TY - JOUR KW - Infections AU - Martins NO AU - Souza RT AU - Cordero EM AU - Maldonado DC AU - Cortez C AU - Marini MM AU - Ferreira ER AU - Bayer-Santos E AU - Almeida IC AU - Yoshida N AU - Silveira JF AB -

Author summary:

Trypanosoma cruzi is the etiologic agent of Chagas’ disease, which infects 6–7 million people worldwide, mostly in Latin America. Currently, there are no vaccines available, and the drugs used for treatment are toxic and are not fully effective. To infect mammalian hosts, T. cruzi relies on the ability to invade host cells, replicate intracellularly and spread the infection in different organs of the mammalian host. Knowledge of the structure and function of T. cruzi surface molecules is fundamental to understanding the mechanisms by which the parasite interacts with its host. T. cruzi infective forms engage a repertoire of surface and secreted molecules, some of which are involved in triggering signaling pathways both in the parasite and the host cell, leading to intracellular Ca2+ mobilization, a process essential for parasite internalization. Here, we described a novel family of T. cruzi surface membrane proteins (TcSMP), including their genomic distribution, expression and cellular localization. We studied the mechanism of action of TcSMP in host-cell invasion and proposed a triggering role for TcSMP in host-cell lysosome exocytosis during metacyclic internalization. TcSMP genes are conserved among different T. cruzi lineages and share orthologs in other Trypanosoma species. These results suggest that the diversification of TcSMP genes in mammalian trypanosomes occurred after continental drift. In T. cruzi this gene family expanded by gene duplication.

BT - PLoS neglected tropical diseases C1 -

http://www.ncbi.nlm.nih.gov/pubmed/26565791?dopt=Abstract

DO - 10.1371/journal.pntd.0004216 IS - 11 J2 - PLoS Negl Trop Dis LA - eng N2 -

Author summary:

Trypanosoma cruzi is the etiologic agent of Chagas’ disease, which infects 6–7 million people worldwide, mostly in Latin America. Currently, there are no vaccines available, and the drugs used for treatment are toxic and are not fully effective. To infect mammalian hosts, T. cruzi relies on the ability to invade host cells, replicate intracellularly and spread the infection in different organs of the mammalian host. Knowledge of the structure and function of T. cruzi surface molecules is fundamental to understanding the mechanisms by which the parasite interacts with its host. T. cruzi infective forms engage a repertoire of surface and secreted molecules, some of which are involved in triggering signaling pathways both in the parasite and the host cell, leading to intracellular Ca2+ mobilization, a process essential for parasite internalization. Here, we described a novel family of T. cruzi surface membrane proteins (TcSMP), including their genomic distribution, expression and cellular localization. We studied the mechanism of action of TcSMP in host-cell invasion and proposed a triggering role for TcSMP in host-cell lysosome exocytosis during metacyclic internalization. TcSMP genes are conserved among different T. cruzi lineages and share orthologs in other Trypanosoma species. These results suggest that the diversification of TcSMP genes in mammalian trypanosomes occurred after continental drift. In T. cruzi this gene family expanded by gene duplication.

PY - 2015 EP - e0004216 T2 - PLoS neglected tropical diseases TI - Molecular Characterization of a Novel Family of Trypanosoma cruzi Surface Membrane Proteins (TcSMP) Involved in Mammalian Host Cell Invasion. UR - http://journals.plos.org/plosntds/article?id=10.1371/journal.pntd.0004216 VL - 9 SN - 1935-2735 ER -