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Beaver, A. K.

Publications and source records attributed to Beaver, A. K..

2 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↗

DNA damage drives antigen diversification through mosaic VSG formation in Trypanosoma brucei

Antigenic variation, using large genomic repertoires of antigen-encoding genes, allows pathogens to evade host antibody. Many pathogens, including the African trypanosome Trypanosoma brucei, extend their antigenic repertoire through genomic diversification. While evidence suggests that T. brucei depends on the generation of new variant surface glycoprotein (VSG) genes to maintain a chronic infection, a lack of experimentally tractable tools for studying this process has obscured its underlying mechanisms. Here, we present a highly sensitive targeted sequencing approach for measuring VSG diversification. Using this method, we demonstrate that a Cas9-induced DNA double-strand break within the VSG coding sequence can induce VSG recombination with patterns identical to those observed during infection. These newly generated VSGs are antigenically distinct from parental clones and thus capable of facilitating immune evasion. Together, these results provide insight into the mechanisms of VSG diversification and an experimental framework for studying the evolution of antigen repertoires in pathogenic microbes.

microbiology↗