While this manuscript was in preparation it was demonstrated by Pothlichet et al. that influenza A virus-induced SOCS-1 and SOCS-3 upregulation requires a TLR-3-independent, RIG-I/ MAVS-dependent pathway [65] . Moreover, over-expression of SOCS-1 and SOCS-3 in infected cells revealed that both molecules inhibit antiviral responses. These studies are perfectly complemented by our findings. Here we confirm involvement of RIG-I/MAVS by showing that 59 triphosphate RNA, the ligand for RIG-I, is a major inducer of SOCS-3. Furthermore, the finding that dsRNA is only a weak inducer of SOCS-3 is also consistent with the independence from the dsRNA sensor TLR-3. The only discrepancy of this work and the study of Pothlichet et al. is that they show a dependence on the type I IFN receptor. This may be due to the different virus-strains and cell types used. It is well known that the capability of type I IFNs to induce SOCS proteins is strongly cell type specific [31] . While in some cell types SOCS-3 expression appears to be type I IFN dependent (e.g. fetal liver cells) [31] it is clearly independent of IFN in other cell types [66] . Recently it was shown that SOCS-3 is not significantly induced by IFNa in A549 cells [18] , the major cell type used in our study. Evidence that cell type specificities may be the cause of discrepancy is additionally provided by the fact that Pothlichet et al. show identical induction kinetics of SOCS-1 and SOCS-3. In contrast the kinetics of the two proteins differ clearly in the cells we used, with SOCS-3 being induced much earlier than SOCS-1 on mRNA and protein level.