The nature of innate immune response dictates the type and duration of adaptive immune response [67, 75] . The mechanism by which NiV VLPs are recognized by host cells and trigger the induction of innate immune response, and how this translates into effective adaptive immunity is not known. Here we have taken the first step ( Figure 6 ) towards understanding this process. With the experimental conditions as described, we observed VLP-induced activation of some of the genes that are known to be involved in the induction of an effective innate immune response [75] . Results presented in the heat map in Figure 6 show that relative to the ''mock'' treated cells, NFKB2 gene (in the NFKB pathway) was up-regulated 89 fold as a result of VLP exposure, and TBK1 (in the IRF pathway) was 7 fold higher. In the light of these findings, we are testing PCR array expression profiles of the same set of 84 genes in 293 and other cells at earlier and later time points to identify their upstream effectors, and NiV VLP-responsive signaling networks. In this respect, the murine system, with the many available immunological reagents and knockout strains may provide the best system to identify these host sensors. Currently there is minimal information on live NiV infection-responsive cellsignaling changes [76] and there is none on array-based transcriptional alterations for comparative analysis. Likewise, it has not been possible to compare the NiV VLP-induced transcription modulation with those induced by other paramyxovirus VLPs since to our knowledge, such studies have not been undertaken so far. Lastly, a growing number of reports point to viral surface glycolproteins as relevant in host cell signaling and triggering of innate immune response. We believe that particles like NiV VLPs, with many virus-like properties (including their surface glycoproteins organized to resemble the parental virus, Figure 2D ) would induce an effective innate immune response for the promotion of the desired adaptive immunity [67, 76] .