Search arXivSearch

arXiv · 2609.13668

Structures of the Basic Reproduction Number $R_0$ Across Compartmental Disease Models

Abstract

The basic reproduction number $R_0$ is the central dimensionless quantity in mathematical epidemiology, characterizing the threshold for disease outbreak and the early growth rate of an epidemic. The algebraic form of $R_0$ varies widely across models of distinct transmission mechanisms, and its interpretation can yield further biological insight into transmission dynamics and disease intervention. We present a structural taxonomy of $R_0$ for compartmental ordinary differential equation models spanning a range of disease transmission features, including staged progression, differential infectivity, competing strains, vector-borne transmission, sexually transmitted infection, recurrent infection, maternal transmission, and gene drive inheritance. For each structural class, we provide a worked example, deriving $R_0$ via the next-generation matrix approach and interpreting the resulting algebraic expression in terms of the underlying transmission pathway. By unifying disparate derivations under a single structural framework, we clarify when and why particular algebraic forms of $R_0$ arise. This review serves both as a research synthesis and as a self-contained pedagogical reference for students and researchers entering the field.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

Zhuolin Qu, Abhi Ashwath. 2026-09-12. Structures of the Basic Reproduction Number $R_0$ Across Compartmental Disease Models. https://arxiv.org/abs/2609.13668

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related papers

A conceptual predator-prey model with super-long transients

Drawing on the understanding of the logistic map, we propose a simple predator-prey model where predators and prey adapt to each other, leading to the co-evolution of the system. The special dynamics observed in periodic windows contribute to the coexistence of multiple time scales, adding to the complexity of the system. Typical dynamics in ecosystems, such as the persistence and coexistence of population cycles and chaotic behaviors, the emergence of super-long transients, regime shifts, and the quantifying of resilience, are encapsulated within this single model. The simplicity of our model allows for detailed analysis, reinforcing its potential as a conceptual tool for understanding ecosystems deeply.

q-bio.PE

Mutation Order and Selection Shape Intratumor Heterogeneity in Tumor Evolution

Cancer progression often requires multiple driver mutations, but the same drivers may be acquired in different orders. How these pathways jointly shape tumor clonal structure remains unclear. We develop a multitype branching-process model in which malignant transformation requires two driver mutations, distinguishing malignant cells by mutation order and the independent transformation event that founded their clone. Under a successive exponential approximation, we establish point-process limits for pathway-specific clone sizes and derive a closed-form expression for the limiting expected Simpson's index of the combined malignant population. When both mutation orders yield malignant cells with the same net growth rate, the index decomposes into effective pathway weights, determined by mutation rates and birth-death dynamics at preceding stages, and within-pathway concentration terms, determined by intermediate-to-malignant growth-rate ratios. A driver's effect on heterogeneity thus depends critically on when it is acquired. A strong driver acquired early expands the intermediate lineage and increases the supply of independent malignant founders, whereas the same driver acquired last strengthens the growth and age advantage of early-founded malignant clones. Under additive fitness effects, these opposing mechanisms can produce a non-monotone relationship between selective advantage and clonal concentration. Threshold-like non-additive fitness effects can generate highly concentrated malignant populations, while order-dependent terminal fitness causes the faster-growing pathway to dominate asymptotically. These results show how mutation order, mutational accessibility, selection, and epistasis jointly determine lineage-level intratumor heterogeneity.

q-bio.PE

Phase transitions in microbial lineage trees

Microbial populations exhibit high cell-to-cell variability, which fundamentally shapes population behavior. A striking consequence is the existence of phase transitions, where small genetic or environmental changes trigger abrupt shifts in population dynamics. While biological phase transitions have often been proposed, connecting observed behavior to the underlying physics has remained challenging. We combine population genetics with statistical physics to show how phase transitions arise naturally in microbial populations. We highlight the existence of a first-order transition in a model of bacterial plasmid engineering and find a strict lower bound on the number of plasmids that can be stably maintained in a population.

q-bio.PE