More Like this

1. Dynamics in a simple evolutionary-epidemiological model for the evolution of an initial asymptomatic infection stage

   https://doi.org/10.1073/pnas.1920761117  

   Saad-Roy, Chadi_M; Wingreen, Ned_S; Levin, Simon_A; Grenfell, Bryan_T (May 2020, Proceedings of the National Academy of Sciences)

   Significance Numerous factors affect early transmission by a newly infected host. A less symptomatic initial infection can persist longer due to reduced immune response, but at the cost of reduced transmission. Assuming simple trade-offs for progression and transmission rates in the initial infectious stage, we couple epidemiological and evolutionary dynamics. We find that fully asymptomatic, less symptomatic, or fully symptomatic first stages are possible evolutionary outcomes, with possible surprising bistability between zero and maximal asymptomatic behavior. This bistability implies that small changes in parameter values followed by reversion to their original values could lead to an alternative stable state with a qualitative difference in degree of first-stage symptoms. Therefore, disease control strategies can have dramatic evolutionary outcomes, cascading to epidemiological consequences. 

   more » « less
2. Evolution of an asymptomatic first stage of infection in a heterogeneous population

   https://doi.org/10.1098/rsif.2021.0175  

   Saad-Roy, Chadi M.; Grenfell, Bryan T.; Levin, Simon A.; van den Driessche, P.; Wingreen, Ned S. (June 2021, Journal of The Royal Society Interface)

   null (Ed.)

   Pathogens evolve different life-history strategies, which depend in part on differences in their host populations. A central feature of hosts is their population structure (e.g. spatial). Additionally, hosts themselves can exhibit different degrees of symptoms when newly infected; this latency is a key life-history property of pathogens. With an evolutionary-epidemiological model, we examine the role of population structure on the evolutionary dynamics of latency. We focus on specific power-law-like formulations for transmission and progression from the first infectious stage as a function of latency, assuming that the across-group to within-group transmission ratio increases if hosts are less symptomatic. We find that simple population heterogeneity can lead to local evolutionarily stable strategies (ESSs) at zero and infinite latency in situations where a unique ESS exists in the corresponding homogeneous case. Furthermore, there can exist more than one interior evolutionarily singular strategy. We find that this diversity of outcomes is due to the (possibly slight) advantage of across-group transmission for pathogens that produce fewer symptoms in a first infectious stage. Thus, our work reveals that allowing individuals without symptoms to travel can have important unintended evolutionary effects and is thus fundamentally problematic in view of the evolutionary dynamics of latency. 

   more » « less
3. Frequency‐dependent transmission of Batrachochytrium salamandrivorans in eastern newts

   https://doi.org/10.1111/tbed.14043  

   Tompros, Adrianna; Dean, Andrew D.; Fenton, Andy; Wilber, Mark Q.; Carter, Edward Davis; Gray, Matthew J. (April 2021, Transboundary and Emerging Diseases)

   null (Ed.)

   Transmission is the fundamental process whereby pathogens infect their hosts and spread through populations, and can be characterized using mathematical functions. The functional form of transmission for emerging pathogens can determine pathogen impacts on host populations and can inform the efficacy of disease management strategies. By directly measuring transmission between infected and susceptible adult eastern newts (Notophthalmus viridescens) in aquatic mesocosms, we identified the most plausible transmission function for the emerging amphibian fungal pathogen Batrachochytrium salamandrivorans (Bsal). Although we considered a range of possible transmission functions, we found that Bsal transmission was best explained by pure frequency dependence. We observed that >90% of susceptible newts became infected within 17 days post-exposure to an infected newt across a range of host densities and initial infection prevalence treatments. Under these conditions, we estimated R_0 = 4.9 for Bsal in an eastern newt population. Our results suggest that Bsal has the capability of driving eastern newt populations to extinction and that managing host density may not be an effective management strategy. Intervention strategies that prevent Bsal introduction or increase host resistance or tolerance to infection may be more effective. Our results add to the growing empirical evidence that transmission of wildlife pathogens can saturate and be functionally frequency-dependent. 

   more » « less
4. Protective microbiomes can limit the evolution of host pathogen defense

   https://doi.org/10.1002/evl3.140  

   Metcalf, C. Jessica E.; Koskella, Britt (October 2019, Evolution Letters)

   Abstract The evolution of host immunity occurs in the context of the microbiome, but little theory exists to predict how resistance against pathogens might be influenced by the need to tolerate and regulate commensal microbiota. We present a general model to explore the optimal investment in host immunity under conditions in which the host can, versus cannot easily distinguish among commensal versus pathogenic bacteria, and when commensal microbiota can, versus cannot protect the host against the impacts of pathogen infection. We find that a loss of immune vigilance associated with innate immunity over evolutionary time can occur due to the challenge of discriminating between pathogenic and other microbe species. Further, we find the greater the protective effect of microbiome species, acting either directly or via competition with a pathogen, or the higher the costs of immunity, the more likely the loss of immune vigilance is. Conversely, this effect can be reversed when pathogens increase host mortality. Generally, the magnitude of costs of immunity required to allow evolution of decreased immune vigilance are predicted to be lowest when microbiome and pathogen species most resemble each other (in terms of host recognition), and when immune effects on the pathogen are weak. Our model framework makes explicit the core trade-offs likely to shape the evolution of immunity in the context of microbiome/pathogen discrimination. We discuss how this informs interpretation of patterns and process in natural systems, including vulnerability to pathogen emergence. 

   more » « less
5. The tumour is in the detail: Local phylogenetic, population and epidemiological dynamics of a transmissible cancer in Tasmanian devils

   https://doi.org/10.1111/eva.13569  

   Hamede, Rodrigo; Fountain‐Jones, Nicholas M.; Arce, Fernando; Jones, Menna; Storfer, Andrew; Hohenlohe, Paul A.; McCallum, Hamish; Roche, Benjamin; Ujvari, Beata; Thomas, Frédéric (June 2023, Evolutionary Applications)

   Abstract Infectious diseases are a major threat for biodiversity conservation and can exert strong influence on wildlife population dynamics. Understanding the mechanisms driving infection rates and epidemic outcomes requires empirical data on the evolutionary trajectory of pathogens and host selective processes. Phylodynamics is a robust framework to understand the interaction of pathogen evolutionary processes with epidemiological dynamics, providing a powerful tool to evaluate disease control strategies. Tasmanian devils have been threatened by a fatal transmissible cancer, devil facial tumour disease (DFTD), for more than two decades. Here we employ a phylodynamic approach using tumour mitochondrial genomes to assess the role of tumour genetic diversity in epidemiological and population dynamics in a devil population subject to 12 years of intensive monitoring, since the beginning of the epidemic outbreak. DFTD molecular clock estimates of disease introduction mirrored observed estimates in the field, and DFTD genetic diversity was positively correlated with estimates of devil population size. However, prevalence and force of infection were the lowest when devil population size and tumour genetic diversity was the highest. This could be due to either differential virulence or transmissibility in tumour lineages or the development of host defence strategies against infection. Our results support the view that evolutionary processes and epidemiological trade‐offs can drive host‐pathogen coexistence, even when disease‐induced mortality is extremely high. We highlight the importance of integrating pathogen and population evolutionary interactions to better understand long‐term epidemic dynamics and evaluating disease control strategies. 

   more » « less