At present, two main mechanisms of type I IFN induction by viruses resulting from the extracytoplasmic or cytoplasmic virus recognition, respectively, are known [12, 13, 14, 15] . The extracytoplasmic induction is initiated by triggering the surfaceexpressed transmembrane protein toll-like receptor (TLR) 4 with certain non-nucleic viral constituents [16, 17, 18] or upon recognition of viral nucleic acids in the endosomes of specialized cells (dendritic cells and macrophages) via different members of the TLR family. These include TLR3, TLR7/TLR8 and TLR9, sensing dsRNA, ssRNA and CpG DNA, respectively. For IFN-ab induction TLR3 and TLR4 signal through the adaptor molecule TIR domain-containing adaptor protein inducing interferon b (TRIF). This results in the activation of interferon regulatory factor (IRF)-3. TLR7, 8 and 9 signal through the adaptor molecule Myeloid differentiation factor 88 (MyD88). An important result of the MyD88-mediated pathway is the activation of IRF-7 (but not of IRF-3), which together with the transcription factors NF-kB and AP-1 initiates the induction of both the IFN-a and IFN-b genes [13, 15] . This induction pathway is responsible for the strong, early IFN-ab response to several replicating and inactivated viruses in pDCs, which express preferentially TLR7 and TLR9 [19, 20, 21] .