Abstract
African trypanosomes are single-celled protozoan parasites that are capable of long-term survival while living extracellularly in the bloodstream and tissues of mammalian hosts. Prolonged infections are possible because trypanosomes undergo antigenic variation—the expression of a large repertoire of antigenically distinct surface coats, which allows the parasite population to evade antibody-mediated elimination. The mechanisms by which antigen genes become activated influence their order of expression, most likely by influencing the frequency of productive antigen switching, which in turn is likely to contribute to infection chronicity. Superimposed upon antigen switching as a contributor to trypanosome infection dynamics is the density-dependent production of cell-cycle arrested parasite transmission stages, which limit the infection while ensuring parasite spread to new hosts via the bite of blood-feeding tsetse flies. Neither antigen switching nor developmental progression to transmission stages is driven by the host. However, the host can contribute to the infection dynamic through the selection of distinct antigen types, the influence of genetic susceptibility or trypanotolerance and the potential influence of host-dependent effects on parasite virulence, development of transmission stages and pathogenicity. In a zoonotic infection cycle where trypanosomes circulate within a range of host animal populations, and in some cases humans, there is considerable scope for a complex interplay between parasite immune evasion, transmission potential and host factors to govern the profile and outcome of infection.
Highlights
African trypanosomes are protozoan parasites of a range of mammalian hosts, infecting humans, livestock and wild animal reservoirs
Even though the variant surface glycoprotein (VSG) cataloguing is still incomplete, the T. brucei genome can contain more than 2000 VSG genes, of which the majority exist in transcriptionally silent subtelomeric arrays, a substantial fraction are found in aneuploid minichromosomes
As the assembly of VSG mosaics initiates and progresses independently in each infection, different hosts will be exposed to completely different antigen repertoires that would prevent any possibility of generating meaningful immunity to the infecting parasite population or to subsequent co-infecting trypanosome populations
Summary
African trypanosomes are protozoan parasites of a range of mammalian hosts, infecting humans, livestock and wild animal reservoirs. Thwarting adaptive host immunity allows trypanosomes to survive and establish chronic infections, enhancing transmission and dissemination They achieve this through an extreme capacity for antigenic variation, allowing the parasite population to evade host antibody responses for months to years (figure 1b). Strategies to achieve infection chronicity, and so increase their capacity for transmission, have become clear, revealing a complex interplay between the parasite’s strategies for immune evasion, their developmental control of transmission potential and the contributions of host immunity in a field setting where hosts can be continually exposed to trypanosome infections [8,9,10,11,12] The interactions between these different parasite and host components of the infection dynamic are likely to drive responses that shape the epidemiology and evolution of the infection over time and in different geographical settings. This review seeks to summarize how the different contributors to the trypanosome infection profile operate and interface to create a complex and finely balanced host–parasite interaction
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