I am a mathematical and computational biologist with a broad interest in evolutionary biology. I have worked on a diverse array of topics, including social evolution, host-pathogen (co)-evolution, and evolutionary conflict. Recently, my research focus has been on the evolution of infectious diseases. Pathogens adapt rapidly to drugs and vaccines and a better understanding of the evolutionary epidemiology of infectious diseases raises many theoretical challenges and has important public health applications. A brief synopsis of some recent research topics can be found below.

Pathogen adaptation in response to vaccination

One way in which pathogens resist vaccines is through immune evasion. In work with Nicole Mideo (Univ. of Toronto) and Lindi Wahl (Western Univ.), we suggested a strategy to overcome immune evasion is to create a ‘mosaic’ of immunity by vaccinating individuals against different epitopes (Evol. Lett. 2021). We provided a proof-of-concept that ‘mosaic’ vaccination can outperform conventional vaccination using a variety of public health metrics. Pathogens also resist vaccines through life-history changes, particularly to virulence. In work with Sylvain Gandon (CNRS), we studied the joint evolutionary dynamics of immune evasion and virulence (Nat. Ecol. Evol. 2022). Our analysis revealed the evolutionary dynamics depend upon the type of protections the vaccine provides.

Population structure and the evolution of multidrug resistance

Multidrug resistance (MDR) poses one of the greatest threats to modern medicine, yet our understanding of why (or why not) it emerges is limited. In work with Sylvain Gandon (CNRS), we blended approaches from population genetics and evolutionary epidemiology to understand the evolution of MDR in structured populations. We used our framework to explain both the transient and equilibrium patterns of MDR observed in Streptococcus pneumoniae surveillance genomic data, clarifying the role played by population structure (eLife 2021).

Evolution and demographic stochasticity

With Troy Day (Queen's Univ.), we developed a general framework for understanding the evolutionary role of demographic stochasticity (individual variation in birth and death rates). Our analysis revealed that in addition to the effect the mutation has upon population size, N, it is also necessary to consider the effect the mutation has upon the variance in per-capita growth rate, V: the trait minimizing the ratio V/N is stochastically favoured. We used this framework to show how demographic stochasticity affects the evolution of disparate biological phenomenon such as social behaviours (PLoS Comp. Biol. 2019) and sterility virulence (Evolution 2019).

Epigenetics and the evolution of pathogen virulence

Epigenetics refers to molecular mechanisms affecting the differential expression of genes in response to external conditions. In collaboration with Francisco Úbeda (Royal Holloway) and Geoff Wild (Western Univ.), we showed that pathogen epigenetic ‘memories’ of prior infections can favour the expression of greater virulence in infections transmitted same-sex rather than between-sexes (Nat. Comm. 2021). This provides an explanation for patterns of virulence observed in some childhood diseases (e.g., chickenpox, polio, measles).

Evolutionary conflict and adaptive phenotypic plasticity

Evolutionary conflict, or the opposing evolutionary interests that arise during interactions between two parties, can lead to both adaptive and maladaptive traits. In work with Troy Day (Queen's Univ.), we studied how evolutionary conflict is impacted by adaptive phenotypic plasticity (APP), in which one party responds to the actions of the other. We showed the conflict experienced by the party without APP is always reduced, whereas the party with APP can experience more, or less, conflict depending upon the circumstances. We applied this insight to explain how plasticity modulates sexual conflict (Nat. Ecol. Evol. 2017) and alters host-pathogen co-evolution (Proc. R. Soc. B 2015; Am. Nat. 2018).