Why do males and females vary in their responses to pathogen attacks?
Sex and infection are intimately linked. Many diseases are spread by sexual contact, males are thought to evolve exaggerated sexual signals to demonstrate their immune robustness, and pathogens have been shown to direct the evolution of recombination. Here, however, infection is influencing the evolution of male and female fitness and less is known about how sex differences influence pathogen fitness.
How does sexual dimorphism influence the evolution and epidemiology of infectious disease?
Does the genetic architecture of dimorphism play into host-pathogen coevolution?
MD Hall and N Mideo. 2019. Linking sex differences to the evolution of infectious disease life-histories. Philosophical transactions B, 373 20170431.
SAY Gipson and MD Hall. 2016. The evolution of sexual dimorphism and its potential impact on host–pathogen coevolution. Evolution 70 (5): 959–968.
SAY Gipson and Hall, MD. Interactions between host sex and age of exposure modify the virulence transmission trade-off. Journal of Evolutionary Biology, 31 (3): 428-437.
Females and males have conflicting evolutionary interests. Selection favours the evolution of different phenotypes within each sex, yet divergence between the sexes is constrained by the shared genetic basis of female and male traits. How this process plays out in a changing environment, such as one under constant pathogen threat, remains largely unknown.
How common should antagonism be in a changing environment?
What are the consequences of sexual antagonism for population persistence?
T Connallon and MD Hall. 2016. Genetic correlations and sex‐specific adaptation in changing environments. Evolution 70(10): 2186–2198.
T Connallon and MD Hall. 2018. Genetic constraints on adaptation: a theoretical primer for the genomics era. Annals of the New York Academy of Sciences, 1422 (1): 65-87.
T Connallon and MD Hall. 2019. Environmental Changes and Sexually Antagonistic Selection. In: eLS. John Wiley & Sons, Ltd: Chichester. DOI: 10.1002/9780470015902.a0028171
The onset of infectious disease depends on a series of events, beginning with the initial encounter between a host and parasite, through to the activation of the host immune system and the exploitation of host resources. This stepwise architecture has an important influence on how we might expect disease and host-pathogen interactions to evolve.
How does an the individual components of the infection process shape the overall evolution of disease?
What are the relative contributions of qualitative and quantitative resistance loci to outcome of host-pathogen interactions?
MD Hall, G Bento and D Ebert. 2017. The evolutionary consequences of stepwise infection processes. Trends in Ecology & Evolution, in press.
Hall, M.D. & Ebert, D. (2013) The genetics of infectious disease susceptibility: has the evidence for epistasis been overestimated? BMC Biology, 11: 79.
Upcoming: Hall, M.D. & Ebert, D. Contrasting the genetic architecture of qualitative and quantitative resistance.