An improved Trypanosoma vivax genome assembly confirms the distinct organisation of its variant antigen repertoire
- 1Institute of Infection, Veterinary and Ecological Sciences, University of Liverpool
Abstract
Trypanosoma vivax is a unicellular parasite spread by biting flies and an important livestock pathogen across sub-Saharan Africa and South America. Alongside its better known relative, T. brucei, it causes animal trypanosomosis. An accurate genome sequence is essential to functional genetics as well as the design of novel diagnostics, drugs and vaccines. However, the existing T. vivax genome sequence is fragmentary, making it difficult to examine genomic features such as the Variant Surface Glycoprotein (VSG) genes that are the basis for antigenic variation, a key phenotype that underpins immune evasion by African trypanosomes. Our aim was to produce a T. vivax genome sequence with improved contiguity to properly characterise the VSG genes. We present a new core genome assembly in 23 scaffolds, forming approximately 10 chromosomes. Many scaffolds are articulated with extensive sub-telomeric domains that, like T. brucei, contain VSG gene arrays but in T. vivax these are near-perfect repeats of intact genes. Using transcriptomic and proteomic analysis of VSG expression during bloodstream infection we show that the active VSG is expressed from a sub-telomeric array while other arrays are silent. We find no evidence for a VSG expression site at the telomeres or elsewhere. Therefore, although monoallelic expression and antigenic switching occur in T. vivax, the familiar regulatory mechanism of T. brucei does not exist in T. vivax. This improved T. vivax genome assembly demonstrates that T. brucei is a poor guide for T. vivax genetics generally and for regulation of antigenic variation specifically.
Related
- NuSAP1 promotes spindle assembly in Trypanosoma brucei by bundling spindle microtubules
- Selective Nerve Block of A- or C-Afferents Confirms Dual Role in Touch Pleasantness but Not Touch-Pain Modulation
- Distinct profiles and antibody production by splenic and lymph node antibody-secreting cells in Trypanosoma cruzi infection
- Transformations de l’agriculture : structures d’exploitation, organisation du travail et dynamiques socio-professionnelles
- Computational identification of responding T cell clones from longitudinal repertoire sequencing
BibTeX
@misc{jackson2026improved,
title = {{An improved Trypanosoma vivax genome assembly confirms the distinct organisation of its variant antigen repertoire}},
author = {A. P. Jackson and R. Young and M. A. Whitehead and P. C. Steketee and A. Darby and L. J. Morrison},
howpublished = {bioRxiv},
year = {2026},
month = oct,
doi = {10.64898/2026.10.08.757617},
url = {https://www.biorxiv.org/content/10.64898/2026.10.08.757617v1},
note = {CC BY},
}
RIS
TY - UNPB
TI - An improved Trypanosoma vivax genome assembly confirms the distinct organisation of its variant antigen repertoire
AU - A. P. Jackson
AU - R. Young
AU - M. A. Whitehead
AU - P. C. Steketee
AU - A. Darby
AU - L. J. Morrison
PY - 2026
DA - 2026/10/08
PB - bioRxiv
DO - 10.64898/2026.10.08.757617
UR - https://www.biorxiv.org/content/10.64898/2026.10.08.757617v1
AB - Trypanosoma vivax is a unicellular parasite spread by biting flies and an important livestock pathogen across sub-Saharan Africa and South America. Alongside its better known relative, T. brucei, it causes animal trypanosomosis. An accurate genome sequence is essential to functional genetics as well as the design of novel diagnostics, drugs and vaccines. However, the existing T. vivax genome sequence is fragmentary, making it difficult to examine genomic features such as the Variant Surface Glycoprotein (VSG) genes that are the basis for antigenic variation, a key phenotype that underpins immune evasion by African trypanosomes. Our aim was to produce a T. vivax genome sequence with improved contiguity to properly characterise the VSG genes. We present a new core genome assembly in 23 scaffolds, forming approximately 10 chromosomes. Many scaffolds are articulated with extensive sub-telomeric domains that, like T. brucei, contain VSG gene arrays but in T. vivax these are near-perfect repeats of intact genes. Using transcriptomic and proteomic analysis of VSG expression during bloodstream infection we show that the active VSG is expressed from a sub-telomeric array while other arrays are silent. We find no evidence for a VSG expression site at the telomeres or elsewhere. Therefore, although monoallelic expression and antigenic switching occur in T. vivax, the familiar regulatory mechanism of T. brucei does not exist in T. vivax. This improved T. vivax genome assembly demonstrates that T. brucei is a poor guide for T. vivax genetics generally and for regulation of antigenic variation specifically.
ER -