The first line of defence against virus infections is innate immunity. The key players are interferons (IFNs) and other cytokines that are rapidly produced in virus infected cells (Reviewed in [13] ). Three major classes of IFNs are known. Type I IFNs comprise the largest group, with multiple distinct IFNa genes, one to three IFNb genes and other genes (IFNv, -e, -d, -k). The first two are induced directly in response to viral infection whereas the others play less defined roles. Type II IFN has a single member, namely IFNc, which is secreted by activated T cells and natural killer cells rather than in direct response to virus infections. A third class of IFNs has been described recently that shares the same pathway to sense viral infection as type I IFNs and is also induced directly in response to viral infection [14, 15, 16] . After an infected cell senses a viral infection, IFNs are produced and released from the cell to induce an antiviral state in both itself and neighbouring cells. Both type I and type II IFNs bind to their cognate cell-surface receptors, thereby activating a signal-transduction pathway that triggers the transcription of several hundreds of genes [17] . These IFN-stimulated genes (ISGs) have either IFNstimulated response elements (ISRE) or GAS (Gamma-activated sequence) elements in their promoter region. Type I IFNs such as IFNa can lead to transcription of ISGs with ISRE or GAS elements, whereas IFNc can only induce ISGs with GAS elements (reviewed in [18] ).