The surface structure of trypanosomes in relation to their molecular phylogeny

• Published in: International journal for parasitology Vol. 31; no. 5-6; pp. 468 - 471
• Main Authors: Overath, Peter, Haag, Jochen, Lischke, Antje, O'hUigin, Colm
• Format: Journal Article Conference Proceeding
• Language: English
• Published: Oxford Elsevier Science 01.05.2001
• Subjects: Animals; Biological and medical sciences; Carps - parasitology; Evolution, Molecular; Fundamental and applied biological sciences. Psychology; Phylogeny; Protozoa; Systematics. Geographical distribution. Morphology. Cytology; Trypanosoma - genetics; Trypanosoma carassii; Trypanosoma cruzi; Trypanosoma cruzi - genetics; Variant Surface Glycoproteins, Trypanosoma - genetics; Variant Surface Glycoproteins, Trypanosoma - immunology; Kinetoplastida; Protozoa; Host parasite relation; Protozoal disease; Taxonomy; Interspecific comparison; Glycoprotein; Parasite; Parasitosis; Phylogeny; Cell surface; Infection; Trypanosomatidae; Mucin; Antigenic variation; Trypanosomiasis
• ISSN: 0020-7519
• DOI: 10.1016/S0020-7519(01)00152-7

Molecular phylogenetic analysis using genes coding for ribosomal RNA and proteins suggests that trypanosomes are monophyletic. Salivarian trypanosomes showing antigenic variation of the variant surface glycoprotein (VSG) diverged from non-Salivarian trypanosomes some 200-300 million years ago. Representatives of the non-Salivarian group, the mammalian parasite, Trypanosoma cruzi, and the fresh-water fish trypanosome, T. carassii, are characterised by surfaces dominated by carbohydrate-rich mucin-like glycoproteins, which are not subject to antigenetic variation. It is suggested that this latter surface structure is typical for non-Salivarian trypanosomes as well as members of the other Kinetoplastid suborder, the Bodonina. This would imply that at some point in time in the evolution of the Salivaria the highly abundant and comparatively poorly immunogenetic mucin-like molecules must have been replaced for equally abundant but highly immunogenic VSG-like molecules. While the selective advantage for such a unique transition is difficult to imagine, the subsequent diversification of VSG genes/molecules may have been comparatively straightforward because even the most limited form of antigenic variation would have extended the duration of infection in the vertebrate and thus would have increased the chance for transfer to the vector.