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This paper presents the design criteria for Visual Cues – visual stimuli that are used in combination with other pedagogical processes and tools in Disruptive Learning interventions in sustainability education – to disrupt learners’ existing frames of mind and help re-orient learners’ mind-sets towards sustainability. The theory of Disruptive Learning rests on the premise that if learners’ frames of mind or frames of reference can be disrupted (in other words, challenged), then learners’ mind-sets can be re-oriented towards sustainability, and indeed learners can be motivated to engage in change agency for sustainability. The use of Visual Cues thus unsettle or challenge learners’ mind-sets, and in doing so, set them on the pathway towards re-orientation in becoming more sustainability oriented, and/or in motivating engagement in sustainability change agency. The findings form part of a broader research study on ESD conducted in a higher education institution in Ireland within an undergraduate degree of teacher education. Kathy Charmaz’ Constructivist Grounded Theory approach guided the entire study, resulting in the articulation of the theory of, and processes within, Disruptive Learning. This paper presents design criteria for Visual Cues that were articulated through a thematic analysis approach from data emerging from reflective diaries, follow-up interviews, audio recordings and observational notes. The findings from this study in respect of design criteria state that Visual Cues must disrupt rather than disturb; must represent (have impressions of) real life contexts, scenarios, practices or events; must provoke controversy; must contain a visual stimulation; and can have a critical question.

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.