Source identification via contact tracing in the presence of asymptomatic patients.

Inferring the source of a diffusion in a large network of agents is a difficult but feasible task, if a few agents act as sensors revealing the time at which they got hit by the diffusion. One of the main limitations of current source identification algorithms is that they assume full knowledge of the contact network, which is rarely the case, especially for epidemics, where the source is called patient zero. Inspired by recent implementations of contact tracing algorithms, we propose a new framework, which we call Source Identification via Contact Tracing Framework (SICTF). In the SICTF, the source identification task starts at the time of the first hospitalization, and initially we have no knowledge about the contact network other than the identity of the first hospitalized agent. We may then explore the network by contact queries, and obtain symptom onset times by test queries in an adaptive way, i.e., both contact and test queries can depend on the outcome of previous queries. We also assume that some of the agents may be asymptomatic, and therefore cannot reveal their symptom onset time. Our goal is to find patient zero with as few contact and test queries as possible. We implement two local search algorithms for the SICTF: the LS algorithm, which has recently been proposed by Waniek et al. in a similar framework, is more data-efficient, but can fail to find the true source if many asymptomatic agents are present, whereas the LS+ algorithm is more robust to asymptomatic agents. By simulations we show that both LS and LS+ outperform previously proposed adaptive and non-adaptive source identification algorithms adapted to the SICTF, even though these baseline algorithms have full access to the contact network. Extending the theory of random exponential trees, we analytically approximate the source identification probability of the LS/ LS+ algorithms, and we show that our analytic results match the simulations. Finally, we benchmark our algorithms on the Data-driven COVID-19 Simulator (DCS) developed by Lorch et al., which is the first time source identification algorithms are tested on such a complex dataset.

Switchover phenomenon induced by epidemic seeding on geometric networks.

It is a fundamental question in disease modeling how the initial seeding of an epidemic, spreading over a network, determines its final outcome. One important goal has been to find the seed configuration, which infects the most individuals. Although the identified optimal configurations give insight into how the initial state affects the outcome of an epidemic, they are unlikely to occur in real life. In this paper we identify two important seeding scenarios, both motivated by historical data, that reveal a complex phenomenon. In one scenario, the seeds are concentrated on the central nodes of a network, while in the second one, they are spread uniformly in the population. Comparing the final size of the epidemic started from these two initial conditions through data-driven and synthetic simulations on real and modeled geometric metapopulation networks, we find evidence for a switchover phenomenon: When the basic reproduction number [Formula: see text] is close to its critical value, more individuals become infected in the first seeding scenario, but for larger values of [Formula: see text], the second scenario is more dangerous. We find that the switchover phenomenon is amplified by the geometric nature of the underlying network and confirm our results via mathematically rigorous proofs, by mapping the network epidemic processes to bond percolation. Our results expand on the previous finding that, in the case of a single seed, the first scenario is always more dangerous and further our understanding of why the sizes of consecutive waves of a pandemic can differ even if their epidemic characters are similar.

Griffiths phases and localization in hierarchical modular networks.

We study variants of hierarchical modular network models suggested by Kaiser and Hilgetag [ Front. in Neuroinform., 4 (2010) 8] to model functional brain connectivity, using extensive simulations and quenched mean-field theory (QMF), focusing on structures with a connection probability that decays exponentially with the level index. Such networks can be embedded in two-dimensional Euclidean space. We explore the dynamic behavior of the contact process (CP) and threshold models on networks of this kind, including hierarchical trees. While in the small-world networks originally proposed to model brain connectivity, the topological heterogeneities are not strong enough to induce deviations from mean-field behavior, we show that a Griffiths phase can emerge under reduced connection probabilities, approaching the percolation threshold. In this case the topological dimension of the networks is finite, and extended regions of bursty, power-law dynamics are observed. Localization in the steady state is also shown via QMF. We investigate the effects of link asymmetry and coupling disorder, and show that localization can occur even in small-world networks with high connectivity in case of link disorder.