Trichomonas vaginalis Pathobiology: New Insights from the Genome Sequence

Institute for Cell and Molecular Biosciences, Newcastle University, Newcastle upon Tyne, UK.
Advances in Parasitology (Impact Factor: 4.36). 01/2011; 77:87-140. DOI: 10.1016/B978-0-12-391429-3.00006-X
Source: PubMed

ABSTRACT The draft genome of the common sexually transmitted pathogen Trichomonas vaginalis encodes one of the largest known proteome with 60,000 candidate proteins. This provides parasitologists and molecular cell biologists alike with exciting, yet challenging, opportunities to unravel the molecular features of the parasite's cellular systems and potentially the molecular basis of its pathobiology. Here, recent investigations addressing selected aspects of the parasite's molecular cell biology are discussed, including surface and secreted virulent factors, membrane trafficking, cell signalling, the degradome, and the potential role of RNA interference in the regulation of gene expression.

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    ABSTRACT: Human trichomonosis, infection with Trichomonas vaginalis, is the most common non-viral sexually transmitted disease in the world. The host-parasite interaction and pathophysiological processes of trichomonosis remain incompletely understood. This review focuses on the advancements reached in the area of the pathogenesis of T. vaginalis, especially in the role of the cysteine proteinases. It highlights various approaches made in this field and lists a group of trichomonad cysteine proteinases involved in diverse processes such as invasion of the mucous layer, cytoadherence, cytotoxicity, cytoskeleton disruption of red blood cells, hemolysis, and evasion of the host immune response. A better understanding of the biological roles of cysteine proteinases in the pathogenesis of this parasite could be used in the identification of new chemotherapeutic targets. An additional advantage could be the development of a vaccine in order to reduce transmission of T. vaginalis.
    Parasite 01/2014; 21:54. DOI:10.1051/parasite/2014054 · 0.82 Impact Factor
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    ABSTRACT: To integrate a selection of the most recent data on Trichomonas vaginalis origins, molecular cell biology and T. vaginalis interactions with the urogenital tract microbiota with trichomoniasis symptoms and clinical management. Transcriptomics and proteomics datasets are accumulating, facilitating the identification and prioritization of key target genes to study T. vaginalis pathobiology. Proteins involved in host sensing and cytoskeletal plasticity during T. vaginalis amoeboid transformation were identified. T. vaginalis was shown to secrete exosomes and a macrophage migration inhibitory factor-like protein that both influence host-parasite interactions. T. vaginalis co-infections with Mycoplasma species and viruses were shown to modulate the inflammatory responses, whereas T. vaginalis interactions with various Lactobacillus species inhibit parasite interactions with human cells. T. vaginalis infections were also shown to be associated with bacterial vaginosis. A broader range of health sequelae is also becoming apparent. Diagnostics for both women and men based on the molecular approaches are being refined, in particular for men. New developments in the molecular and cellular basis of T. vaginalis pathobiology combined with data on the urogenital tract microbiota and immunology have enriched our knowledge on human-microbe interactions that will contribute to increasing our capacity to prevent and treat T. vaginalis and other sexually transmitted infections.
    Current Opinion in Infectious Diseases 12/2014; 23(1). DOI:10.1097/QCO.0000000000000128 · 5.03 Impact Factor
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    ABSTRACT: The parasite Trichomonas vaginalis is the causative agent of trichomoniasis, a prevalent sexually transmitted infection. Here, we report the cellular analysis of T. vaginalis tetraspanin family (TvTSPs). This family of membrane proteins has been implicated in cell adhesion, migration and proliferation in vertebrates. We found that the expression of several members of the family is up-regulated upon contact with vaginal ectocervical cells (VECs). We demonstrate that most TvTSPs are localized on the surface and intracellular vesicles and that the C-terminal intracellular tails of surface TvTSPs are necessary for proper localization. Analyses of full length TvTSP8 and a mutant that lacks the C-terminal tail indicates that surface localized TvTSP8 is involved in parasite aggregation, suggesting a role for this protein in parasite: parasite interaction. This article is protected by copyright. All rights reserved.
    Cellular Microbiology 02/2015; DOI:10.1111/cmi.12431 · 4.82 Impact Factor


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