (IFN). The mechanism by which CSFV orchestrates this inhibition was investigated and it is shown that, like the related pestivirus bovine viral diarrhea virus (BVDV), this involves the N^pro protein targeting interferon regulatory factor-3 (IRF-3) for degradation by proteasomes and thus preventing IRF-3 from activating transcription from the IFN- promoter. Like BVDV, the steady-state levels of IRF-3 mRNA are not reduced markedly by CSFV infection or N^pro overexpression. Moreover, IFN- stimulation of CSFV-infected cells induces the antiviral protein MxA, indicating that, as in BVDV-infected cells, the JAK/STAT pathway is not targeted for inhibition.

Present address: Division of Virology, National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.

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