Alternating phenotypic expression of two classes of Trichomonas vaginalis surface markers.

The antigenic heterogeneity of Trichomonas vaginalis is due in part to the membrane disposition of immunogens (repertoire A) among some but not all isolates and among subpopulations of trichomonads of certain isolates. Heterogeneous T. vaginalis isolates undergo phenotypic variation for the A repertoire of immunogens. The presence of immunogens on (A+ phenotype) or the absence of them from (A- phenotype) trichomonal surfaces clearly influences the virulence traits of the pathogenic human trichomonads. A- parasites, for example, possess an enhanced ability to cause cytadherence-dependent killing of HeLa cells as compared with A+ parasites. A relation between phenotype of repertoire A and adherence was further substantiated by fractionating parasites of a parent T. vaginalis isolate, yielding adherent and nonadherent subpopulations. Trichomonad proteins were identified as putative adhesin candidates (repertoire B); adhesins were synthesized only by adherent (B+ parasites). Flow cytofluorometry of B+ and B- (nonadherent) subpopulations with antibody to proteins of the A repertoire demonstrated corresponding A- B+ and A+ B- phenotypes, respectively. Data support the hypothesis that trichomonads of some isolates of T. vaginalis undergo alternating expression of at least two classes of surface markers.