KILLING OF TRICHOMONAS-VAGINALIS BY COMPLEMENT-MEDIATED LYSIS IS NOT ASSOCIATED WITH THE PRESENCE OF TRICHOMONAS-VAGINALIS VIRUS

We have examined the possible relationship between trichomonad killing by human serum and the presence of virus-encoded double-stranded ribo nucleic acid in T. vaginalis (TVV). Indirect immunofluorescence assay revealed that non-immune serum (NIS) and T. vaginalis-immune serum (TV IS) had immunoglobulin G (IgG) antibody titres of 1:8 and 1:256, respe ctively, against T. vaginalis. Among the 12 isolates of T. vaginalis e xamined, 9 were infected with TVV. Upon long-term (> 9 months) culture , of the 9 infected isolates, 3 isolates lost the virus during the pas sage process. Five of 9 TVV-infected isolates were completely killed b y 10% NIS while the other 4 TVV-infected isolates had viability over t he range 22-81%. Three fresh non-TVV-infected isolates had viability o ver the range 12-89%. On the other hand, no trichomonads survived in t he presence of 10% TVIS. Viability of the virus-lost isolates during l ong-term culture was not altered when compared with that of their corr esponding fresh isolates. Heat-inactivated-NIS and -TVIS had no killin g effect on trichomonads while absorbed-NIS and -TVIS (ATVIS) had a si milar killing effect to NIS. Further studies on the role of antibody a nd complement in the killing of trichomonads by serum revealed no sign ificant difference in trichomonad viability between treatments of Mg2-ethylene glycol-bis-(beta-aminoethyl ether)- N,N,N,N'-tetraacetic aci d (Mg2+-EGTA)-TVIS and of Mg2+-EGTA-ATVIS. Zymosan-treated ATVIS did n ot kill trichomonads but zymosan-treated TVIS had a marked killing eff ect. Taken together, these results not only indicate that killing of t richomonads by an antibody-independent alternative pathway activation is not associated with the presence of TVV, but also suggest that the TVV-expressed surface immunogens do not have a major part to play in a ctivating the classical pathway.