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Journal of Virology, April 2002, p. 3936-3942, Vol. 76, No. 8
0022-538X/02/$04.00+0 DOI: 10.1128/JVI.76.8.3936-3942.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Centro de Biología Molecular "Severo Ochoa," Universidad Autónoma, Cantoblanco, 28049 Madrid, Spain
Received 23 October 2001/ Accepted 10 January 2002
African swine fever virus (ASFV) encodes a homologue of the inhibitor of apoptosis (IAP) that promotes cell survival by controlling the activity of caspase-3. Here we show that ASFV IAP is also able to activate the transcription factor NF-
B. Thus, transient transfection of the viral IAP increases the activity of an NF-
B reporter gene in a dose-responsive manner in Jurkat cells. Similarly, stably transfected cells expressing ASFV IAP have elevated basal levels of c-rel, an NF-
B-dependent gene. NF-
B complexes in the nucleus were increased in A224L-expressing cells compared with control cells upon stimulation with phorbol myristate acetate (PMA) plus ionomycin. This resulted in greater NF-
B-dependent promoter activity in ASFV IAP-expressing than in control cells, both in basal conditions and after PMA plus ionophore stimulation. The elevated NF-
B activity seems to be the consequence of higher I
B kinase (IKK) basal activity in these cells. The NF-
B-inducing activity of ASFV IAP was abrogated by an IKK-2 dominant negative mutant and enhanced by expression of tumor necrosis factor receptor-associated factor 2.
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