Abstract

Tsetse flies transmit the disease African trypanosomosis, which affects humans and cattle. The control of tsetse flies via the sterile insect technique (SIT) requires mass production of the target tsetse species. This mass production can however be severely hindered by infections with the Glossina pallidipes salivary gland hypertrophy virus (GpSGHV; Hytrosaviridae). Although GpSGHV asymptomatically infects many Glossina species, it is in reared G. pallidipes that symptomatic infections may occur, characterized by the salivary gland hypertrophy (SGH) syndrome, and cause reproductive dysfunctions, leading to colony collapse. GpSGHV can be vertically transmitted to the offspring, as well as horizontally during the in vitro blood feeding technique in mass rearing facilities. The aim of this PhD research was to determine the mechanisms that trigger the occurrence of symptomatic GpSGHV infections in tsetse colonies. This thesis has first explored how the genetics and ecology of SGHVs and their hosts may have influenced the evolution, pathogenesis and transmission modes of these viruses. Secondly, experiments were designed to determine the GpSGHV prevalence and diversity in different tsetse species, both under field and laboratory settings, and to investigate how GpSGHV is able to evade tsetse immune surveillance to induce SGH outbreaks in colonized G. pallidipes. Altogether, these findings provide insights into the precautions to be taken during the establishment of new tsetse colonies in order to prevent SGH outbreaks, particularly in places where multiple Glossina species are mass produced. These data are a milestone in the implementation of SIT-mediated control of tsetse and trypanosomosis in sub-Saharan Africa.

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