Trichomonas vaginalis is a major sexually transmitted parasite that inhabits primarily the vaginal tract of women. Very little is known about precise virulence factors of the pathogenic human trichomonads, although recent reports (1-3) indicate that the ability of these parasites to undergo phenotypic variation may be related to expression of certain virulence attributes . For example, parasites that lacked a repertoire of major immunogens on their surface (negative phenotype) displayed enhanced cytadherence and killing of host cells (3). On the other hand, trichomonads possessing surface immunogens (positive phenotype) had a diminished ability to cause contact-dependent cytotoxicity of HeLa cells; however, the positive phenotype organisms were still capable of shifting to the negative phenotype (3). More recent studies examining the phenotypes of fresh isolates of T. vaginalis (3, 4) confirmed the presence of only two types of parasite populations. On the basis of mAb reactivity via indirect immunofluorescence, isolates comprised homogeneous, negative phenotype trichomonads or heterogeneous populations containing both positive and negative phenotype trichomonads (3, 4). Isolates that were stable negative phenotype populations did not undergo phenotypic variation (3, 4). However, purified subpopulations of positive and negative phenotype trichomonads newly fractionated from the heterogeneous parents were both capable of phenotypic variation upon further in vitro cultivation (3,4).Another recent and as yet poorly understood observation that may be relevant to the biology of this host-parasite relationship is the presence of a virus-encoded double-stranded ribonucleic acid (dsRNA)' among some but not all isolates of T. vaginalis (5-7) . The virus shown in Fig. I has an icosahedral morphology and a diameter of 33 nm. It consists of a single, linear dsRNA with an estimated size of 5 .5 kb and a major protein of 85 kD . There is no detectable homology