Trypanosoma cruzi Infection: Cellular and Molecular Basis

Dear Colleagues,

Trypanosoma cruzi, the causative agent of Chagas disease (also called American trypanosomiasis), is a parasitic protist that affects millions of people worldwide. No vaccines are available to prevent this disease, and current drug treatments have serious side effects and are not completely effective. The survival of T. cruzi in the mammalian hosts depends on the parasite's ability to infect host cells, reproduce, and live in the blood of the host long enough to warrant is transmission through a bloodsucking insect vector. However, as few genetic tools are available to work with T. cruzi, the cellular, biochemical, and molecular mechanisms for the pathogenesis of this parasite’s infection have not been completely known. Elucidating the cellular and molecular basis of T. cruzi infections will not only provide important information for better understanding the parasite–host interactions but also discover new potential drug targets for the prevention of this parasite in humans. With the recent application of the CRISPR/cas9 technique for gene knockout, gene downregulation, and endogenous gene tagging in T. cruzi, our research is making tremendous advances in defining its pathogenetic machinery. The scope of this Special Issue includes the identification and characterization of cell structures, organelles, genes, enzymes, transporters, or metabolic pathways required for the process of T. cruzi infection. We will accept reviews or original contributions.

Dr. Guozhong Huang
Prof. Dr. Roberto Docampo
Guest Editors

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