Samuel V. Hulse

The paper models how pathogens evolve transmission timing in relation to host life stages and phenology, finding that synchronized germination and flowering maximizes disease prevalence.

This study uses a coevolutionary model to show that pathogen evolution drives age-specific infection patterns, leading to reciprocal specialization in host resistance.

The paper develops a multi-locus model of disease resistance to explore how genetic architectures shape evolutionary trade-off functions and their implications for genetic polymorphisms.