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Lejon, V.

Publications and source records attributed to Lejon, V..

3 recordsLinked to original sources

Targets of the human antibody response to the variant surface glycoprotein of Trypanosoma brucei

Human African Trypanosomiasis (HAT) is a severe disease endemic to Sub-Saharan Africa caused by the parasite Trypanosoma brucei. Diagnosis of the chronic form of HAT relies heavily on serological screening tests that detect specific antibodies. Trypanosoma brucei parasites rely on the antigenic variation of their variant surface glycoproteins (VSG) to evade host antibody recognition. Although VSG is the primary target of host antibodies, studies of the antibody response to VSG have been limited by low-throughput approaches that allow for the analysis of only a few VSG proteins at a time, primarily in animal models. Here, we use phage immunoprecipitation sequencing (PhIP-seq) to characterize the antibody response to VSG in HAT patient serum. Using a comprehensive T7 bacteriophage display library containing peptides representing 12,108 unique T. brucei VSGs, our analysis revealed significant differences in the anti-VSG antibody between the acute and chronic forms of HAT. Our results show that, in chronic HAT, the top lobe of the VSG is the primary interface of antibody interactions. By characterizing the targets of anti-VSG immunity, we also identified a potential bias in the CATT, the most common test used for HAT screening. Finally, we were able to identify sets of seroprevalent VSG peptides for each form of the disease that successfully distinguish between infected and uninfected individuals. Our results demonstrate the utility of characterizing host antibody responses against African trypanosomes, which can reveal unique features of parasite biology while also uncovering new diagnostic targets.

microbiology↗

Variant surface glycoprotein expression in human African trypanosomiasis patients

Trypanosoma brucei gambiense is the primary causative agent of human African trypanosomiasis (HAT), a vector-borne disease endemic to West and Central Africa. The extracellular parasite evades antibody recognition within the host bloodstream by altering its Variant Surface Glycoprotein (VSG) coat through a process of antigenic variation. The serological tests which are widely used to screen for HAT use VSG as one of the target antigens. However, the VSGs expressed during human infection have not been characterized. Here we use VSG-seq to analyze the VSGs expressed in the blood of patients infected with T. b. gambiense and compared them to VSG expression in T. b. rhodesiense infections in humans as well as T. b. brucei infections in mice. The 44 VSGs expressed during T. b. gambiense infection revealed a striking bias towards expression of type B N-termini (82% of detected VSGs). This bias is specific to T. b. gambiense, which is unique among T. brucei subspecies in its chronic clinical presentation and anthroponotic nature, pointing towards a potential link between VSG expression and pathogenesis. The expressed T. b. gambiense VSGs also share very little similarity to sequences from 36 T. b. gambiense whole genome sequencing datasets, particularly in areas of the VSG protein exposed to host antibodies, suggesting that wild T. brucei VSG repertoires vary more than previously expected. Overall, this work demonstrates new features of antigenic variation in T. brucei gambiense and highlights the importance of understanding VSG repertoires in nature. Significance StatementHuman African Trypanosomiasis is a neglected tropical disease primarily caused by the extracellular parasite Trypanosoma brucei gambiense. To avoid elimination by the host, these parasites repeatedly replace their Variant Surface Glycoprotein (VSG) coat. Despite the important role of VSGs in prolonging infection, VSG expression during human infections is poorly understood. A better understanding of natural VSG gene expression dynamics can clarify the mechanisms that T. brucei uses to alter its VSG coat and improve trypanosomiasis diagnosis in humans. We analyzed the expressed VSGs detected in the blood of patients with trypanosomiasis. Our findings indicate that there are features of antigenic variation unique to human-infective T. brucei subspecies and VSGs expressed in natural infection may vary more than previously expected.

microbiology↗

Genomic evidence for population specific selection in Nilo-Saharan and Niger-Congo linguistic groups in Africa

BackgroundThere are over 2000 genetically diverse ethno-linguistic groups in Africa that could help decipher human evolutionary history and the genetic basis of phenotypic variation. We have sequenced 300 genomes from Niger-Congo populations from six sub-Saharan African countries (Uganda, Democratic Republic of Congo, Cameroon, Zambia, Ivory Coast, Guinea) and a Nilo-Saharan population from Uganda. Of these, we analysed 289 samples for population structure, genetic admixture, population history and signatures of selection. These samples were collected as part of the TrypanoGEN consortium project [1].\n\nResultsThe population genetic structure of the 289 individuals revealed four clusters, which correlated with ethno-linguistic group and geographical latitude. These were the West African Niger-Congo A, Central African Niger-Congo B, East African Niger-Congo B and the Nilo-Saharan. We observed a spatial distribution of positive natural selection signatures in genes previously associated with AIDS, Tuberculosis, Malaria and Human African Trypanosomiasis among the TrypanoGEN samples. Having observed a marked difference between the Nilo-Saharan Lugbara and Niger-Congo populations, we identified four genes (APOBEC3G, TOP2B, CAPN9, LANCL2), which are highly differentiated between the two ethnic groups and under positive selection in the Lugbara population (_iHS -log p > 3.0, Rsb -log p > 3.0, Fst > 0.1 bonferroni p > 1.8x10e4).\n\nConclusionThe signatures that differentiate ethnically distinct populations could provide information on the specific ecological adaptations with respect to disease history and susceptibility/resistance. For instance in this study we identified APOBEC3G which is believed to be involved in the susceptibility of the Nilo-Saharan Lugbara population to Hepatitis B virus infection.

genomics↗