Abstract
Infectious diseases are recognised as one of the greatest global threats
to biodiversity and ecosystem functioning. Consequently, there is a
growing urgency to understand the speed at which adaptive phenotypes can
evolve and spread in natural populations to inform future management.
Here we provide evidence of rapid genomic changes in wild Australian
blacklip abalone (Haliotis rubra ) following a major population
crash associated with an infectious disease. A genome wide association
study on H. rubra was conducted using pooled whole genome
re-sequencing data from commercial fishing stocks varying in historical
exposure to haliotid herpesvirus-1 (HaHV-1). Approximately 25,000 SNP
loci associated with virus exposure were identified, many of which
mapped to genes known to contribute to HaHV-1 immunity in the New
Zealand pāua (H. iris ) and herpesvirus response pathways in
haliotids and other animal systems. These findings indicate genetic
changes across a single generation in H. rubra fishing stocks
decimated by HaHV-1, with stock recovery determined by rapid
evolutionary changes leading to virus resistance. This is a novel
example of rapid adaptation in natural populations of a non-model marine
organism, highlighting the pace at which selection can potentially act
to counter disease in wildlife communities.