The transmission of many animal and plant diseases relies on the behavior of arthropod vectors. In particular, the specific preference for infected or uninfected hosts observed in many vector species ...is expected to affect the circulation of vector-borne diseases. Here I develop a theoretical framework to study the epidemiology and evolution of the manipulation of host choice behavior of vectors. I show that vector preference strategies have dramatic epidemiological consequences. I also explore the evolution of vector host choice under different scenarios regarding control of the vector behavior by the pathogen. This analysis yields multiple evolutionary outcomes and explains the diversity of host choice behaviors observed in a broad range of vector-borne diseases. In particular, this analysis helps us understand why several pathogens have evolved manipulation strategies that vary with the infectious status of their vector species while other pathogens seem unable to evolve such complex conditional strategies. I argue that contrasting the behavior of infected and uninfected vectors is key to revealing the mechanistic constraints acting on the evolution of the manipulation of vector behavior.
The limited supply of vaccines against severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) raises the question of targeted vaccination. Many countries have opted to vaccinate older and more ...sensitive hosts first to minimize the disease burden. However, what are the evolutionary consequences of targeted vaccination? We clarify the consequences of different vaccination strategies through the analysis of the speed of viral adaptation measured as the rate of change of the frequency of a vaccine-adapted variant. We show that such a variant is expected to spread faster if vaccination targets individuals who are likely to be involved in a higher number of contacts. We also discuss the pros and cons of dose-sparing strategies. Because delaying the second dose increases the proportion of the population vaccinated with a single dose, this strategy can both speed up the spread of the vaccine-adapted variant and reduce the cumulative number of deaths. Hence, strategies that are most effective at slowing viral adaptation may not always be epidemiologically optimal. A careful assessment of both the epidemiological and evolutionary consequences of alternative vaccination strategies is required to determine which individuals should be vaccinated first.
There is no doubt that the novel coronavirus SARS-CoV-2 that causes COVID-19 is mutating and thus has the potential to adapt during the current pandemic. Whether this evolution will lead to changes ...in the transmission, the duration, or the severity of the disease is not clear. This has led to considerable scientific and media debate, from raising alarms about evolutionary change to dismissing it. Here we review what little is currently known about the evolution of SARS-CoV-2 and extend existing evolutionary theory to consider how selection might be acting upon the virus during the COVID-19 pandemic. Although there is currently no definitive evidence that SARS-CoV-2 is undergoing further adaptation, continued evidence-based analysis of evolutionary change is important so that public health measures can be adjusted in response to substantive changes in the infectivity or severity of COVID-19.
Evolutionary theory predicts that selection favors increased transmission, longer pre-symptomatic periods, fewer asymptomatic cases, and lower disease severity for SARS-CoV-2. However, viral mutations are expected to affect combinations of these traits, making it challenging to predict the direction and disease impact of evolution.
Adaptation in spatially heterogeneous environments results from the balance between local selection, mutation, and migration. We study the interplay among these different evolutionary forces and ...demography in a classical two-habitat scenario with asexual reproduction. We develop a new theoretical approach that goes beyond the Adaptive Dynamics framework, and allows us to explore the effect of high mutation rates on the stationary phenotypic distribution. We show that this approach improves the classical Gaussian approximation, and captures accurately the shape of this equilibrium phenotypic distribution in one- and two-population scenarios. We examine the evolutionary equilibrium under general conditions where demography and selection may be nonsymmetric between the two habitats. In particular, we show how migration may increase differentiation in a source-sink scenario. We discuss the implications of these analytic results for the adaptation of organisms with large mutation rates, such as RNA viruses.
Avian malaria is the oldest experimental system for investigating the biology and transmission of Plasmodium parasites. Recent molecular protocols for detecting and characterizing avian malaria ...lineages in the field are providing an ever-growing picture of the prevalence, distribution, host range, and diversity hotspots of avian malaria across the world. The unparalleled genetic diversity uncovered rivals anything that has been found in other vertebrate malarias and seems to be matched by an equally rich phenotypic diversity, providing endless opportunities for exploring the selective pressures under which hosts and parasites evolve. We review the most important milestones in avian Plasmodium research and explain why this is a unique animal model to understand the ecology and evolution of malaria.
Avian malaria is the oldest experimental system for investigating the biology and transmission of Plasmodium parasites.
Avian Plasmodium has been found infecting thousands of bird species in all geographic regions except Antarctica. Its prevalence and genetic diversity rivals anything that has been found in any other vertebrate malaria.
Several avian Plasmodium lineages and their most common natural vector, the mosquito Culex pipiens, are widespread and easy to maintain in the laboratory – meaning that the system is also easily amenable to laboratory experiments.
The unparalleled genetic diversity of avian malaria uncovered thus far is likely matched by an equally rich phenotypic diversity, providing a unique opportunity for exploring the selective pressures under which hosts and parasites evolve. This will be best achieved by combining empirical and experimental studies in the field, with experimental infections in controlled laboratory conditions.
Patterns of local adaptation are expected to emerge when selection is spatially heterogeneous and sufficiently strong relative to the action of other evolutionary forces. The observation of local ...adaptation thus provides important insight into evolutionary processes and the adaptive divergence of populations. The detection of local adaptation, however, suffers from several conceptual, statistical and methodological issues. Here, we provide practical recommendations regarding (1) the definition of local adaptation, (2) the analysis of transplant experiments and (3) the optimisation of the experimental design of local adaptation studies. Together, these recommendations provide a unified approach for measuring local adaptation and understanding the adaptive divergence of populations in a wide range of biological systems.
The evolution of multidrug resistance (MDR) is a pressing public health concern. Yet many aspects, such as the role played by population structure, remain poorly understood. Here, we argue that ...studying MDR evolution by focusing upon the dynamical equations for linkage disequilibrium (LD) can greatly simplify the calculations, generate more insight, and provide a unified framework for understanding the role of population structure. We demonstrate how a general epidemiological model of MDR evolution can be recast in terms of the LD equations. These equations reveal how the different forces generating and propagating LD operate in a dynamical setting at both the population and metapopulation levels. We then apply these insights to show how the LD perspective: (i) explains equilibrium patterns of MDR, (ii) provides a simple interpretative framework for transient evolutionary dynamics, and (iii) can be used to assess the consequences of different drug prescription strategies for MDR evolution.
Following the initiation of the unprecedented global vaccination campaign against Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2), attention has now turned to the potential impact of ...this large-scale intervention on the evolution of the virus. In this Essay, we summarize what is currently known about pathogen evolution in the context of immune priming (including vaccination) from research on other pathogen species, with an eye towards the future evolution of SARS-CoV-2.
Metapopulation dynamics can strongly affect the ecological and evolutionary processes involved in host–parasite interactions. Here, I analyse a deterministic host–parasite coevolutionary model and ...derive analytic approximations for the level of local adaptation as a function of (1) host migration rate, (2) parasite migration rate, (3) parasite specificity and (4) parasite virulence. This analysis confirms the results of previous simulation studies: the difference between host and parasite migration rates may explain the level of local adaptation of both species. I also show that both higher specificity and higher virulence generally lead to higher levels of local adaptation of the species which is already ahead in the coevolutionary arms race. The present analysis also provides a simple geometric interpretation for local adaptation which captures the complexity of the temporal dynamics of host–parasite coevolution.
Phages are promising tools to fight antibiotic-resistant bacteria, and as for now, phage therapy is essentially performed in combination with antibiotics. Interestingly, combined treatments including ...phages and a wide range of antibiotics lead to an increased bacterial killing, a phenomenon called phage-antibiotic synergy (PAS), suggesting that antibiotic-induced changes in bacterial physiology alter the dynamics of phage propagation. Using single-phage and single-cell techniques, each step of the lytic cycle of phage HK620 was studied in E. coli cultures treated with either ceftazidime, cephalexin or ciprofloxacin, three filamentation-inducing antibiotics. In the presence of sublethal doses of antibiotics, multiple stress tolerance and DNA repair pathways are triggered following activation of the SOS response. One of the most notable effects is the inhibition of bacterial division. As a result, a significant fraction of cells forms filaments that stop dividing but have higher rates of mutagenesis. Antibiotic-induced filaments become easy targets for phages due to their enlarged surface areas, as demonstrated by fluorescence microscopy and flow cytometry techniques. Adsorption, infection and lysis occur more often in filamentous cells compared to regular-sized bacteria. In addition, the reduction in bacterial numbers caused by impaired cell division may account for the faster elimination of bacteria during PAS. We developed a mathematical model to capture the interaction between sublethal doses of antibiotics and exposition to phages. This model shows that the induction of filamentation by sublethal doses of antibiotics can amplify the replication of phages and therefore yield PAS. We also use this model to study the consequences of PAS on the emergence of antibiotic resistance. A significant percentage of hyper-mutagenic filamentous bacteria are effectively killed by phages due to their increased susceptibility to infection. As a result, the addition of even a very low number of bacteriophages produced a strong reduction of the mutagenesis rate of the entire bacterial population. We confirm this prediction experimentally using reporters for bacterial DNA repair. Our work highlights the multiple benefits associated with the combination of sublethal doses of antibiotics with bacteriophages.
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