Biology subjects

Visher, E.

Publications and source records attributed to Visher, E..

5 recordsLinked to original sources

bioRxiv2023

The direction of local adaptation on pathogen exploitation rates reverses with environmental context

Host heterogeneity and spatial population structure each influence parasite evolution but may also interact because space structures contacts between host types. Here, we experimentally evolve granulosis virus in microcosms of its Plodia interpunctella (Indian meal moth) host that differ in both spatial structure and host genetic diversity. We control spatial structure by manipulating the viscosity of the food that the larvae live within and host genetic diversity by adding larvae from either a single or two inbred lines to opposite ends of the microcosm. We preserve spatial structure across passages and assay virus from different positions within the microcosm on both host genotypes. We find that the lower contact rates between host genotypes resulting from spatial structure can lead to the evolution of locally specialized virus, even when the host population is genetically diverse overall. We also find that spatial structure changes how viruses specialize: viruses evolved in well-mixed environments had lower exploitation of familiar hosts, while those in spatially structured environments exhibited higher exploitation of familiar hosts. These results demonstrate that spatial structure and host heterogeneity interact to shape pathogen specialization and that the evolutionary consequences of host diversity depends on the population structure.

evolutionary biology↗

bioRxiv2022

The evolution of host resistance to a virus is determined by resources, historical contingency, and time scale

Hosts can often evolve resistance to parasites (and other stressors), but such resistance is generally thought to be constrained by trade-offs with other traits. These trade-offs determine the hosts optimal resistance strategy and whether resistance cycles, diversifies, and/or is maintained in the absence of parasite. However, trade-offs are often inconsistently measured across experiments and can depend on environmental conditions. Here, we extend a selection experiment evolving resistance to viral infection under variable resource quality in the Plodia interpunctella model system to explore the evolutionary conditions leading to an incongruent earlier measurement of costless resistance. We find that environmental resource quality, historical contingency, and the time scale of selection all affect trade-offs in our long-term selection experiment. Specifically, populations selected for resistance with the dual stressor of low resource quality are slowed, but not prevented, from evolving resistance. Second, variation in starting populations or early sampled adaptations led to contingency towards context-dependent resistance. Finally, some costs to resistance observed at early time points were compensated over longer evolutionary time scales. Our work therefore informs perspectives for the predictability of adaptation and how variation in specific evolutionary conditions can alter the evolutionary trajectories of a population towards costly or costless resistance strategies.

evolutionary biology↗

bioRxiv2021

The Evolution of Host Specialization in an Insect Pathogen

Niche breadth coevolution between biotic partners underpins theories of diversity and co-existence and influences patterns of disease emergence and transmission in host-parasite systems. Despite these broad implications, we still do not fully understand how the breadth of parasites infectivity evolves, the nature of any associated costs, or the genetic basis of specialization. Here, we serially passage a granulosis virus on multiple inbred populations of its Plodia interpunctella host to explore the dynamics and outcomes of specialization. In particular, we collect time series of phenotypic and genetic data to explore the dynamics of host genotype specialization throughout the course of experimental evolution and examine two fitness components. We find that the Plodia interpunctella granulosis virus consistently evolves increases in overall specialization, but that our two fitness components evolve independently such that lines specialize in either productivity or infectivity. Furthermore, we find that specialization in our experiment is a highly polygenic trait best explained by a combination of evolutionary mechanisms including conditionally positive fitness asymmetries and mutation accumulation. These results are important for understanding the evolution of specialization in host-parasite interactions and its broader implications for co-existence, diversification, and infectious disease management.

evolutionary biology↗

bioRxiv2021

Bats host the most virulent--but not the most dangerous--zoonotic viruses

Identifying virus characteristics associated with the largest public health impacts on human populations is critical to informing zoonotic risk assessments and surveillance strategies. Efforts to assess "zoonotic risk" often use trait-based analyses to identify which viral and reservoir host groups are most likely to source zoonoses but have not fully addressed how and why the impacts of zoonotic viruses vary in terms of disease severity ( virulence), capacity to spread within human populations ( transmissibility), or total human mortality ( death burden). We analyzed trends in human case fatality rates, transmission capacities, and total death burdens across a comprehensive dataset of mammalian and avian zoonotic viruses. Bats harbor the most virulent zoonotic viruses even when compared to birds, which alongside bats, have been hypothesized to be "special" zoonotic reservoirs due to molecular adaptations that support the physiology of flight. Reservoir host groups more closely related to humans--in particular, Primates--harbor less virulent, but more highly transmissible viruses. Importantly, disproportionately high human death burden, arguably the most important metric of zoonotic risk, is not associated with any animal reservoir, including bats. Our data demonstrate that mechanisms driving death burdens are diverse and often contradict trait-based predictions. Ultimately, total human mortality is dependent on context-specific epidemiological dynamics, which are shaped by a combination of viral traits and conditions in the animal host population and across and beyond the human-animal interface. Understanding the conditions that predict high zoonotic burden in humans will require longitudinal studies of epidemiological dynamics in wildlife and human populations. Significance statementThe clear need to mitigate zoonotic risk has fueled increased viral discovery in specific reservoir host taxa. We show that a combination of viral and reservoir traits can predict zoonotic virus virulence and transmissibility in humans, supporting the hypothesis that bats harbor exceptionally virulent zoonoses. However, pandemic prevention requires thinking beyond zoonotic capacity, virulence, and transmissibility to consider collective burden on human health. For this, viral discovery targeting specific reservoirs may be inefficient as death burden correlates with viral, not reservoir, traits, and depends on context-specific epidemiological dynamics across and beyond the human-animal interface. These findings suggest that longitudinal studies of viral dynamics in reservoir and spillover host populations may offer the most effective strategy for mitigating zoonotic risk.

ecology↗

bioRxiv2018

When parasites are selected to kill the young

The impact of infectious disease is often very different in juveniles and adults, but theory has focused on the drivers of stage-dependent defense in hosts rather than the potential for stage-dependent virulence evolution. Stage-structure has the potential to be important to the evolution of pathogens because it exposes parasites to heterogeneous environments in terms of both host characteristics and transmission routes. We develop a stage-structured (juvenile-adult) epidemiological model and examine the evolutionary outcomes of stage-specific virulence under the classic assumption of a transmission-virulence trade-off. We show that selection on virulence against adults remains consistent with the classic theory. However, the evolution of juvenile virulence is sensitive to both demography and transmission pathway with higher virulence against juveniles being favored either when the transmission pathway is assortative (juveniles preferentially interact together) and the juvenile stage is short, or in contrast when the transmission pathway is disassortative and the juvenile stage is long. These results highlight the potentially profound effects of host stage-structure on determining parasite virulence in nature. This new perspective may have broad implications for both understanding and managing disease severity. Impact summaryUnderstanding the evolution of parasite virulence remains one of the most important questions in evolutionary ecology. Virulence is often very different in young and old hosts, but previous theory has presumed that these differences are attributed to adaptation in host defense rather than parasite adaptation. However, stage-structure within host populations can expose parasites to heterogeneous environments, which may lead to differential selection on parasite virulence (stage-specific virulence). Surprisingly, no study has investigated the effects of hosts stage-structure on the evolution of stage-specific virulence. We present a theoretical analysis to examine when selection can favor higher virulence against juveniles (juvenile-virulence) versus adults (adult-virulence). Our key result is that higher juvenile-virulence is selected for either when the transmission is assortative within age classes and maturation is slow, or when the transmission is disassortative (occurring predominantly between-classes) and maturation is relatively fast. These at first sight contrasting outcomes can be understood as adaptation to the exploitation of the more available host stage. Although the data on assortativity in infectious disease systems is limited, empirical studies for the virulence of Great Island Virus in guillemots (Uria aalge) and for salmon louse in pink salmon (Oncorhynchus gorbuscha) are consistent with our predictions. Our work provides testable predictions for stage-specific virulence and presents a novel mechanism that may explain variation in virulence in nature. There are also management implications for conservation, public health, vaccination programs, and farming to understanding the drivers of stage dependent virulence.

ecology↗