In fact, the genome sequencing project has revealed that T. vaginalis genome has undergone expansion on a scale unprecedented in unicellular eukaryotes [36], and such gene family expansions are likely to improve the specific adaptation of the organism to its environment [37]. Furthermore, there are variations between the 5S rRNA genes of T. vaginalis and GSK2126458 in vitro T. tenax (personal communication). This fact may explain the Tipifarnib molecular weight expression levels of identical genes within the two highly related species.

Without a doubt, such a modification in the gene inventory in the genomes of pathogens would be an important evolutionary signal. In fact, several studies have shown a relationship between virulence, differential gene acquisition and copy number, and gene expression in both bacteria and viruses [38], and this may be what resulted to distinguish T. vaginalis from the oral trichomonad. Therefore, it is altogether reasonable that the levels of transcription and synthesis of proteins in these two trichomonad species may account for adaptability for survival in their respective oral cavity and urogenital regions. Finally, our results may begin to delineate recent findings regarding how both T. vaginalis and PLX4032 T. tenax are associated with broncho-pulmonary infections in patients with Pneumocystis carinii or with underlying cancers or other

lung diseases [18–24]. As mentioned above, the respiratory-lung environment is itself distinct from the oral cavity and urogenital region, but this niche obviously permits survival of both regardless of the extent of gene expression for T. vaginalis and T. tenax. While lung infection by the oral trichomonads can be envisioned, the mechanisms by which the urogenital parasites establish residence in the oral cavity for subsequent oropharyngeal and respiratory infections is unclear. Future considerations must now be given regarding methods of Phosphoprotein phosphatase transmission of T. vaginalis into lung tissues. It is possible that this parasite colonizes the oral cavity through oral sex and survives for extended periods prior to aspiration

and infection. It is equally theoretically possible that T. tenax is a genetic variant of T. vaginalis distinguished by rates of gene transcription. It may be unlikely that T. tenax infects the urogenital region of women. One reason for this may be that this trichomonad is nonadherent to HeLa epithelial 9 cells [39] and vaginal epithelial cells (not shown). As T. tenax has the genes encoding adhesins, such as AP65 [32–35], this inability to bind epithelial cells, a property preparatory to infection and colonization, may help explain the tropism of T. tenax to the oral cavity. It is conceivable that the decreased level of expression of these adhesin genes in T. tenax accounts for this inability to adhere to vaginal epithelial cells. These possibilities will require future experimental examination.