Research article

Variant Surface Glycoprotein gene repertoires in Trypanosoma brucei have diverged to become strain-specific

O Clyde Hutchinson^1,3 , Kim Picozzi² , Nicola G Jones¹ , Helen Mott¹ , Reuben Sharma^1,4 , Susan C Welburn² and Mark Carrington¹

¹  Department of Biochemistry, 80 Tennis Court Road, Cambridge, CB2 1GA, UK

²  Centre for Tropical Veterinary Medicine, University of Edinburgh, Easter Bush Veterinary Centre, Roslin, Midlothian, EH25 9RG, UK

³  Institute of Zoology, Zoological Society of London, Regents Park, London, NW1 4RY, UK

⁴  Faculty of Veterinary Medicine, Universiti Putra Malaysia, 43400 UPM, Serdang, Selangor, Malaysia

author email corresponding author email

BMC Genomics 2007, 8:234doi:10.1186/1471-2164-8-234

Published:	13 July 2007

Abstract

Background

In a mammalian host, the cell surface of African trypanosomes is protected by a monolayer of a single variant surface glycoprotein (VSG). The VSG is central to antigenic variation; one VSG gene is expressed at any one time and there is a low frequency stochastic switch to expression of a different VSG gene. The genome of Trypanosoma brucei contains a repertoire of > 1000 VSG sequences. The degree of conservation of the genomic VSG repertoire in different strains has not been investigated in detail.

Results

Eighteen expressed VSGs from Ugandan isolates were compared with homologues (> 40 % sequence identity) in the two available T. brucei genome sequences. Fourteen homologues were present in the genome of Trypanosoma brucei brucei TREU927 from Kenya and fourteen in the genome of T. b. gambiense Dal972 from Cote d'Ivoire. The Ugandan VSGs averaged 71% and 73 % identity to homologues in T. b. brucei and T. b. gambiense respectively. The sequence divergence between homologous VSGs from the three different strains was not random but was more prevalent in the parts of the VSG believed to interact with the host immune system on the living trypanosome.

Conclusion

It is probable that the VSG repertoires in the different isolates contain many common VSG genes. The location of divergence between VSGs is consistent with selection for strain-specific VSG repertoires, possibly to allow superinfection of an animal by a second strain. A consequence of strain-specific VSG repertoires is that any vaccine based on large numbers of VSGs from a single strain will only provide partial protection against other strains.