Rodrigues Juliany Cola Fernandes, Godinho Joseane Lima Prado, de Souza Wanderley
Laboratório de Ultraestrutura Celular Hertha Meyer, Instituto de Biofísica Carlos Chagas Filho, Centro de Ciências da Saúde, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil,
Subcell Biochem. 2014;74:1-42. doi: 10.1007/978-94-007-7305-9_1.
Leishmania and Trypanosoma belong to the Trypanosomatidae family and cause important human infections such as leishmaniasis, Chagas disease, and sleeping sickness. Leishmaniasis, caused by protozoa belonging to Leishmania, affects about 12 million people worldwide and can present different clinical manifestations, i.e., visceral leishmaniasis (VL), cutaneous leishmaniasis (CL), mucocutaneous leishmaniasis (MCL), diffuse cutaneous leishmaniasis (DCL), and post-kala-azar dermal leishmaniasis (PKDL). Chagas disease, also known as American trypanosomiasis, is caused by Trypanosoma cruzi and is mainly prevalent in Latin America but is increasingly occurring in the United States, Canada, and Europe. Sleeping sickness or human African trypanosomiasis (HAT), caused by two sub-species of Trypanosoma brucei (i.e., T. b. rhodesiense and T. b. gambiense), occurs only in sub-Saharan Africa countries. These pathogenic trypanosomatids alternate between invertebrate and vertebrate hosts throughout their lifecycles, and different developmental stages can live inside the host cells and circulate in the bloodstream or in the insect gut. Trypanosomatids have a classical eukaryotic ultrastructural organization with some of the same main organelles found in mammalian host cells, while also containing special structures and organelles that are absent in other eukaryotic organisms. For example, the mitochondrion is ramified and contains a region known as the kinetoplast, which houses the mitochondrial DNA. Also, the glycosomes are specialized peroxisomes containing glycolytic pathway enzymes. Moreover, a layer of subpellicular microtubules confers mechanic rigidity to the cell. Some of these structures have been investigated to determine their function and identify potential enzymes and metabolic pathways that may constitute targets for new chemotherapeutic drugs.
利什曼原虫和锥虫属于锥虫科，可引发重要的人类感染疾病，如利什曼病、恰加斯病和昏睡病。由利什曼原虫属原生动物引起的利什曼病，全球约有1200万人受其影响，可呈现不同的临床表现，即内脏利什曼病（VL）、皮肤利什曼病（CL）、黏膜皮肤利什曼病（MCL）、弥漫性皮肤利什曼病（DCL）和黑热病后皮肤利什曼病（PKDL）。恰加斯病，也称为美洲锥虫病，由克氏锥虫引起，主要流行于拉丁美洲，但在美国、加拿大和欧洲也日益常见。昏睡病或人类非洲锥虫病（HAT），由布氏锥虫的两个亚种（即罗德西亚布氏锥虫和冈比亚布氏锥虫）引起，仅发生在撒哈拉以南非洲国家。这些致病性锥虫在其整个生命周期中在无脊椎动物和脊椎动物宿主之间交替，不同的发育阶段可寄生于宿主细胞内，并在血液或昆虫肠道中循环。锥虫具有典型的真核超微结构组织，拥有一些与哺乳动物宿主细胞相同的主要细胞器，同时还含有其他真核生物所没有的特殊结构和细胞器。例如，线粒体呈分支状，包含一个称为动质体的区域，其中储存着线粒体DNA。此外，糖体是含有糖酵解途径酶的特殊过氧化物酶体。而且，一层表膜下微管赋予细胞机械刚性。其中一些结构已被研究以确定其功能，并识别可能构成新型化疗药物靶点的潜在酶和代谢途径。
