Trypanosome sociology and antigenic variation
- PMID: 2682484
- DOI: 10.1017/s0031182000083402
Trypanosome sociology and antigenic variation
Abstract
Survival of the trypanosome (Trypanosoma brucei) population in the mammalian body depends upon paced stimulation of the host's humoral immune response by different antigenic variants and serial sacrifice of the dominant variant (homotype) so that minority variants (heterotypes) can continue the infection and each become a homotype in its turn. New variants are generated by a spontaneous switch in gene expression so that the trypanosome puts on a surface coat of a glycoprotein differing in antigenic specificity from its predecessor. Homotypes appear in a characteristic order for a given trypanosome clone but what determines this order and the pacing of homotype generation so that the trypanosome does not quickly exhaust its repertoire of variable antigens, is not clear. The tendency of some genes to be expressed more frequently than others may reflect the location within the genome and mode of expression of the genes concerned and may influence homotype succession. Differences in the doubling time of different variants or in the rate at which trypanosomes belonging to a particular variant differentiate into non-dividing (vector infective) stumpy forms have also been invoked to explain how a heterotype's growth characteristics may determine when it becomes a homotype. Recent estimations of the frequency of variable antigen switching in trypanosome populations after transmission through the tsetse fly vector, however, suggest a much higher figure (0.97-2.2 x 10(-3) switches per cell per generation) than that obtained for syringe-passed infections (10(-5)-10(-7) switches per cell per generation) and it seems probable that most of the variable antigen genes are expressed as minority variable antigen types very early in the infection. Instability of expression is a feature of trypanosome clones derived from infective tsetse salivary gland (metacyclic) trypanosomes and it is suggested that high switching rates in tsetse-transmitted infections may delay the growth of certain variants to homotype status until later in the infection.
Similar articles
-
A Host-Pathogen Interaction Reduced to First Principles: Antigenic Variation in T. brucei.Results Probl Cell Differ. 2015;57:23-46. doi: 10.1007/978-3-319-20819-0_2. Results Probl Cell Differ. 2015. PMID: 26537376 Review.
-
Antigenic variation in trypanosomes: enhanced phenotypic variation in a eukaryotic parasite.Adv Parasitol. 2001;49:1-70. doi: 10.1016/s0065-308x(01)49037-3. Adv Parasitol. 2001. PMID: 11461029 Review.
-
Antigenic variation during the developmental cycle of Trypanosoma brucei.J Protozool. 1984 Feb;31(1):41-7. J Protozool. 1984. PMID: 6204043 Review.
-
Multiple mechanisms of immune evasion by African trypanosomes.Mol Biochem Parasitol. 1998 Mar 1;91(1):51-66. doi: 10.1016/s0166-6851(97)00209-0. Mol Biochem Parasitol. 1998. PMID: 9574925 Review.
-
High frequency of antigenic variation in Trypanosoma brucei rhodesiense infections.Parasitology. 1989 Aug;99 Pt 1:67-75. doi: 10.1017/s0031182000061035. Parasitology. 1989. PMID: 2797873
Cited by
-
Tissue spaces are reservoirs of antigenic diversity for Trypanosoma brucei.Nature. 2024 Dec;636(8042):430-437. doi: 10.1038/s41586-024-08151-z. Epub 2024 Oct 30. Nature. 2024. PMID: 39478231 Free PMC article.
-
Antigenic variation in vector-borne pathogens.Emerg Infect Dis. 2000 Sep-Oct;6(5):449-57. doi: 10.3201/eid0605.000502. Emerg Infect Dis. 2000. PMID: 10998374 Free PMC article. Review.
-
Maintainence of parasitaemia - is it to die for?Kinetoplastid Biol Dis. 2003 Jun 24;2(1):2. doi: 10.1186/1475-9292-2-2. Kinetoplastid Biol Dis. 2003. PMID: 12869207 Free PMC article.
-
Suramin exposure alters cellular metabolism and mitochondrial energy production in African trypanosomes.J Biol Chem. 2020 Jun 12;295(24):8331-8347. doi: 10.1074/jbc.RA120.012355. Epub 2020 Apr 30. J Biol Chem. 2020. PMID: 32354742 Free PMC article.
-
T. brucei infection reduces B lymphopoiesis in bone marrow and truncates compensatory splenic lymphopoiesis through transitional B-cell apoptosis.PLoS Pathog. 2011 Jun;7(6):e1002089. doi: 10.1371/journal.ppat.1002089. Epub 2011 Jun 30. PLoS Pathog. 2011. PMID: 21738467 Free PMC article.