epidemic modelers

Abstract: Signal dispersion, stress propagation in interbank systems, and transmission probabilities in epidemic and reliability models are all captured by studying paths on directed graphs where the path weight is defined as the product of its edge weights. Connectivity in such networks is naturally quantified by aggregating these multiplicative path weights across nodes. This paper provides a comprehensive treatise on connectivity and ranking measures based on multiplicative path weights. We demonstrate how standard all-path connectivity, such as the standard Katz centrality, can be extended beyond its classical spectral threshold. In addition, we derive closed-form expressions for connectivity based on first-hit paths and introduce a new version of Katz centrality. Furthermore, for random edge weights, we derive resolvent-based expressions for the first and second moments, alongside variance bounds, under a path-indexed coupling framework. Finite irreducible Markov chains are a subclass of the models studied, and we show that the scaled matrix of first-hit path probabilities is the probability-generating function for first-passage and return times, and that differentiation yields the classical first-passage times. Numerical examples illustrate the application of our results in a variety of settings.

Abstract: Modeling the temporal evolution of macroscopic properties of complex systems is an important scientific task. To predict this evolution without full microscopic simulation, a common approach encodes microstates into compact latent states, learns their evolution, and reads out macroscopic predictions from the latent trajectory. These latent states are often learned through microstate reconstruction. However, with limited latent capacity, reconstruction can favor high-variance microscopic details over information needed for macroscopic prediction. Yet jointly learning latent states and their transition without reconstruction often fails to obtain latent dynamics that support accurate macroscopic prediction. We show that this failure can arise from latent scale collapse: shrinking the latent state scale reduces training loss while macroscopic evolution error remains large. Here, we propose a reconstruction-free framework to learn latent states with their dynamics for prescribed macroscopic prediction. Training alternates between updating the latent representation with the transition and next-state latent targets fixed, and updating the transition with the latent representation fixed. At inference, the trained model predicts macroscopic states recursively from an initial microstate. Our theoretical analysis characterizes reconstruction misalignment and scale collapse under joint training, and gives a sufficient condition for local convergence to correct latent dynamics for our method. Experiments on epidemic spreading on a lattice, mixing of two particle species, and polymer stretching demonstrate that the proposed method achieves substantially better macroscopic prediction over baselines.

Abstract: Temporal-network models attribute memory in contact data to either node self-excitation (branching ratio n_node) or tie reinforcement (kappa), carrying major consequences for epidemic spreading. We prove that when event initiators are observed, the two mechanisms are orthogonal: the Fisher information is block-diagonal and neither trades off against the other. In undirected proximity data, where initiators are unobserved, marginalising over them couples the mechanisms into a structural confound that survives posterior smoothing. On empirical proximity, messaging, and email records, however, a cruder failure dominates: fitted node memory is pinned to the inter-event marginal law and remains virtually invariant across latent label posterior samples (coefficient of variation below 1%). An inter-event-order shuffle test and burstiness-memory diagnostics reveal that exponential-Hawkes node memory is recovered from none, while tie reinforcement remains identifiable throughout. This near-unidentifiability is intrinsic, not an artefact of the exponential kernel: refitting flexible scale-free (sum-of-exponentials) kernels on synthetic power-law self-exciting processes fails to distinguish genuine node memory from memoryless renewal controls, with identical collapses recurring on algorithmic networks (edit bots, cloud microservices) and cortical spiking. Downstream epidemic consequences are quantitative: simulations fitted to empirical contact records under-predict outbreak sizes by up to a factor of 2.5 and shift the epidemic threshold. We conclude that observational temporal networks face a two-fold identifiability boundary: contact directionality is essential to decouple tie reinforcement, whereas heavy-tailed node self-excitation is intrinsically unidentifiable from contact timings alone.