Figure 2: A model depicting a probable cellular response to highly pathogenic avian influenza (HPAI)-H5N1 virus infection in A549 cells which are not activated in response to RG modified H5N1 virus infection. Influenza virus infection results in activation of various signaling events in the host cells. In response to HPAI-H5N1 infection, Toll-like receptor (TLR) mediated signaling events result in activation of inflammatory cytokines like CXCL10, CCL5 through activation of specific transcription factors like NF-κB and v-JUN, as observed in our study. However, this mechanism does not get activated in response to RG modified H5N1 as evident by the downregulation of cytokine genes. The transcription factors like NF-κB and JUN were also found to be down-regulated during RG modified H5N1 infection [34].