We examined the kinetics of ISG56 and MxA activation by live SNV and compared this to viral replication kinetics in Huh7 cells. SNV induced a strong ISG response upon initial infection, however, this response was transient and almost completely abated by one day post infection, despite the continuous accumulation of viral Ssegment vRNA in Huh7 cells. We verified that Huh7 cells were productively infected, since we were also able to use their supernatants to infect fresh Vero E6 cells and focus assays performed on Vero E6 cells showed titers of up to 104 ffu/mL. These results indicate that either the products of viral replication are not required for ISG stimulation, or that the virus can efficiently antagonize innate immune responses following replication, thus inhibiting ISG activation. We then asked whether the ISG-activating potential in Huh7 is a function of viral titer upon initial infection. For this, we generated a time-course series of SNV stocks in Vero E6 cells and assayed both their viral titer on fresh Vero E6 cells and their ISG-inducing potential on Huh7 cells. We observed that ISG induction is dissociable from the viral titer, with the highest ISG-inducing activity exhibited by the 20 dpi virus stocks, which had the lowest viral titers. To test whether a soluble mediator of innate immunity is responsible for the observed ISG transcription, we examined whether the ISGactivating fraction is physically dissociable from intact viral particles by filtration. We applied SNV stocks to a 100-kDa cutoff Amicon centrifugation filters and collected the filtrate and retentate, both of which we resuspended to the starting volume by the addition of cell culture medium. We were unable to LEE011 CDK inhibitor detect replication-competent virus in the filtrate by titration. When these components were applied to Huh7 cells, we observed that the ISG activating fraction was contained within the filtrate, indicating that a soluble component derived from the Vero E6 cell stocks, or viral components of less than 100-kDa relative mass are responsible for ISG inductions. Initially, the microbes may live by mutual co-operation, but, at a stage when local concentrations are high or resources are limited, competitive interactions do occur. For example, quorum sensing molecules that coordinate and reinforce community behaviour in many bacterial species are released and are recognized by bacteria and used for competitive survival. Another competitive strategy possibly employed by bacteria is recognition by physical contact. Physical contact allows bacteria to recognize a competitor, the immediate benefit being ability to rapidly mobilise mechanisms to utilise available resources, thereby outcompeting the competitor. Although the former phenomenon is very well characterized, the latter method of sensing competition is hardly discussed and needs to be investigated in detail.