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Hoang, K. L.

Publications and source records attributed to Hoang, K. L..

3 recordsLinked to original sources

Rising temperatures favour parasite virulence and parallel molecular evolution following a host jump

Climate change is facilitating the poleward emergence of parasites, increasing the risk of jumping into new animal species, including humans. Whether more virulent or transmissible variants will spread during these climate-driven outbreaks is unclear. We experimentally evolved a wild parasitic bacterium, across the thermal range (20-30{degrees}C) and extremes (35{degrees}C) of Cape Verde - the site of field collection - in a novel, temperate animal host. At the parasites typical warm environmental temperature, we found that virulence escalated across evolutionary time. Parasites evolved at hot temperatures, towards the limit of host-parasite survival, displayed a cryptic virulence boost, deadlier once infecting animals at cooler temperatures. Patterns of molecular evolution were constrained to parallel changes in fewer loci at extreme temperatures. Our findings suggest that rising temperatures will leave predictable phenotypic and genomic signatures on evolving parasites as they emerge with climate change.

evolutionary biology↗

Incomplete immunity in a natural animal-microbiota interaction boosts pathogen virulence

Strong partial immunity in recovered hosts is predicted to favour more virulent pathogens upon re-infection in the population. We present empirical evidence that the incomplete immunity generated by commensal host microbiota can similarly select for higher pathogen virulence. We tracked the evolutionary trajectories of a widespread pathogen (Pseudomonas aeruginosa) experimentally passaged through populations of nematode hosts which had been immune-primed by a natural commensal. Immune protection selected for pathogens more than twice as likely to kill the nematode as those evolved in non-primed or immune-compromised animals. Despite the higher virulence that emerged, pathogen molecular evolution in immune-primed hosts was slower and more constrained compared to evolution in immune-compromised hosts, where substantial genetic differentiation was exhibited. These findings directly attribute the partial protective immunity provided by host-microbiome interactions as a significant selective force shaping the virulence and evolutionary dynamics of novel infectious diseases.

evolutionary biology↗

How symbiosis and ecological context influence the variable expression of transgenerational wing induction upon fungal infection of aphids

Aphids, like most animals, mount a diverse set of defenses against pathogens. For aphids, two of the best studied defenses are symbiont-conferred protection and transgenerational wing induction. Aphids can harbor bacterial symbionts that provide protection against pathogens, parasitoids and predators, as well as against other environmental stressors. In response to signals of danger, aphids also protect not themselves but their offspring by producing more winged than unwinged offspring as a way to ensure that their progeny may be able to escape deteriorating conditions. Such transgenerational wing induction has been studied most commonly as a response to overcrowding of host plants and presence of predators, but recent evidence suggests that pea aphids (Acyrthosiphon pisum) may also begin to produce a greater proportion of winged offspring when infected with fungal pathogens. Here, we explore this phenomenon further by asking how protective symbionts, pathogen dosage and environmental conditions influence this response. Overall, while we find some evidence that protective symbionts can modulate transgenerational wing induction in response to fungal pathogens, we observe that transgenerational wing induction in response to fungal infection is highly variable. That variability cannot be explained entirely by symbiont association, by pathogen load or by environmental stress, leaving the possibility that a complex interplay of genotypic and environmental factors may together influence this trait.

evolutionary biology↗