Andrade L O, Machado C R, Chiari E, Pena S D, Macedo A M
Departamento de Bioquímica e Immunologia, Universidade Federal de Minas Gerais, Belo Horizonte-MG, Brazil.
Mol Biochem Parasitol. 1999 May 25;100(2):163-72. doi: 10.1016/s0166-6851(99)90035-x.
Chagas disease, caused by the protozoan Trypanosoma cruzi, presents variable clinical course but the phenomena underlying this variability remain largely unknown. T. cruzi has a clonal population structure and infecting strains are often multiclonal. T. cruzi genetic variability could be a determinant of differential tissue tropism or distribution and consequently of the clinical forms of the disease. We tested this hypothesis by using low-stringency single specific primer polymerase chain reaction (LSSP-PCR) to type genetically the parasites in tissues of experimental infected mice. BALB/c mice were simultaneously inoculated with two different T. cruzi populations (JG strain and Coll.7G2 clone). Doubly infected animals showed clear differential tissue distribution for the two populations (chronic phase). Our results indicate a significant influence of the genetic polymorphism of infecting T. cruzi populations in the pathogenesis of chronic Chagas disease.
恰加斯病由原生动物克氏锥虫引起,临床病程多变,但这种变异性背后的现象在很大程度上仍不为人知。克氏锥虫具有克隆群体结构,感染菌株通常是多克隆的。克氏锥虫的基因变异性可能是不同组织嗜性或分布差异的决定因素,因此也是该疾病临床形式的决定因素。我们通过使用低严谨度单特异性引物聚合酶链反应(LSSP-PCR)对实验感染小鼠组织中的寄生虫进行基因分型来验证这一假设。将BALB/c小鼠同时接种两种不同的克氏锥虫群体(JG株和Coll.7G2克隆)。双重感染的动物在两个群体中显示出明显的组织分布差异(慢性期)。我们的结果表明,感染克氏锥虫群体的基因多态性对慢性恰加斯病的发病机制有重大影响。