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. 1984 Feb;43(2):735–738. doi: 10.1128/iai.43.2.735-738.1984

Resistance of cattle to tsetse-transmitted challenge with Trypanosoma brucei or Trypanosoma congolense after spontaneous recovery from syringe-passaged infections.

V M Nantulya, A J Musoke, F R Rurangirwa, S K Moloo
PMCID: PMC264362  PMID: 6693173

Abstract

Groups of cattle were inoculated intravenously with cloned populations of bloodstream forms of Trypanosoma brucei or Trypanosoma congolense. All five steers infected with T. brucei ILTat 2.1 and six of the eight steers infected with T. congolense IL 13-E14 became aparasitemic within 16 and 32 weeks postinfection, respectively. Examination of sera from animals infected with T. brucei by indirect immunofluorescence and neutralization assays revealed the presence of antibodies against all the metacyclic variable antigen types (VATs) of the infecting clone. The neutralizing capacity of the sera increased with the course of infection from 1:10 at 2 months to 1:100 at 3 to 4 months postinfection. The recovered animals were completely immune to challenge by Glossina morsitans subsp. centralis infected with clone IL Tat 2.1, which had initiated the infection, as well as with another clone (IL Tat 2.2) belonging to the same serodeme, but they were susceptible to a tsetse-transmitted heterologous challenge with isolate STIB 367-H. Similar results were obtained with sera from T. congolense IL 13-E14-infected steers. The six steers infected with a different T. congolense ILNat 3.1 clone did not recover spontaneously; however, 2 months postinfection, sera from five of them also contained neutralizing antibodies against ILNat 3.1 metacyclic VATs. These results indicate that some of the bloodstream VATs that arise during the course of a chronic infection possess surface epitopes in their variable surface glycoproteins that are identical to those of the metacyclic VATs. It is suggested that in chronic infection, the infecting trypanosomes could exhaust their VAT repertoire, including those that cross-react with metacyclics, thereby leading to both "self-cure" and subsequent immunity to homologous cyclically transmitted challenge.

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Selected References

These references are in PubMed. This may not be the complete list of references from this article.

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