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1.
Afr J Infect Dis ; 11(1): 26-43, 2017.
Artículo en Inglés | MEDLINE | ID: mdl-28337491

RESUMEN

BACKGROUND: The Ebola virus disease outbreak of 2014 was the largest, longest and most devastating in the history of the disease. It demonstrated the social and economic impact an emerging infectious disease can have in a globalized world. Health systems in affected countries were stretched to the point of near collapse, while social relations and traditional practices were negatively impacted. Heads of African research institutions, African government representatives, leaders of global pharmaceutical companies, global infectious disease experts and close to 100 young African researchers from 25 countries; Assembled in Geneva on 19 and 20th October 2015, for the inaugural UNESCO-Merck Africa Summit sponsored by the United Nations Educational, Science and Culture Organization and Merck KGA. GOAL OF SUMMIT: The primary goal of the summit was to develop strategies to increase health research capacity in Africa, with special focus on Ebola and enhancing pandemic preparation for emerging infectious diseases. The summit was also provide a forum to showcase the research taking place in Africa, and provided platform for African researchers to network. Some of the key issues discussed included; strategies for enhancing policy frameworks to promote knowledge translation, strengthening of health systems, enhancing knowledge and data sharing, and increasing innovation in Africa. CONCLUSIONS: Summit attendees recognized that Africa still bore the heaviest burden of infectious disease, and increased commitment by African governments to fund health research, offered the best hope for developing health solutions and interventions to improve the health of Africans. Improved health in turn would enhance the productivity of Africans, further supporting the socio-economic transformation currently taking place on the continent.

2.
Mucosal Immunol ; 7(2): 268-79, 2014 Mar.
Artículo en Inglés | MEDLINE | ID: mdl-23801306

RESUMEN

Cohort studies of female commercial sex workers (CSWs) in Kenya were among the first to identify highly HIV-1-exposed seronegative (HESN) individuals. As natural resistance is usually mediated by innate immune mechanisms, we focused on determining whether expression and function of innate signaling pathways were altered locally in the genital mucosa of HESN CSWs. Our results demonstrated that selected pattern-recognition receptors (PRRs) were significantly reduced in expression in cervical mononuclear cells (CMCs) from HESN compared with the new HIV-negative (HIV-N) and HIV-positive (HIV-P) groups. Although baseline levels of secreted cytokines were reduced in CMCs of HESN, they were highly stimulated following exposure to ssRNA40 in vitro. Importantly, cervical epithelial cells from HESN also expressed reduced levels of PRRs, but Toll-like receptor 3 (TLR3) and TLR7 as well as nuclear factor-κB and activator protein 1 were highly expressed and activated. Lastly, inflammatory cytokines interleukin (IL)-1ß, IL-8, and RANTES (regulated and normal T cell expressed and secreted) were detected at lower levels in cervicovaginal lavage of HESN compared with the HIV-N and HIV-P groups. Overall, our study reveals a local microenvironment of HIV resistance in the genital mucosa consisting of a finely controlled balance of basal immune quiescence with a focused and potent innate anti-viral response critical to resistance to sexual transmission of HIV-1.


Asunto(s)
Infecciones por VIH/inmunología , VIH-1/inmunología , Inmunidad Innata , Inmunidad Mucosa/inmunología , Trabajadores Sexuales , Cuello del Útero/inmunología , Cuello del Útero/metabolismo , Cuello del Útero/virología , Citocinas/biosíntesis , Citocinas/metabolismo , Células Epiteliales/metabolismo , Femenino , Infecciones por VIH/metabolismo , Seronegatividad para VIH , VIH-1/genética , Humanos , Indolamina-Pirrol 2,3,-Dioxigenasa/metabolismo , Mediadores de Inflamación/metabolismo , Kenia , Modelos Biológicos , Membrana Mucosa/inmunología , Membrana Mucosa/metabolismo , Membrana Mucosa/virología , FN-kappa B/metabolismo , Receptores de Reconocimiento de Patrones/metabolismo , Receptor Toll-Like 7/metabolismo , Receptor Toll-Like 8/metabolismo , Factor de Transcripción AP-1/metabolismo , Ubiquitinas/metabolismo
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