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Journal of Virology, September 2002, p. 8979-8988, Vol. 76, No. 18
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.18.8979-8988.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Inhibition of Beta Interferon Transcription by Noncytopathogenic Bovine Viral Diarrhea Virus Is through an Interferon Regulatory Factor 3-Dependent Mechanism

Susan J. Baigent,1 Gang Zhang,1 Martin D. Fray,1,{dagger} Helen Flick-Smith,1,{ddagger} Stephen Goodbourn,2 and John W. McCauley1*

Institute for Animal Health, Compton Laboratory, Compton, Newbury, Berkshire RG20 7NN,1 Department of Biochemistry and Immunology, St. George's Hospital Medical School, University of London, London SW17 0RE, United Kingdom2

Received 11 March 2002/ Accepted 12 June 2002

The induction and inhibition of the interferon (IFN) response and apoptosis by bovine viral diarrhea virus (BVDV) has been examined. Here we show that prior infection of cells by noncytopathogenic BVDV (ncp BVDV) fails to block transcriptional responses to alpha/beta IFN. In contrast, ncp BVDV-infected cells fail to produce IFN-{alpha}/ß or MxA in response to double-stranded RNA (dsRNA) or infection with a heterologous virus (Semliki Forest virus [SFV]). ncp BVDV preinfection is unable to block cp BVDV- or SFV-induced apoptosis. The effects of ncp BVDV infection on the transcription factors controlling the IFN-ß induction pathway have been analyzed. The transcription factor NF-{kappa}B was not activated following ncp BVDV infection, but ncp BVDV infection was not able to block the activation of NF-{kappa}B by either SFV or tumor necrosis factor alpha. Furthermore, ncp BVDV infection did not result in the activation of stress kinases (JNK1 and JNK2) or the phosphorylation of transcription factors ATF-2 and c-Jun; again, ncp BVDV infection was not able to block their activation by SFV. Interferon regulatory factor 3 (IRF-3) was shown to be translocated to the nuclei of infected cells in response to ncp BVDV, although DNA-binding of IRF-3 was not seen in nuclear extracts. In contrast, an IRF-3-DNA complex was observed in nuclear extracts from cells infected with SFV, but the appearance of this complex was blocked when cells were previously exposed to ncp BVDV. We conclude that the inhibition of IFN induction by this pestivirus involves a block to IRF-3 function, and we speculate that this may be a key characteristic for the survival of pestiviruses in nature.

* Corresponding author. Mailing address: Institute for Animal Health, Compton Laboratory, Compton, Newbury, Berkshire RG20 7NN, United Kingdom. Phone: 44 1635 577269. Fax: 44 1635 577263. E-mail: john.mccauley{at}bbsrc.ac.uk.

{dagger} Present address: MDF, Medical Research Council, Harwell, Didcot, Oxfordshire OX11 0RD, United Kingdom.

{ddagger} Present address: HF-S, DSTL, Porton Down, Salisbury, Wiltshire SP4 0JQ, United Kingdom.

Journal of Virology, September 2002, p. 8979-8988, Vol. 76, No. 18
0022-538X/02/$04.00+0     DOI: 10.1128/JVI.76.18.8979-8988.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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