Antigenic type of first relapse variants arising from a strain of Trypanosoma (Trypanozoon) brucei

McNeillage, Gillian J.C.; Herbert, W.J.; Lumsden, W. H. R.

doi:10.1016/0014-4894(69)90046-0

Cited by 34 publications

(6 citation statements)

References 15 publications

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“…(8) found that 1.21 and 1.69 were activated very early in all goats examined following fly transmission of EATRO 795; the other bloodstream ILTat VATs in the present study were not examined. In related trypanosome stocks (isolates), the ILTat 1.69 (ETat 1.7), 1.21 (ETat 1.9), and 1.22 (GUTat 7.1, ETat 1.2) VATs have been identified, and all have been shown to be activated early in infection (6,46). ILTats 1.22 and 1.64 (GUTat 7.13) are also expressed in the metacyclic population in the tsetse fly (6,19), and expression of the former has been studied in considerable detail (7-9, 30, 44).…”

Section: Discussionmentioning

confidence: 99%

Predominance of Duplicative VSG Gene Conversion in Antigenic Variation in African Trypanosomes

Robinson

Burman

Melville

et al. 1999

Molecular and Cellular Biology

131

113

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A number of mechanisms have been described by which African trypanosomes undergo the genetic switches that differentially activate their variant surface glycoprotein genes (VSGs) and bring about antigenic variation. These mechanisms have been observed mainly in trypanosome lines adapted, by rapid syringe passaging, to laboratory conditions. Such "monomorphic" lines, which routinely yield only the proliferative bloodstream form and do not develop through their life cycle, have VSG switch rates up to 4 or 5 orders of magnitude lower than those of nonadapted lines. We have proposed that nonadapted, or pleomorphic, trypanosomes normally have an active VSG switch mechanism, involving gene duplication, that is depressed, or from which a component is absent, in monomorphic lines. We have characterized 88 trypanosome clones from the first two relapse peaks of a single rabbit infection with pleomorphic trypanosomes and shown that they represent 11 different variable antigen types (VATs). The pattern of appearance in the first relapse peak was generally reproducible in three more rabbit infections. Nine of these VATs had activated VSGs by gene duplication, the tenth possibly also had done so, and only one had activated a VSG by the transcriptional switch mechanism that predominates in monomorphic lines. At least 10 of the donor genes have telomeric silent copies, and many reside on minichromosomes. It appears that trypanosome antigenic variation is dominated by one, relatively highly active, mechanism rather than by the plethora of pathways described before.

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Section: Discussionmentioning

confidence: 99%

Predominance of Duplicative VSG Gene Conversion in Antigenic Variation in African Trypanosomes

Robinson

Burman

Melville

et al. 1999

Molecular and Cellular Biology

131

113

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“…TREU 164 represents passage 21 in mice from parasites originating from a capsule of bovine blood on which Glossina pallidipes captured at Lugala, Busoga, Uganda, in 1960, were allowed to feed. The pedigree of TREU 164 has been published [23]. The ETat3 variant derived from TREU 164 was triply cloned at Yale and referred to as YTat1.…”

Section: Methodsmentioning

confidence: 99%

Infections with Immunogenic Trypanosomes Reduce Tsetse Reproductive Fitness: Potential Impact of Different Parasite Strains on Vector Population Structure

Rio

Medlock

et al. 2008

PLoS Negl Trop Dis

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The parasite Trypanosoma brucei rhodesiense and its insect vector Glossina morsitans morsitans were used to evaluate the effect of parasite clearance (resistance) as well as the cost of midgut infections on tsetse host fitness. Tsetse flies are viviparous and have a low reproductive capacity, giving birth to only 6–8 progeny during their lifetime. Thus, small perturbations to their reproductive fitness can have a major impact on population densities. We measured the fecundity (number of larval progeny deposited) and mortality in parasite-resistant tsetse females and untreated controls and found no differences. There was, however, a typanosome-specific impact on midgut infections. Infections with an immunogenic parasite line that resulted in prolonged activation of the tsetse immune system delayed intrauterine larval development resulting in the production of fewer progeny over the fly's lifetime. In contrast, parasitism with a second line that failed to activate the immune system did not impose a fecundity cost. Coinfections favored the establishment of the immunogenic parasites in the midgut. We show that a decrease in the synthesis of Glossina Milk gland protein (GmmMgp), a major female accessory gland protein associated with larvagenesis, likely contributed to the reproductive lag observed in infected flies. Mathematical analysis of our empirical results indicated that infection with the immunogenic trypanosomes reduced tsetse fecundity by 30% relative to infections with the non-immunogenic strain. We estimate that a moderate infection prevalence of about 26% with immunogenic parasites has the potential to reduce tsetse populations. Potential repercussions for vector population growth, parasite–host coevolution, and disease prevalence are discussed.

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“…The different VATs of a repertoire are genetically determined and the corresponding genes are expressed, one at a time, in a semi-ordered sequence. Indeed, in a given trypanosome stock, "predominant" VATs are always observed early in chronic infections and others only late (2)(3)(4)(5)(6)(7)(8).…”

Section: Introductionmentioning

confidence: 99%

Translocation alters the activation rate of a trypanosome surface antigen gene

et al. 1984

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Antigenic type of first relapse variants arising from a strain of Trypanosoma (Trypanozoon) brucei

Cited by 34 publications

References 15 publications

Predominance of Duplicative VSG Gene Conversion in Antigenic Variation in African Trypanosomes

Predominance of Duplicative VSG Gene Conversion in Antigenic Variation in African Trypanosomes

Infections with Immunogenic Trypanosomes Reduce Tsetse Reproductive Fitness: Potential Impact of Different Parasite Strains on Vector Population Structure

Translocation alters the activation rate of a trypanosome surface antigen gene

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