An IkappaB homolog encoded by African swine fever virus provides a novel mechanism for downregulation of proinflammatory cytokine responses in host macrophages
Abstract
Cytokines stimulate inflammatory defenses against viral infections. In order to evade host defenses, viruses have developed strategies to counteract antiviral cytokines. African swine fever virus (ASFV) is a large, double-stranded DNA virus that infects macrophages. This study demonstrates that ASFV effectively inhibited phorbol myristic acid-induced synthesis of antiviral, proinflammatory cytokines alpha interferon, tumor necrosis factor alpha, and interleukin-8 in infected macrophages as assessed by enzyme-linked immunosorbent assay and reverse transcriptase PCR. In contrast, levels of mRNA and protein for transforming growth factor beta, an anti-inflammatory cytokine, were increased by ASFV infection, suggesting that ASFV-induced inhibition of cytokine synthesis may be limited to cytokines activated by NFkappaB. An interleukin-8 promoter, containing an NFkappaB enhancer site, driving expression of a luciferase reporter gene was used to show that NFkappaB-dependent transcription was inhibited by the virus and by a cloned ASFV gene, A238L. This gene encodes a protein with homology to IkappaB, the inhibitor of NFkappaB. Electrophoretic mobility shift assay showed that cells expressing the A238L gene inhibited NFkappaB binding t...Continue Reading
References
Targeted disruption of the p50 subunit of NF-kappa B leads to multifocal defects in immune responses
The DNA polymerase-encoding gene of African swine fever virus: sequence and transcriptional analysis
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