Abstract
Research exploring the proteome of Toxoplasma gondii oocysts has gained momentum over the past few years. However, little is known about the oocyst's protein repertoires that contribute to differential virulence among T. gondii strains. Here, we used isobaric tag for relative and absolute quantitation-based proteomic analysis of oocysts of two T. gondii strains exhibiting the virulent PYS (ToxoDB#9) phenotype versus the less virulent PRU (Type II, ToxoDB#1) phenotype. Our aim was to determine protein expression patterns that contribute to the virulence of a particular phenotype. A total of 2,551 proteins were identified, of which 374 were differentially expressed proteins (DEPs) (|log2 fold change| ≥ 0.58 and P < 0.05). DEPs included 192 increased and 182 decreased proteins. Gene Ontology and KEGG pathway analyses revealed a large number of DEPs enriched in various metabolic processes. Protein interaction network analysis using STRING identified inosine monophosphate dehydrogenase (IMPDH), Bifunctional GMP synthase/glutamine amidotransferase protein, Glucose-6-phosphate 1-dehydrogenase, and Citrate synthase as the top four hubs. Of the 22 virulence proteins commonly expressed in the oocysts of the two strains, 13 and 2 proteins were increased in PYS strain and PRU strain, respectively. Also, 10 and 3 of the 22 identified oocyst wall proteins showed higher expression in oocysts of PRU strain and PYS strain, respectively. These findings revealed new proteomic differences in the oocysts of T. gondii strains of different genotypic backgrounds.
Highlights
The apicomplexan protozoan parasite Toxoplasma gondii has a remarkable ability to infect a wide range of mammals, birds and humans [1,2,3,4]
Of the 22 virulence proteins commonly expressed in the oocysts of the two strains, 13 and 2 proteins were increased in PYS strain and PRU strain, respectively
10 and 3 of the 22 identified oocyst wall proteins showed higher expression in oocysts of PRU strain and PYS strain, respectively. These findings revealed new proteomic differences in the oocysts of T. gondii strains of different genotypic backgrounds
Summary
The apicomplexan protozoan parasite Toxoplasma gondii has a remarkable ability to infect a wide range of mammals, birds and humans [1,2,3,4]. Infection can occur via ingestion of the cat-borne oocysts through contaminated food or water, ingestion of cysts in the tissues of an infected intermediate host or transplacentally from infected mothers to their offspring [5]. Oocysts have an exceptional ability to adapt to adverse environmental conditions outside the host [7]. They can remain viable for at least 1 year at 4oC [8]. Exposure to ultraviolet irradiation at doses even exceeding those used to treat water did not fully inactivate T. gondii oocysts [10]. Two chemicals commonly used to treat sewage and drinking water, failed to inactivate all infective oocysts [11]. Clinical illness can be more severe when hosts acquire the infection through ingestion of oocysts [12]
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