18 research outputs found

    Automated Visual Attention Manipulation

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    Abstract. In this paper a system for visual attention manipulation is introduced and formally described. This system is part of the design of a software agent that supports naval crew in her task to compile a tactical picture of the situation in the field. A case study is described in which the system is used to manipulate a human subject’s attention. To this end the system includes a Theory of Mind about human attention and uses this to estimate the subject’s current attention, and to determine how features of displayed objects have to be adjusted to make the attention shift in a desired direction. Manipulation of attention is done by adjusting illumination according to the calculated difference between a model describing the subject’s attention and a model prescribing it.

    The viral chemokine MCK-2 of murine cytomegalovirus promotes infection as part of a gH/gL/MCK-2 complex.

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    Human cytomegalovirus (HCMV) forms two gH/gL glycoprotein complexes, gH/gL/gO and gH/gL/pUL(128,130,131A), which determine the tropism, the entry pathways and the mode of spread of the virus. For murine cytomegalovirus (MCMV), which serves as a model for HCMV, a gH/gL/gO complex functionally homologous to the HCMV gH/gL/gO complex has been described. Knock-out of MCMV gO does impair, but not abolish, virus spread indicating that also MCMV might form an alternative gH/gL complex. Here, we show that the MCMV CC chemokine MCK-2 forms a complex with the glycoprotein gH, a complex which is incorporated into the virion. We could additionally show that mutants lacking both, gO and MCK-2 are not able to produce infectious virus. Trans-complementation of these double mutants with either gO or MCK-2 showed that both proteins can promote infection of host cells, although through different entry pathways. MCK-2 has been extensively studied in vivo by others. It has been shown to be involved in attracting cells for virus dissemination and in regulating antiviral host responses. We now show that MCK-2, by forming a complex with gH, strongly promotes infection of macrophages in vitro and in vivo. Thus, MCK-2 may play a dual role in MCMV infection, as a chemokine regulating the host response and attracting specific target cells and as part of a glycoprotein complex promoting entry into cells crucial for virus dissemination
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