Abstract

Unlike Trypanosoma cruzi, the causative agent of Chagas’ disease, T. rangeli is an infective, non-pathogenic parasite for humans, but pathogenic for vectors from the Rhodnius genus. Several T. rangeli genotypes (KP1+/A, B, KP1-/C, KP1-/D and E) have been described based on kinetoplast DNA (kDNA) polymorphisms, the spliced leader or miniexon, the intergenic transcribed spacer (ITS) and the small ribosomal subunit (SSUrRNA). These are selectively transmitted by two Rhodnius phylogenetic lines, thereby indicating co-evolutionary processes between parasite and vector genotypes. The Robustus line (Rhodnius prolixus, R. robustus and R. neglectus) exclusively transmits the KP1+/A genotype and the Pallescens line (R. pallescens, R. colombiensis and R. ecuadoriensis) only transmits the KP1-/C genotype. Even though little knowledge is available regarding the molecular basis of parasitevector interaction, the present work presents unpublished observations about KP1+/A and KP1-/C genotype ability to complete the life-cycle of some of the 19 Rhodnius species and the detection of trypanolytic factors in R. prolixus, R. robustus and R. neglectus against the KP1-/C genotype and some T. cruzi genotypes. Several advances regarding molecular, transcriptome and genomic studies dealing with T. rangeli are presented and compared to T. cruzi; these are the starting point for understanding the selective vectorial transmission of T. rangeli and T. cruzi, T. rangeli pathogenicity for the vector, as well as T. rangeli inability and T. cruzi ability to invade mammalian cells.

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