IFN-induction and RNAi by shRNAs appear to be independent functions of the same RNA (57). Our results also showed that IFN-induction by sh-B971 is independent of its ability to suppress target mRNA expression through RNAi. On the other hand, it might be possible to screen for duel functional siRNAs that confer therapeutic benefits by both RNAi and immunostimulation (58) . For example, siRNAs that target either viral genomes or cellular cofactors of the viruses can be screened for their ability to trigger IFN activation in hopes of find 'super siRNAs' with increased efficacy against IFN-sensitive viruses. The early diversification of influenza A/H1N1pdm Background Since its initial detection in April 2009, the A/H1N1pdm influenza virus has spread rapidly in humans, with over 5,700 human deaths. However, little is known about the evolutionary dynamics of H1N1pdm and its geographic and temporal diversification. Methods Phylogenetic analysis was conducted upon the concatenated coding regions of whole-genome sequences from 290 H1N1pdm isolates sampled globally between April 1 – July 9, 2009, including relatively large samples from the US states of Wisconsin and New York. Results At least 7 phylogenetically distinct viral clades have disseminated globally and co-circulated in localities that experienced multiple introductions of H1N1pdm. The epidemics in New York and Wisconsin were dominated by two different clades, both phylogenetically distinct from the viruses first identified in California and Mexico, suggesting an important role for founder effects in determining local viral population structures. Conclusions Determining the global diversity of H1N1pdm is central to understanding the evolution and spatial spread of the current pandemic, and to predict its future impact on human populations. Our results indicate that H1N1pdm has already diversified into distinct viral lineages with defined spatial patterns.  Immunoglobulin Superfamily Virus Receptors and the Evolution of Adaptive Immunity  Obligate intracellular pathogens depend on cell-surface molecules to attach and enter into host cells. Pathogen receptors may be highly specialized proteins, such as complement receptors or neurotransmitter receptors, or more ubiquitous components of cell membranes, such as integrins or sialic acid-containing oligosaccharides. The immunoglobulin superfamily (IgSF) of molecules contains several members that are expressed at the cell surface, bind diverse ligands, and contribute to a variety of cellular activities, including adhesion and immune responses. Many viruses have usurped the adhesive properties of IgSF proteins to mediate attachment (Table 1) . Strategies used by viruses to engage IgSF receptors provide clues to general mechanisms by which IgSF proteins bind different types of ligands, including antigens.