ArticleScientific reports2018
Faster growth with shorter antigens can explain a VSG hierarchy during African trypanosome infections: a feint attack by parasites.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Article
- Competition among variants is predictable and contributes to the antigenic variation dynamics of African trypanosomes.PLoS pathogens · 2023Article
- Genetic and immunological basis of human African trypanosomiasis.Current opinion in immunology · 2021Review
- VSG mRNA levels are regulated by the production of functional VSG protein.Molecular and biochemical parasitology · 2021Article
- Transgenic functional complementation with a transmission -associated protein restores spirochete infectivity by tick bite.Ticks and tick-borne diseases · 2020Article
- Variant antigen diversity in Trypanosoma vivax is not driven by recombination.Nature communications · 2020Article
- Developmental competence and antigen switch frequency can be uncoupled inProceedings of the National Academy of Sciences of the United States of America · 2019Article
- Evolution of Antigenic Variation in African Trypanosomes: Variant Surface Glycoprotein Expression, Structure, and Function.BioEssays : news and reviews in molecular, cellular and developmental biology · 2018Review
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
The parasitic African trypanosome, Trypanosoma brucei, evades the adaptive host immune response by a process of antigenic variation that involves the clonal switching of variant surface glycoproteins (VSGs). The VSGs that come to dominate in vivo during an infection are not entirely random, but display a hierarchical order. How this arises is not fully understood. Combining available genetic data with mathematical modelling, we report a VSG-length-dependent hierarchical timing of clonal VSG dominance in a mouse model, consistent with an inverse correlation between VSG length and trypanosome growth-rate. Our analyses indicate that, among parasites switching to new VSGs, those expressing shorter VSGs preferentially accumulate to a detectable level that is sufficient to trigger a targeted immune response. This may be due to the increased metabolic cost of producing longer VSGs. Subsequent elimination of faster-growing parasites then allows slower-growing parasites with longer VSGs to accumulate. This interaction between the host and parasite is able to explain the temporal distribution of VSGs observed in vivo. Thus, our findings reveal a length-dependent hierarchy that operates during T. brucei infection. This represents a 'feint attack' diversion tactic utilised by these persistent parasites to out-maneuver the host adaptive immune system.
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Registered trials
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