ABSTRACT.    Trichomonas vaginalis is responsible for trichomoniasis, the most common nonviral sexually transmitted disease. The infection is closely related to higher susceptibility to HIV, invasive cervical cancer, and increased risk for preterm delivery during pregnancy. T. vaginalis developed different pathogenicity strategies, based on colonization of vaginal mucosa and production of toxic molecules. During vaginal infection, T. vaginalis induces target-cells damage by a contact-dependent mechanism that involves secreted proteins. The recent publication of the draft genome sequence of T. vaginalis contributed to shed light on some aspects of its pathogenicity mechanisms: sequence analysis led us to the identification of 12 different genes (TvSaplip1 to TvSaplip12) containing saposin-like domains. TvSaplips are homologous to the pore-forming toxins secreted by Entamoeba histolytica and Naegleria fowleri, belonging to the conserved family of saposin-like proteins. All members of the Saplip family have in common a ~75 aminoacid polypeptide motif characterized by an invariable 6-cysteine pattern and the abundance of hydrophobic residues, resulting in a common folding characterized by 5 alfa-helices interconnected by three disulfide bridges between the conserved cysteine residues. Real Time PCR experiments showed that all the TvSaplip genes except TvSaplip9 are transcribed. The transcription levels of TvSaplip genes have been then evaluated in Real Time PCR upon contact with human target cells, in order to obtain clues on which of the TvSaplip genes might be involved in the cytopathic effect mediated by T. vaginalis.