Induction of the interferon (IFN)-alpha/beta gene transcription in virus-infected cells is an event central to innate immunity. Mice lacking the transcription factor IRF-3 are more vulnerable to virus infection. In embryonic fibroblasts, virus-induced IFN-alpha/beta gene expression levels are reduced and the spectrum of the IFN-alpha mRNA subspecies altered. Furthermore, cells additionally defective in IRF-7 expression totally fail to induce these genes in response to infections by any of the virus types tested. In these cells, a normal profile of IFN-alpha/beta mRNA induction can be achieved by coexpressing both IRF-3 and IRF-7. These results demonstrate the essential and distinct roles of thetwo factors, which together ensure the transcriptional efficiency and diversity of IFN-alpha/beta genes for the antiviral response.

The interferon regulatory factor (IRF) family of transcription factors regulate the interferon (IFN) system, among which IRF-3 is involved in the virus-induced IFN-L L gene expression. Here we show that another member IRF-7 is critical for the IFN-K K gene induction. Unlike the IRF-3 gene, the IRF-7 gene is induced by IFNs through activation of the ISGF3 transcription factor, and IRF-7 undergoes virus-induced nuclear translocation. In cells lacking p48, an essential component of IFN stimulated gene factor 3 (ISGF3), ectopic expression of IRF-7 but not IRF-3 can rescue the deficiency to induce IFN-K K genes. These results indicate that IRF-7 is a key factor in the positive feedback regulation of IFN-K K/L L production.z 1998 Federation of European Biochemical Societies.

The IFN-L L promoter is controlled primarily by the virus-inducible enhancer elements, the IRF-Es. Here we show that IRF-3, an IRF family transcription factor, translocates to the nucleus from the cytoplasm upon virus infection in NIH/3T3 cells. The nuclear IRF-3 is phosphorylated, interacts with the co-activators CBP/ p300, and binds specifically to the IFN-L L IRF-E. Furthermore, overexpression of IRF-3 causes a marked increase in virusinduced IFN-L L mRNA expression. Thus, IRF-3 is a candidate transcription factor mediating the activation of the IFN-L L gene.z 1998 Federation of European Biochemical Societies.

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The brain–machine interface (BMI) or brain–computer interface is a new interface technology that uses neurophysiological signals from the brain to control external machines or computers. This technology is expected to support daily activities, especially for persons with disabilities. To expand the range of activities enabled by this type of interface, here, we added augmented reality (AR) to a P300-based BMI. In this new system, we used a see-through head-mount display (HMD) to create control panels with flicker visual stimuli to support the user in areas close to controllable devices. When the attached camera detects an AR marker, the position and orientation of the marker are calculated, and the control panel for the pre-assigned appliance is created by the AR system and superimposed on the HMD. The participants were required to control system-compatible devices, and they successfully operated them without significant training. Online performance with the HMD was not different from that using an LCD monitor. Posterior and lateral (right or left) channel selections contributed to operation of the AR–BMI with both the HMD and LCD monitor. Our results indicate that AR–BMI systems operated with a see-through HMD may be useful in building advanced intelligent environments.

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