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Biochem Biophys Res Commun. 2010 Aug 13;399(1):72-8. doi: 10.1016/j.bbrc.2010.07.044. Epub 2010 Jul 16.

Foot-and-mouth disease virus leader proteinase inhibits dsRNA-induced type I interferon transcription by decreasing interferon regulatory factor 3/7 in protein levels.

Author information

1
Huazhong Agricultural University, Wuhan, PR China.

Abstract

The leader proteinase (L(pro)) of foot-and-mouth disease virus (FMDV) has been identified as an interferon-beta (IFN-beta) antagonist that disrupts the integrity of transcription factor nuclear factor kappaB (NF-kappaB). In this study, we showed that the reduction of double stranded RNA (dsRNA)-induced IFN-alpha1/beta expression caused by L(pro) was also associated with a decrease of interferon regulatory factor 3/7 (IRF-3/7) in protein levels, two critical transcription factors for activation of IFN-alpha/beta. Furthermore, overexpression of L(pro) significantly reduced the transcription of multiple IRF-responsive genes including 2',5'-OAS, ISG54, IP-10, and RANTES. Screening L(pro) mutants indicated that the ability to process eIF-4G of L(pro) is not required for suppressing dsRNA-induced activation of the IFN-alpha1/beta promoter and decreasing IRF-3/7 expression. Taken together, our results demonstrate that, in addition to disrupting NF-kappaB, L(pro) also decreases IRF-3/7 expression to suppress dsRNA-induced type I IFN production, suggesting multiple strategies used by FMDV to counteract the immune response to viral infection.

PMID:
20638368
DOI:
10.1016/j.bbrc.2010.07.044
[Indexed for MEDLINE]

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