Viral infection of fibroblastic and endothelial cells leads to the transient synthesis of interferon-b(IFN-b). The down-regulation of IFN-bsynthesis after infection results both from transcriptional repression of the IFN-bgene and rapid degradation of mRNA. As with many cytokine mRNAs, IFN-bmRNA contains an AU-rich element (ARE) in its 3¢-untranslated region (UTR). AREs are known tomediate mRNAdeadenylation and destabilization. Depending on the class of ARE, deadenylation was shown to occur through synchronous or asynchronous mechanisms
