Summary Trafficking of cell-associated HIV-1 from the genital mucosa to lymphoid organs represents a critical first step toward systemic infection. Mature DCs capture and transmit HIV-1 to T cells, but insights into DC-to-T cell viral spread dynamics within a 3-dimensional environment is lacking. Using live-cell imaging, we show that mature DCs rapidly compartmentalize HIV-1 within surface-accessible invaginations near the uropod. HIV-1 capture did not interfere with DC migration toward lymph node homing chemo-attractants and their ability to enter lymphatic vessels. However, HIV-captured DCs engaged in prolonged contacts with autologous CD4+ T cells, which led to high T cell infection. Interestingly, we show that surface bound, virion-associated Env induced signal transduction in motile T cells that facilitated prolonged DC:T cell interactions, partially through high-affinity LFA-1 expression. Together, we describe a mechanism by which surface bound HIV-1 particles function as signaling receptors that regulate T cell motility, cell-cell contact dynamics, and productive infection.

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Background Creating an airtight seal is vital in making a Negative pressure wound therapy setup functional and effective but in some conditions, this may be difficult to achieve. Case presentation We present the methods of use of improvised negative pressure therapy in the difficult settings of external fixation and complete scotch cast with a window for wound dressing in two patients managed at LAUTECH Teaching Hospital, Ogbomoso. The simple use of opsite initially over the foam dressing and reinforcing it with cling film and subsequently wrapping strips of opsite around the pin sites and the potential leak sites as described in this report is very effective and with lower cost when compared with other methods. Conclusion The use of cling film and opsite only in maintaining an airtight seal in difficult settings of negative pressure wound therapy is simple and cost-effective with good wound outcomes.