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Mihaljevic, J. R.

Publications and source records attributed to Mihaljevic, J. R..

2 recordsLinked to original sources

Untangling the dynamics of persistence and colonization in microbial communities

A central goal of community ecology is to infer biotic interactions from observed distributions of co-occurring species. Evidence for biotic interactions, however, can be obscured by shared environmental requirements, posing a challenge for statistical inference. Here we introduce a dynamic statistical model that quantifies the effects of spatial and temporal covariance in longitudinal co-occurrence data. We separate the fixed pairwise effects of species occurrences on persistence and colonization rates, a potential signal of direct interactions, from latent pairwise correlations in occurrence, a potential signal of shared environmental responses. We apply our modeling approach to a pressing epidemiological question by examining how human papillomavirus (HPV) types coexist. Our results suggest that while HPV types respond similarly to common host traits, direct interactions are sparse and weak, so that HPV type diversity depends largely on shared environmental drivers. Our modeling approach is widely applicable to microbial communities and provides valuable insights that should lead to more directed hypothesis testing and mechanistic modeling.

ecology

Using biological control data to understand host-pathogen dynamics

A key assumption of models of infectious disease is that population-scale spread is driven by transmission between host individuals at small scales. This assumption, however, is rarely tested, likely because observing disease transmission between host individuals is non-trivial in many infectious diseases. Quantifying the transmission of insect baculoviruses at a small scale is in contrast straightforward. We fit a disease model to data from baculovirus epizootics (= epidemics in animals) at the scale of whole forests, while using prior parameter distributions constructed from branch-scale experiments. Our experimentally-constrained model fits the large-scale data very well, supporting the role of small-scale transmission mechanisms in baculovirus epizootics. We further compared our experimentally-based model to an unconstrained model that ignores our experimental data, serving as a proxy for models that include large-scale mechanisms. This analysis supports our hypothesis that small-scale mechanisms are important, especially individual variability in host susceptibility to the virus. Comparison of transmission rates in the two models, however, suggests that large-scale mechanisms increase transmission compared to our experimental estimates. Our study shows that small-scale and large-scale mechanisms drive forest-wide epizootics of baculoviruses, and that synthesizing mathematical models with data collected across scales is key to understanding the spread of infectious disease.

ecology