Antigenic variation in cyclically transmitted Trypanosoma brucei. Variable antigen type composition of metacyclic trypanosome populations from the salivary glands of Glossina morsitans

Parasitology ◽  
1981 ◽  
Vol 83 (3) ◽  
pp. 595-607 ◽  
Author(s):  
S. L. Hajduk ◽  
Cathy R. Cameron ◽  
J. D. Barry ◽  
K. Vickerman
Keyword(s):  
Salivary Glands ◽  
Trypanosoma Brucei ◽  
Indirect Immunofluorescence ◽  
Antigenic Variation ◽  
Tsetse Flies ◽  
Glossina Morsitans ◽  
Type Composition ◽  
Variable Antigen ◽  
Monospecific Antisera

SUMMARYTsetse flies (Glossina morsitans) were fed on the blood of mice containing any one of 5 variable antigen types (VATs) of Trypanosoma brucei AnTAR 1 serodeme. The VATs of the metacyclic trypanosomes subsequently detected in the flies' saliva probes were investigated using monospecific antisera to AnTAR 1 VATs in indirect immunofluorescence and trypanolysis reactions; these sera included 3 raised against AnTats 1.6, 1.30 and 1.45, previously identified as components of the metacyclic population (M-VATs), and against the 5 VATs originally ingested by the flies. The percentage of metacyclics reacting with a particular M-VAT antiserum remained more or less constant (AnTat 1.6, 6·0–8·3%; AnTat 1.30, 13·7–18·2%; AnTat 1.45, 2·0–8·0%), regardless of the age of the fly or the ingested VAT. As these 3 VATs accounted for no more than 30% of the metacyclic population, the existence of at least one more VAT is envisaged. The ingested VAT could not be detected among the AnTAR 1 metacyclic trypanosomes.

Antigenic variation in cyclically transmitted Trypanosoma brucei. Variable antigen type composition of the first parasitaemia in mice bitten by trypanosome-infected Glossina morsitans

Parasitology ◽  
1981 ◽  
Vol 83 (3) ◽  
pp. 609-621 ◽  
Author(s):  
S. L. Hajduk ◽  
K. Vickerman
Keyword(s):  
Salivary Glands ◽  
Trypanosoma Brucei ◽  
Antigenic Variation ◽  
Tsetse Flies ◽  
Glossina Morsitans ◽  
Type Composition ◽  
X Irradiation ◽  
Variable Antigen ◽  
Monospecific Antisera ◽  
Cyclical Transmission

SUMMARYTsetse flies were infected with 5 different variable antigen types (VATs) or with a mixture of VATs of the AnTAR 1 serodeme of Trypanosoma brucei. Metacyclic forms from the salivary glands of infected flies were used to initiate infections in mice. Immunofluorescence and trypanolysis reactions employing 24 monospecific antisera were used to analyse the VATs present in the mice following cyclical transmission. Regardless of the VAT used to infect tsetse flies, the first VATs detectable in the bloodstream were those previously identified as metacyclic VATs (M-VATs). These were present until at least 5 days after infection, at which time lytic antibodies against at least 2 of the M-VATs were detectable in the blood of infected mice. In mice immunosuppressed by X-irradiation the M-VATs were detectable in the bloodstream for longer periods, but the percentage of the population labelled with anti-metacyclic sera showed a decrease on day 5 as in non-irradiated animals. The VAT ingested by the tsetse was always detectable early during the first parasitaemia following cyclical transmission and was usually the first VAT detected after the M-VATs. Neutralization of selected M-VATs before infecting mice resulted in elimination of the neutralized M-VAT from the first parasitaemia but had no effect on the expression of other VATs in the early infection.

Trypanosome infections and survival in tsetse

Parasitology ◽  
1998 ◽  
Vol 116 (S1) ◽  
pp. S23-S28 ◽  
Author(s):  
I. Maudlin ◽  
S. C. Welburn ◽  
P. J. M. Milligan
Keyword(s):  
Salivary Gland ◽  
Salivary Glands ◽  
Trypanosoma Brucei ◽  
Glossina Morsitans Morsitans ◽  
Trypanosoma Congolense ◽  
Vectorial Capacity ◽  
Trypanosome Infection ◽  
Trypanosoma Brucei Rhodesiense ◽  
Glossina Morsitans ◽  
Differential Effects

SummaryThe effect of trypanosome infection on vector survival was observed in a line of Glossina morsitans morsitans selected for susceptibility to trypanosome infection. The differential effects of midgut and salivary gland infections on survival were examined by exposing flies to infection with either Trypanosoma congolense which colonizes midgut and mouthparts or Trypanosoma brucei rhodesiense which colonizes midgut and salivary glands. A comparison of the survival distributions of uninfected flies with those exposed to infection showed that salivary gland infection significantly reduces tsetse survival; midgut infection had little or no effect on the survival of tsetse. The significance of these findings is discussed in relation to the vectorial capacity of wild flies.

Trypanosome sociology and antigenic variation

Parasitology ◽  
1989 ◽  
Vol 99 (S1) ◽  
pp. S37-S47 ◽  
Author(s):  
K. Vickerman
Keyword(s):  
Trypanosoma Brucei ◽  
Antigenic Variation ◽  
Growth Characteristics ◽  
Tsetse Fly ◽  
Antigenic Specificity ◽  
Surface Coat ◽  
Humoral Immune ◽  
Variable Antigen ◽  
Minority Variants ◽  
Stimulation Of

SUMMARYSurvival of the trypanosome (Trypanosoma brucei) population in the mammalian body depends upon paced stimulation of the host's humoral immune response by different antigenic variants and serial sacrifice of the dominant variant (homotype) so that minority variants (heterotypes) can continue the infection and each become a homotype in its turn. New variants are generated by a spontaneous switch in gene expression so that the trypanosome puts on a surface coat of a glycoprotein differing in antigenic specificity from its predecessor. Homotypes appear in a characteristic order for a given trypanosome clone but what determines this order and the pacing of homotype generation so that the trypanosome does not quickly exhaust its repertoire of variable antigens, is not clear. The tendency of some genes to be expressed more frequently than others may reflect the location within the genome and mode of expression of the genes concerned and may influence homotype succession. Differences in the doubling time of different variants or in the rate at which trypanosomes belonging to a particular variant differentiate into non-dividing (vector infective) stumpy forms have also been invoked to explain how a heterotype's growth characteristics may determine when it becomes a homotype. Recent estimations of the frequency of variable antigen switching in trypanosome populations after transmission through the tsetse fly vector, however, suggest a much higher figure (0·97–2·2 × 10−3switches per cell per generation) than that obtained for syringe-passed infections (10−5–10−7switches per cell per generation) and it seems probable that most of the variable antigen genes are expressed as minority variable antigen types very early in the infection. Instability of expression is a feature of trypanosome clones derived from infective tsetse salivary gland (metacyclic) trypanosomes and it is suggested that high switching rates in tsetse-transmitted infections may delay the growth of certain variants to homotype status until later in the infection.

Infection of post-teneral tsetse flies (Glossina morsitans morsitans and Glossina morsitans centralis) with Trypanosoma brucei brucei

1988 ◽  
Vol 66 (6) ◽  
pp. 1289-1292 ◽  
Author(s):  
R. H. Gooding
Keyword(s):  
Trypanosoma Brucei ◽  
Significant Proportion ◽  
Glossina Morsitans Morsitans ◽  
Tsetse Flies ◽  
Glossina Morsitans ◽  
Trypanosoma Brucei Brucei ◽  
Male And Female ◽  
Glossina Morsitans Centralis

A significant proportion of post-teneral male Glossina morsitans morsitans Westwood and post-teneral male and female Glossina morsitans centralis Machado develop mature infections of Trypanosoma brucei brucei Plimmer and Bradford without being starved before feeding upon infected rabbits.

Sleeping Sickness: In vitro Cultivation of Trypanosoma brucei from the Salivary Glands of Glossina morsitans

1978 ◽  
Vol 64 (6) ◽  
pp. 1039 ◽  
Author(s):  
M. Nyindo ◽  
M. Chimtawi ◽  
J. Owor ◽  
J. S. Kaminjolo ◽  
N. Patel ◽  
...  
Keyword(s):  
Salivary Glands ◽  
Trypanosoma Brucei ◽  
Sleeping Sickness ◽  
In Vitro Cultivation ◽  
Glossina Morsitans

scholarly journals Oxidative Phosphorylation Is Required for Powering Motility and Development of the Sleeping Sickness Parasite Trypanosoma brucei in the Tsetse Fly Vector

mBio ◽  
2022 ◽  
Author(s):  
Caroline E. Dewar ◽  
Aitor Casas-Sanchez ◽  
Constentin Dieme ◽  
Aline Crouzols ◽  
Lee R. Haines ◽  
...  
Keyword(s):  
Oxidative Phosphorylation ◽  
Salivary Glands ◽  
Trypanosoma Brucei ◽  
Blood Meal ◽  
Sleeping Sickness ◽  
Tsetse Fly ◽  
Tsetse Flies ◽  
African Trypanosomes ◽  
Complex Development

African trypanosomes cause disease in humans and their livestock and are transmitted by tsetse flies. The insect ingests these parasites with its blood meal, but to be transmitted to another mammal, the trypanosome must undergo complex development within the tsetse fly and migrate from the insect's gut to its salivary glands.

The effects of genetic exchange on variable antigen expression in Trypanosoma brucei

Parasitology ◽  
1991 ◽  
Vol 103 (3) ◽  
pp. 379-386 ◽  
Author(s):  
C. M. R. Turner ◽  
N. Aslam ◽  
E. Smith ◽  
N. Buchanan ◽  
A. Tait
Keyword(s):  
Trypanosoma Brucei ◽  
Antigen Expression ◽  
Genetic Exchange ◽  
Direct Immunofluorescence ◽  
Tsetse Flies ◽  
Double Labelling ◽  
Hybrid Progeny ◽  
Parental Stock ◽  
Variable Antigen ◽  
Antibody Specificities

The inheritance of variant surface antigens in Trypanosoma brucei has been determined by identifying variable antigen types (VATs) in each of two cloned parental stocks and then examining the presence and abundance of these VATs in hybrid progeny produced when these stocks undergo genetic exchange during co-transmission through tsetse flies. Nine VATs have been identified from the repertoire of the parental stock STIB 247L and 5 VATs have been identified from the parental stock STIB 386AA; the identified VATs were exclusive to each stock. Their inheritance was elucidated using two assays. In the first, repertoire antisera (RAS) containing antibody specificities to many different VATs were raised in rabbits to the 2 parental stocks and 6 progeny clones. The presence of VAT-specific antibodies in these RAS was then determined by antibody-dependent complement-mediated lysis. In the second assay, the 2 parental stocks and 4 hybrid progeny clones were each independently transmitted through tsetse flies and VATs observed using VAT-specific antisera in indirect immunofluorescence of metacyclic trypanosomes and in bloodstream forms of fly-bitten mice. The results from both assays showed that (1) both metacyclic- and bloodstream-VATs were inherited into the progeny, (2) each hybrid progeny clone contained some VATs from both parents, (3) hybrids did not express all the VATs from either parent, (4) there was little apparent pattern as to which VATs had been inherited and which had not and (5) the VAT repertoires of the hybrid progeny appeared to be larger than those of the parents. In addition, two results indicated that control of VAT expression remains unaltered after genetic exchange. Firstly, the immunofluorescence results showed that VATs present in hybrid trypanosomes were expressed at the same stage during an infection and at approximately the same prevalence as in the parent. Secondly, a double-labelling experiment using direct immunofluorescence indicated that individual hybrid trypanosomes did not generally simultaneously express more than one VAT. Taken together, these results demonstrate that recombinant VAT repertoires are created when trypanosomes undergo genetic exchange and that genetic exchange is a mechanism whereby the generation of new serodemes can occur.

Antigenic variation in Trypanosoma brucei infections: an holistic view

1999 ◽  
Vol 112 (19) ◽  
pp. 3187-3192
Author(s):  
C.M. Turner
Keyword(s):  
Immune Responses ◽  
Trypanosoma Brucei ◽  
Antigenic Variation ◽  
Tsetse Fly ◽  
High Rate ◽  
T Helper 1 ◽  
Holistic View ◽  
Humoral Immune ◽  
Humoral Immune Responses ◽  
Variable Antigen

Trypanosoma brucei parasites undergo clonal phenotypic (antigenic) variation to promote their transmission between mammals and tsetse-fly vectors. This process is classically considered to be a mechanism for evading humoral immune responses, but such an explanation cannot account for the high rate of switching between variable antigens or for their hierarchical (i.e. non-random) expression. I suggest that these anomalies can be explained by a new model: that antigenic variation has evolved as a bifunctional, rather than as a unifunctional, strategy that not only evades humoral immune responses but also enables competition between parasite strains in concomitantly infected hosts. This competition causes a depression of cellular responses. My proposal gives rise to a number of testable predictions. First, low numbers of trypanosomes should express some variable antigen types (VATs) in infections several weeks before these VATs are detectable. Second, as an infection progresses, the number of VATs expressed simultaneously in the population should decrease. Third, immunisation to generate a T helper 1 response against those VATs that are expressed most frequently should lower parasitaemias and reduce virulence.

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