Host-parasite interactions which influence the virulence of Trypanosoma (Trypanozoon) brucei brucei organisms.

Subclones were prepared in mice from T. b. brucei ILTat 1.4 parasites. Subclones which did not differentiate to stumpy forms in mice were highly virulent and did not stimulate detectable antibody responses. A subclone which did give rise to stumpy forms in mice, was less virulent and did stimulate an antibody response specific for the trypanosome surface glycoprotein. Clones and subclones of T.b. brucei parasites which did not give rise to stumpy forms in mice, did give rise to stumpy forms in Bovidae. Plasma from cattle infected with those parasites did not stimulate differentiation of T.b. brucei parasites in mice. Murine pleomorphic and monomorphic T.b. brucei parasites retained their respective phenotypes in co-infected mice. Both types of parasites were equally pleomorphic in Bovidae. We conclude that some clones of T.b. brucei remain monomorphic in mice as a result of a high avidity interaction between slender forms and host molecules which inhibit differentiation of T.b. brucei parasites.