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HIV causes rapid CD4+ T cell depletion in the gut mucosa, resulting in immune deficiency and defects in the intestinal epithelial barrier. Breakdown in gut barrier integrity is linked to chronic inflammation and disease progression. However, the early effects of HIV on the gut epithelium, prior to the CD4+ T cell depletion, are not known. Further, the impact of early viral infection on mucosal responses to pathogenic and commensal microbes has not been investigated. We utilized the SIV model of AIDS to assess the earliest host-virus interactions and mechanisms of inflammation and dysfunction in the gut, prior to CD4+ T cell depletion. An intestinal loop model was used to interrogate the effects of SIV infection on gut mucosal immune sensing and response to pathogens and commensal bacteria in vivo. At 2.5 days post-SIV infection, low viral loads were detected in peripheral blood and gut mucosa without CD4+ T cell loss. However, immunohistological analysis revealed the disruption of the gut epithelium manifested by decreased expression and mislocalization of tight junction proteins. Correlating with epithelial disruption was a significant induction of IL-1β expression by Paneth cells, which were in close proximity to SIV-infected cells in the intestinal crypts. The IL-1β response preceded the induction of the antiviral interferon response. Despite the disruption of the gut epithelium, no aberrant responses to pathogenic or commensal bacteria were observed. In fact, inoculation of commensal Lactobacillus plantarum in intestinal loops led to rapid anti-inflammatory response and epithelial tight junction repair in SIV infected macaques. Thus, intestinal Paneth cells are the earliest responders to viral infection and induce gut inflammation through IL-1β signaling. Reversal of the IL-1β induced gut epithelial damage by Lactobacillus plantarum suggests synergistic host-commensal interactions during early viral infection and identify these mechanisms as potential targets for therapeutic intervention.

Abstract. This paper describes an algorithm for maintaining an approximating triangulation of a deforming surface in R 3 . The surface is the envelope of an infinite family of spheres defined and controlled by a finite collection of weighted points. The triangulation adapts dynamically to changing shape, curvature, and topology of the surface.

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This article presents the design, implementation and application of Mobile‐C, an IEEE Foundation for Intelligent Physical Agents (FIPA) compliant agent platform for mobile C/C++ agents. IEEE FIPA standards are a set of specifications designed to ensure the interoperation between agents in a heterogeneous network. Mobile‐C conforms to the FIPA standards both at agent and platform level. Mobile‐C extends FIPA standards to support mobile agents by integrating an embeddable C/C++ interpreter—Ch—into the platform as a mobile agent execution engine and defining a mobile agent mobility protocol to direct agent migration process. Agent migration in Mobile‐C is achieved through FIPA agent communication language (ACL) messages encoded in XML. Using FIPA ACL messages for agent migration provides a straightforward but effective way for inter‐platform agent migration in FIPA compliant agent systems as both agent communication and migration can share the same communication mechanism. Choosing scriptable C/C++ as a mobile agent language allows mobile agents easy interfacing with low‐level software modules and underlying hardware. Mobile‐C has been used to simulate highway traffic detection and management. The agent‐based traffic detection and management system uses agent technology for real‐time distributed traffic information fusion. Mobile agents in the system are used for dynamic code deployment and performing unanticipated actions. The application of agent technology shows a great potential for enhancing the interoperability, flexibility and distributed computing capabilities of intelligent transportation systems. Copyright © 2006 John Wiley & Sons, Ltd.