The phosphorylated transcription factors dimerise and bind to IRF-9 [17] . The newly formed heterotrimer, called IFNstimulated gene factor 3 (ISGF3), translocates into the nucleus and binds to IFN-stimulated response elements (ISRE), to initiate gene transcription of ISGs. Treatment of cells with type I IFN upregulates expression of an array of genes including SP110, IRF-1 and many others [18] . Among these ISGs the 29, 59oligoadenylate synthetase 1 (OAS1), the Mx proteins and the dsRNA-activated protein kinase (PKR) are described to directly interfere with viral replication [19] . Both, PKR and the OAS1/ RNaseL system are capable of inhibiting cellular and viral translation.