We use Drosophila melanogaster as our model host to investigate resistance and tolerance to infections.
Resistance & tolerance
Our main current research topic relates to host-pathogen interactions and strategies that a host can use to deal with its pathogens, those being resistance and tolerance (for a review please see Kutzer & Armitage 2016).
Pathogen control (resistance), is probably the more familiar of two defence strategies that a host can employ when it encounters a pathogen. It might be possible to avoid infection via behavioural or barrier defences (Cremer, Armitage & Schmid-Hempel 2007), but when this is not possible and a pathogen enters the host, the immune system fights against the pathogen. This can reduce the number of pathogens or can even clear the infection completely. A host infected by a lower number of pathogens is thought ot be more resistant than a host with more pathogens.
However, when the immune system is activated it can damage self-tissue and the immune system can also be costly to use. Therefore, in some ways, being more resistant is not necessarily better. This is where the second strategy, tolerance, comes into focus. Tolerance describes the ability of hosts to control the amount of damage that an infection causes by decreasing the damage or fitness loss caused by infection. Unlike resistance, tolerance does not negatively affect the pathogen’s fitness inside the host.
We tested the influence of diet (protein in the form of yeast) on resistance and tolerance in D. melanogaster during the acute phase of the infection, using two different bacterial species. We found that diet and the time after infection influenced variation in host tolerance (Kutzer & Armitage 2016b). We then extended this work to test whether there are genotypic differences in resistance and tolerance: we found considerable genetic variation in host resistance but fecundity tolerance was unaffected by genotype (Kutzer, Kurtz & Armitage 2018). We are building on this work to try to understand more about the evolution of resistance and tolerance and how immune priming (previous experience of a pathogen) affects both of these defence strategies.