arXiv subjects

Dylan H. Morris

Publications and source records attributed to Dylan H. Morris.

4 recordsLinked to original sources

arXiv2026

Collaborative estimation and evaluation of SARS-CoV-2 variant nowcasting in the United States

The ability to estimate and predict pathogen variant dynamics can inform public health responses, including planning for increased transmission or severity, shifts in population immunity, or changes to vaccine or therapeutic effectiveness. The COVID-19 pandemic demonstrated the importance of monitoring SARS-CoV-2 variant evolution through viral genome sequencing, enabling predictive models to estimate variant frequencies in the recent past, present, and short-term future. Collaborative forecasting Hubs provided a valuable way to centralize predictive modeling of epidemiological indicators such as cases, hospitalizations, and deaths during the pandemic; however, none existed for variant dynamics. Here, we discuss the creation of the United States SARS-CoV-2 Variant Nowcast Hub, designed to solicit estimates of the relative abundance of a specified set of SARS-CoV-2 variants at the U.S. state level. We discuss the design decisions and challenges in building the Hub and its scoring procedures. Using submissions from the Hub's first respiratory virus season (nowcast dates October 9th, 2024 to June 4th, 2025), we evaluate five individual models and a baseline model. We found that the baseline model, which pools sequences across the U.S., performs well overall, with most individual models performing similarly or slightly worse. Locations with lower sequencing volumes exhibited greater variability in model performance. Models submitted for a single location outperformed those submitted for all locations, potentially due to greater timeliness and magnitude of local data. Much remains to be investigated regarding relative model performance across different phases of variant emergence, and we conclude by proposing future directions within and beyond this Hub.

stat.AP↗

arXiv2022

Social dilemmas of sociality due to beneficial and costly contagion

Levels of sociality in nature vary widely. Some species are solitary; others live in family groups; some form complex multi-family societies. Increased levels of social interaction can allow for the spread of useful innovations and beneficial information, but can also facilitate the spread of harmful contagions, such as infectious diseases. It is natural to assume that these contagion processes shape the evolution of complex social systems, but an explicit account of the dynamics of sociality under selection pressure imposed by contagion remains elusive. We consider a model for the evolution of sociality strategies in the presence of both a beneficial and costly contagion. We study the dynamics of this model at three timescales: using a susceptible-infectious-susceptible (SIS) model to describe contagion spread for given sociality strategies, a replicator equation to study the changing fractions of two different levels of sociality, and an adaptive dynamics approach to study the long-time evolution of the population level of sociality. For a wide range of assumptions about the benefits and costs of infection, we identify a social dilemma: the evolutionarily-stable sociality strategy (ESS) is distinct from the collective optimum -- the level of sociality that would be best for all individuals. In particular, the ESS level of social interaction is greater (respectively less) than the social optimum when the good contagion spreads more (respectively less) readily than the bad contagion. Our results shed light on how contagion shapes the evolution of social interaction, but reveals that evolution may not necessarily lead populations to social structures that are good for any or all.

physics.soc-ph↗

arXiv2021

A PDE Model for Protocell Evolution and the Origin of Chromosomes via Multilevel Selection

The evolution of complex cellular life involved two major transitions: the encapsulation of self-replicating genetic entities into cellular units and the aggregation of individual genes into a collectively replicating genome. In this paper, we formulate a minimal model of the evolution of proto-chromosomes within protocells. We model a simple protocell composed of two types of genes: a "fast gene" with an advantage for gene-level self-replication and a "slow gene" that replicates more slowly at the gene level, but which confers an advantage for protocell-level reproduction. Protocell-level replication capacity depends on cellular composition of fast and slow genes. We use a partial differential equation to describe how the composition of genes within protocells evolves over time under within-cell and between-cell competition. We find that the gene-level advantage of fast replicators casts a long shadow on the multilevel dynamics of protocell evolution: no level of between-protocell competition can produce coexistence of the fast and slow replicators when the two genes are equally needed for protocell-level reproduction. By introducing a "dimer replicator" consisting of a linked pair of the slow and fast genes, we show analytically that coexistence between the two genes can be promoted in pairwise multilevel competition between fast and dimer replicators, and provide numerical evidence for coexistence in trimorphic competition between fast, slow, and dimer replicators. Our results suggest that dimerization, or the formation of a simple chromosome-like dimer replicator, can help to overcome the shadow of lower-level selection and work in concert with deterministic multilevel selection to allow for the coexistence of two genes that are complementary at the protocell-level but compete at the level of individual gene-level replication.

q-bio.PE↗

arXiv2021

Optimal, near-optimal, and robust epidemic control

In the absence of drugs and vaccines, policymakers use non-pharmaceutical interventions such as social distancing to decrease rates of disease-causing contact, with the aim of reducing or delaying the epidemic peak. These measures carry social and economic costs, so societies may be unable to maintain them for more than a short period of time. Intervention policy design often relies on numerical simulations of epidemic models, but comparing policies and assessing their robustness demands clear principles that apply across strategies. Here we derive the theoretically optimal strategy for using a time-limited intervention to reduce the peak prevalence of a novel disease in the classic Susceptible-Infectious-Recovered epidemic model. We show that broad classes of easier-to-implement strategies can perform nearly as well as the theoretically optimal strategy. But neither the optimal strategy nor any of these near-optimal strategies is robust to implementation error: small errors in timing the intervention produce large increases in peak prevalence. Our results reveal fundamental principles of non-pharmaceutical disease control and expose their potential fragility. For robust control, an intervention must be strong, early, and ideally sustained.

q-bio.PE↗