Influenza A virus genome contains eight pieces of segmented negative-sense RNA which encode 11 proteins. Therefore the virus has to exploit host cell factors to promote its replication and suppress antiviral response. The function of viral proteins during influenza A virus infections is rather well characterized. However, the host response activated by viral infection is less well understood. The development of genome-wide screening techniques such as RNAi has resulted in the identification of hundreds of new host factors that are involved in influenza A virus replication in different cell lines [28] [29] [30] [31] [32] [33] . The cellular responses to influenza infection as well as other respiratory viruses have also been studied using proteomics in human cell lines with both two-dimensional gel electrophoresis (2-DE) based approach [34] [35] [36] and newer MS-based strategies [37] [38] [39] . These studies have shown that similar cellular pathways are activated in response to different viruses. However, these studies have also pointed out that the cellular responses to influenza infection are in part cell-type specific and more studies using human primary cells are needed to elucidate the host response in detail.