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Within host selection for faster replicating bacterial symbionts

Publication . Chrostek, Ewa; Teixeira, Luis

Wolbachia is a widespread, intracellular symbiont of arthropods, able to induce reproductive distortions and antiviral protection in insects. Wolbachia can also be pathogenic, as is the case with wMelPop, a virulent variant of the endosymbiont of Drosophila melanogaster. An extensive genomic amplification of the 20kb region encompassing eight Wolbachia genes, called Octomom, is responsible for wMelPop virulence. The Octomom copy number in wMelPop can be highly variable between individual D. melanogaster flies, even when comparing siblings arising from a single female. Moreover, Octomom copy number can change rapidly between generations. These data suggest an intra-host variability in Octomom copy number between Wolbachia cells. Since wMelPop Wolbachia with different Octomom copy numbers grow at different rates, we hypothesized that selection could act on this intra-host variability. Here we tested if total Octomom copy number changes during the lifespan of individual Drosophila hosts, revealing selection for different Wolbachia populations. We performed a time course analysis of Octomom amplification in flies whose mothers were controlled for Octomom copy number. We show that despite the Octomom copy number being relatively stable it increases slightly throughout D. melanogaster adult life. This indicates that there is selection acting on the intra-host variation in the Octomom copy number over the lifespan of individual hosts. This within host selection for faster replicating bacterial symbionts may be in conflict with between host selection against highly pathogenic Wolbachia.

2018-01-18Journal article

Open access

Disease tolerance and immunity in host protection against infection

Publication . Soares, Miguel P.; Teixeira, Luis; Moita, Luis F.

The immune system probably evolved to limit the negative effects exerted by pathogens on host homeostasis. This defence strategy relies on the concerted action of innate and adaptive components of the immune system, which sense and target pathogens for containment, destruction or expulsion. Resistance to infection refers to these immune functions, which reduce the pathogen load of an infected host as the means to preserve homeostasis. Immune-driven resistance to infection is coupled to an additional, and arguably as important, defence strategy that limits the extent of dysfunction imposed on host parenchymal tissues during infection, without exerting a direct negative effect on pathogens. This defence strategy, known as disease tolerance, relies on tissue damage control mechanisms that prevent the deleterious effects of pathogens and that uncouples immune-driven resistance mechanisms from immunopathology and disease. In this Review, we provide a unifying view of resistance and disease tolerance in the framework of immunity to infection.

2017-02Journal article

Open access