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1. Time-series modeling of epidemics in complex populations: Detecting changes in incidence volatility over time

   https://doi.org/10.1371/journal.pcbi.1012882  

   Aber, Rachael; Di, Yanming; Dalziel, Benjamin D (July 2025, PLOS Computational Biology)

   Hill, Edward M (Ed.)

   Trends in infectious disease incidence provide important information about epidemic dynamics and prospects for control. Higher-frequency variation around incidence trends can shed light on the processes driving epidemics in complex populations, as transmission heterogeneity, shifting landscapes of susceptibility, and fluctuations in reporting can impact the volatility of observed case counts. However, measures of temporal volatility in incidence, and how volatility changes over time, are often overlooked in population-level analyses of incidence data, which typically focus on moving averages. Here we present a statistical framework to quantify temporal changes in incidence dispersion and to detect rapid shifts in the dispersion parameter, which may signal new epidemic phases. We apply the method to COVID-19 incidence data in 144 United States (US) counties from January 1st, 2020 to March 23rd, 2023. Theory predicts that dispersion should be inversely proportional to incidence, however our method reveals pronounced temporal trends in dispersion that are not explained by incidence alone, but which are replicated across counties. In particular, dispersion increased around the major surge in cases in 2022, and highly overdispersed patterns became more frequent later in the time series. These increases potentially indicate transmission heterogeneity, changes in the susceptibility landscape, or that there were changes in reporting. Shifts in dispersion can also indicate shifts in epidemic phase, so our method provides a way for public health officials to anticipate and manage changes in epidemic regime and the drivers of transmission. 

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2. Multimodal pathogen transmission as a limiting factor in host distribution

   https://doi.org/10.1002/ecy.3956  

   Uricchio, Lawrence H.; Bruns, Emily L.; Hood, Michael E.; Boots, Mike; Antonovics, Janis (January 2023, Ecology)

   Abstract Theoretical models suggest that infectious diseases could play a substantial role in determining the spatial extent of host species, but few studies have collected the empirical data required to test this hypothesis. Pathogens that sterilize their hosts or spread through frequency‐dependent transmission could have especially strong effects on the limits of species' distributions because diseased hosts that are sterilized but not killed may continue to produce infectious stages and frequency‐dependent transmission mechanisms are effective even at very low population densities. We collected spatial pathogen prevalence data and population abundance data for alpine carnations infected by the sterilizing pathogenMicrobotryum dianthorum, a parasite that is spread through both frequency‐dependent (vector‐borne) and density‐dependent (aerial spore transmission) mechanisms. Our 13‐year study reveals rapid declines in population abundance without a compensatory decrease in pathogen prevalence. We apply a stochastic, spatial model of parasite spread that accommodates spatial habitat heterogeneity to investigate how the population dynamics depend on multimodal (frequency‐dependent and density‐dependent) transmission. We found that the observed rate of population decline could plausibly be explained by multimodal transmission, but is unlikely to be explained by either frequency‐dependent or density‐dependent mechanisms alone. Multimodal pathogen transmission rates high enough to explain the observed decline predicted that eventual local extinction of the host species is highly likely. Our results add to a growing body of literature showing how multimodal transmission can constrain species distributions in nature. 

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3. Ecological and Evolutionary Insights About Emerging Infectious Diseases from the COVID-19 Pandemic

   https://doi.org/10.1146/annurev-ecolsys-102320-101234  

   Kilpatrick, A Marm (November 2023, Annual Review of Ecology, Evolution, and Systematics)

   The coronavirus disease 2019 (COVID-19) pandemic challenged the workings of human society, but in doing so, it advanced our understanding of the ecology and evolution of infectious diseases. Fluctuating transmission of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) demonstrated the highly dynamic nature of human social behavior, often without government intervention. Evolution of SARS-CoV-2 in the first two years following spillover resulted primarily in increased transmissibility, while in the third year, the globally dominant virus variants had all evolved substantial immune evasion. The combination of viral evolution and the buildup of host immunity through vaccination and infection greatly decreased the realized virulence of SARS-CoV-2 due to the age dependence of disease severity. The COVID-19 pandemic was exacerbated by presymptomatic, asymptomatic, and highly heterogeneous transmission, as well as highly variable disease severity and the broad host range of SARS-CoV-2. Insights and tools developed during the COVID-19 pandemic could provide a stronger scientific basis for preventing, mitigating, and controlling future pandemics. 

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4. What Does Tolerance Mean for Animal Disease Dynamics When Pathology Enhances Transmission?

   https://doi.org/10.1093/icb/icz065  

   Henschen, Amberleigh E.; Adelman, James S. (May 2019, Integrative and Comparative Biology)

   Abstract Host competence, or how well an individual transmits pathogens, varies substantially within and among animal populations. As this variation can alter the course of epidemics and epizootics, revealing its underlying causes will help predict and control the spread of disease. One host trait that could drive heterogeneity in competence is host tolerance, which minimizes fitness losses during infection without decreasing pathogen load. In many cases, tolerance should increase competence by extending infectious periods and enabling behaviors that facilitate contact among hosts. However, we argue that the links between tolerance and competence are more varied. Specifically, the different physiological and behavioral mechanisms by which hosts achieve tolerance should have a range of effects on competence, enhancing the ability to transmit pathogens in some circumstances and impeding it in others. Because tissue-based pathology (damage) that reduces host fitness is often critical for pathogen transmission, we focus on two mechanisms that can underlie tolerance at the tissue level: damage-avoidance and damage-repair. As damage-avoidance reduces transmission-enhancing pathology, this mechanism is likely to decrease host competence and pathogen transmission. In contrast, damage-repair does not prevent transmission-relevant pathology from occurring. Rather, damage-repair provides new, healthy tissues that pathogens can exploit, likely extending the infectious period and increasing host competence. We explore these concepts through graphical models and present three disease systems in which damage-avoidance and damage-repair alter host competence in the predicted directions. Finally, we suggest that by incorporating these links, future theoretical studies could provide new insights into infectious disease dynamics and host–pathogen coevolution. 

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5. The cost of travel: How dispersal ability limits local adaptation in host–parasite interactions

   https://doi.org/10.1111/jeb.13754  

   Johnson, Pieter; Calhoun, Dana M.; Moss, Wynne E.; McDevitt‐Galles, Travis; Riepe, Tawni B.; Hallas, Joshua M.; Parchman, Thomas L.; Feldman, Chris R.; Achatz, Tyler J.; Tkach, Vasyl V.; et al (December 2020, Journal of Evolutionary Biology)

   Abstract Classical theory suggests that parasites will exhibit higher fitness in sympatric relative to allopatric host populations (local adaptation). However, evidence for local adaptation in natural host–parasite systems is often equivocal, emphasizing the need for infection experiments conducted over realistic geographic scales and comparisons among species with varied life history traits. Here, we used infection experiments to test how two trematode (flatworm) species (Paralechriorchis syntomenteraandRibeiroia ondatrae) with differing dispersal abilities varied in the strength of local adaptation to their amphibian hosts. Both parasites have complex life cycles involving sequential transmission among aquatic snails, larval amphibians and vertebrate definitive hosts that control dispersal across the landscape. By experimentally pairing 26 host‐by‐parasite population infection combinations from across the western USA with analyses of host and parasite spatial genetic structure, we found that increasing geographic distance—and corresponding increases in host population genetic distance—reduced infection success forP. syntomentera, which is dispersed by snake definitive hosts. For the avian‐dispersedR. ondatrae, in contrast, the geographic distance between the parasite and host populations had no influence on infection success. Differences in local adaptation corresponded to parasite genetic structure; although populations ofP. syntomenteraexhibited ~10% mtDNA sequence divergence, those ofR. ondatraewere nearly identical (<0.5%), even across a 900 km range. Taken together, these results offer empirical evidence that high levels of dispersal can limit opportunities for parasites to adapt to local host populations. 

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