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Background  Trichomonosis, caused by  Trichomonas vaginalis , is the number one, nonviral sexually transmitted infection that has adverse consequences for the health of women and children. The interaction of  T. vaginalis  with vaginal epithelial cells (VECs), a step preparatory to infection, is mediated in part by the prominent surface protein AP65. The bovine trichomonad,  Tritrichomonas foetus , adheres poorly to human VECs. Thus, we established a transfection system for heterologous expression of the  T. vaginalis  AP65 in  T. foetus , as an alternative approach to confirm adhesin function for this virulence factor.    Results  In this study, we show stable transfection and expression of the  T.   vaginalis ap65  gene in  T. foetus  from an episomal pBS- ap65-neo  plasmid. Expression of the gene and protein was confirmed by RT-PCR and immunoblots, respectively. AP65 in transformed  T. foetus  bound to host cells. Specific mAbs revealed episomally-expressed AP65 targeted to the parasite surface and hydrogenosome organelles. Importantly, surface-expression of AP65 in  T. foetus  paralleled increased levels of adherence of transfected bovine trichomonads to human VECs.    Conclusion  The  T. vaginalis  AP65 adhesin was stably expressed in  T. foetus , and the data obtained using this heterologous system strongly supports the role of AP65 as a prominent adhesin for  T. vaginalis . In addition, the heterologous expression in  T. foetus  of a  T. vaginalis  gene offers an important, new approach for confirming and characterizing virulence factors.

Heterologous expression in Tritrichomonas foetus of functional Trichomonas vaginalis AP65 adhesin.