Abstract
American trypanosomiasis or Chagas disease (CD), discovered in 1909 by the Brazilian physician Carlos Chagas, is a vector-borne complex disease caused by the haemoflagellate protozoan parasite Trypanosoma cruzi [1]. One hundred years after its discovery, CD is still epidemiologically relevant, afflicting 12–14 million neglected individuals in 18 endemic countries in Latin America, as well as in non-endemic countries in North America, Europe, and Asia [2, 3]. In the last three decades, governmental initiatives targeting the main vector in endemic areas resulted in successful decline of the incidence of acute infection. For instance, in Brazil, the numbers of acute infection dropped from more than 100,000 new cases/year during the 1980s to less than 500 new cases/year during 2001–2006 [2, 4]. However, the current epidemiological data indicate that we must devote our efforts and agenda to the implementation of sustainable policies for CD control. These measures should incorporate guaranteeing access to the trypanocidal treatment and therapies required by patients, particularly pregnant women and children, developing new drugs and therapeutic strategies, identifying progression markers, as well as elucidating pathogenic mechanisms leading to the distinct clinical forms of CD [3, 4].
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Acknowledgment
This work was supported by grants from CNPq, FAPERJ, DECIT/MS/CNPq/MCT, INCT/CNPq, and fellowship from CNPq
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Lannes-Vieira, J., Pereira, I.R., Vinagre, N.F., Arnez, L.E.A. (2011). TNF-α and TNFR in Chagas Disease: From Protective Immunity to Pathogenesis of Chronic Cardiomyopathy. In: Wallach, D., Kovalenko, A., Feldmann, M. (eds) Advances in TNF Family Research. Advances in Experimental Medicine and Biology, vol 691. Springer, New York, NY. https://doi.org/10.1007/978-1-4419-6612-4_23
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