Luikart, G. | Search bioRxiv

bioRxiv2020

Natural resistance to worms exacerbates bovine tuberculosis severity independently of worm coinfection

Pathogen interactions arising during coinfection can exacerbate disease severity, for example, when the immune response mounted against one pathogen negatively affects defense of another. It is also possible that host immune responses to a pathogen shaped by historical evolutionary interactions between host and pathogen, may modify host immune defenses in ways that have repercussions for other pathogens. In this case, negative interactions between two pathogens could emerge even in the absence of concurrent infection. Parasitic worms and tuberculosis (TB) are involved in one of the most geographically extensive of pathogen interactions, and during coinfection, worms can exacerbate TB disease outcomes. Here, we show that in a wild mammal, natural resistance to worms affects bovine tuberculosis (BTB) severity independently of active worm infection. We found that worm-resistant individuals were more likely to die of BTB than were non-resistant individuals, and their disease progressed more quickly. Anthelmintic treatment moderated, but did not eliminate, the resistance effect, and the effects of resistance and treatment were additive with untreated, resistant individuals experiencing the highest mortality. Interestingly, resistance and anthelmintic treatment had non-overlapping effects on BTB pathology. The effects of resistance manifested in the lungs (the primary site of BTB infection), while the effects of treatment manifested almost entirely in the lymph nodes (the site of disseminated disease), suggesting that resistance and active worm infection affect BTB progression via distinct mechanisms. Our findings reveal that interactions between pathogens can occur as a consequence of processes arising on very different timescales.

ecology↗

bioRxiv2019

The genomic architecture of fitness is a major driver of population viability during rapid environmental change

AO_SCPLOWBSTRACTC_SCPLOWThe rapid global loss of biodiversity calls for improved predictions of how populations will evolve and respond demographically to ongoing environmental change. The heritability (h2) of selected traits has long been known to affect evolutionary and demographic responses to environmental change. However, effects of the genetic architecture underlying the h2 of a selected trait on population responses to selection are less well understood. We use deterministic models and stochastic simulations to show that the genetic architecture underlying h2 can dramatically affect population viability during environmental change. Polygenic trait architectures (many loci, each with a small phenotypic effect) conferred higher population viability than genetic architectures with the same initial h2 and large-effect loci under a wide range of scenarios. Population viability also depended strongly on the initial frequency of large-effect beneficial alleles, with moderately low initial allele frequencies conferring higher viability than rare or already-frequent large-effect alleles. Greater population viability associated with polygenic architectures appears to be due to higher short term evolutionary potential compared to architectures with large-effect loci. These results suggest that integrating information on the trait genetic architecture into quantitiative genetic and population viability analysis will substantially improve our understanding and prediction of evolutionary and demographic responses following environmental change.

evolutionary biology↗