Department of Especial Education, UNESP São Paulo State University, 17525-900 Campus Marília, SP, Brazil.
J Trop Med. 2012;2012:357948. doi: 10.1155/2012/357948. Epub 2012 Mar 8.
The etiologic agent of Chagas Disease is the Trypanosoma cruzi, transmitted through blood-sucking insect vectors of the Triatominae subfamily, representing one of the most serious public health concerns in Latin America. There are geographic variations in the prevalence of clinical forms and morbidity of Chagas disease, likely due to genetic variation of the T. cruzi and the host genetic and environmental features. Increasing evidence has supported that inflammatory cytokines and chemokines are responsible for the generation of the inflammatory infiltrate and tissue damage. Moreover, genetic polymorphisms, protein expression levels, and genomic imbalances are associated with disease progression. This paper discusses these key aspects. Large surveys were carried out in Brazil and served as baseline for definition of the control measures adopted. However, Chagas disease is still active, and aspects such as host-parasite interactions, genetic mechanisms of cellular interaction, genetic variability, and tropism need further investigations in the attempt to eradicate the disease.
恰加斯病的病原体是克氏锥虫，通过中肠亚目的吸血昆虫传播，是拉丁美洲最严重的公共卫生问题之一。恰加斯病的临床形式和发病率存在地理差异，可能与克氏锥虫和宿主遗传和环境特征的遗传变异有关。越来越多的证据表明，炎症细胞因子和趋化因子是产生炎症浸润和组织损伤的原因。此外，遗传多态性、蛋白表达水平和基因组失衡与疾病进展有关。本文讨论了这些关键方面。在巴西进行了大规模调查，为所采取的控制措施提供了基准。然而，恰加斯病仍然活跃，宿主-寄生虫相互作用、细胞相互作用的遗传机制、遗传变异性和趋向性等方面需要进一步研究，以试图消灭这种疾病。
