Recent studies of the biology of Trypanosoma vivax.
Recent biological investigations of the African trypanosomes have been moving away from their previous preoccupation with the phenomenon of antigenic variation. The feeling has arisen that antigenic variation, as demonstrated by the Trypanozoon and Nannomonas subgenera of trypanosomes, is too extensive, the number of serodemes too large and the coexistence of different species in many areas too complicated, to allow any immunoprophylaxis based on antibodies to variable antigens. This is, of course, not to rule out possible biochemical intervention in the biosynthesis or export of VSG molecules by trypanosomes. However, in the case of T. vivax, more information is required concerning antigenic variation and coat structure in this organism before these avenues of investigation are discarded. Ways of improving the yield of mature metacyclic trypanosomes in vitro must be found, so that the contribution of metacyclic variable antigens to the induction of immunity in T. vivax infection can be elucidated. The number of bloodstream VATs must be determined (perhaps by genetic rather than serological means), as there is evidence both for VAT exhaustion contributing to the self-cure of infected hosts, and for a possible limit to the number of VATs which can be expressed in infections in Africa. In South America nothing is known of the number of serodemes of T. vivax which exist, although such knowledge is obviously required, especially if immunity to bloodstream variants is the more important mechanism of inducing immunity to this trypanosome and true cyclical transmission is rare in, or absent from, that subcontinent. Further, in a fragile organism, with a coat of suspect integrity, the method of VSG packing and the relative exposure of underlying surface molecules seems to hold out even more hope for an immunological intervention based on cell surface but invariant molecules than is the case with T. brucei or T. congolense, although this is being attempted with the latter species. In T. brucei infections the appearance of the non-dividing stumpy population acts as a stimulus to the induction of humoral immune responses. In ruminants, antibody responses to T. vivax, at least as judged from lysis tests, lag behind the appearance of the different VATs by some days. It would be important to determine, therefore, whether, if late bloodstream forms could be induced more frequently in the ruminant, the speed of anti-VAT responses could be enhanced. Whilst self-cure appears to be relatively common in T. vivax infections, it is unlikely that it results in sterile immunity.(ABSTRACT TRUNCATED AT 400 WORDS)
Gardiner
P R
PR
International Laboratory for Research on Animal Diseases, Nairobi, Kenya.
D000818:Animals; D000940:Antigenic Variation; D000953:Antigens, Protozoan / Q000235:genetics / Q000276:immunology; D014345:Trypanosoma / Q000254:growth & development / Q000276:immunology / Q000502:physiology*; D014353:Trypanosomiasis, African / Q000276:immunology / Q000469:parasitology* / Q000635:transmission
D000953:Antigens, Protozoan