HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via CrossRef Google Scholar Articles by Doceul, V. Articles by Seago, J. PubMed PubMed Citation Articles by Doceul, V. Articles by Seago, J. Agricola Articles by Doceul, V. Articles by Seago, J.

The N^pro product of classical swine fever virus interacts with IB, the NF-B inhibitor

Virginie Doceul^1,

Penny P. Powell^1,

¹ BBSRC Institute for Animal Health, Pirbright Laboratory, Ash Road, Pirbright, Surrey GU24 0NF, UK
² Veterinary Laboratories Agency, New Haw, Addlestone, Surrey KT15 3NB, UK

Correspondence
Julian Seago
julian.seago{at}bbsrc.ac.uk

Classical swine fever virus (CSFV) belongs to the genus Pestivirus and is the causative agent of classical swine fever, a haemorrhagic disease of pigs. The virus replicates in host cells without activating interferon (IFN) production and has been reported to be an antagonist of double-stranded RNA-induced apoptosis. The N-terminal protease (N^pro) of CSFV is responsible for this evasion of the host innate immune response. In order to identify cellular proteins that interact with the N^pro product of CSFV, a yeast two-hybrid screen of a human library was carried out, which identified IB, the inhibitor of NF-B, a transcription factor involved in the control of apoptosis, the immune response and IFN production. The N^pro–IB interaction was confirmed using yeast two-hybrid analysis and additional co-precipitation assays. It was also shown that N^pro localizes to both the cytoplasmic and nuclear compartments in stably transfected cells and in CSFV-infected cells. Following stimulation by tumour necrosis factor alpha, PK-15 cell lines expressing N^pro exhibited transient nuclear accumulation of pIB, but no effect of CSFV infection on IB localization or NF-B p65 activation was observed.

Present address: Department of Virology, Faculty of Medicine, Imperial College London, St Mary's Campus, Norfolk Place, London W2 1PG, UK.

Present address: University of East Anglia, Norwich NR4 7TJ, UK.