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Register a new userInitial growth rates of malware epidemics fail to predict their reach
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Empirical studies show that epidemiological models based on an epidemics initial spread rate often fail to predict the true scale of that epidemic. Most epidemics with a rapid early rise die out before affecting a significant fraction of the population, whereas the early pace of some pandemics is rather modest. Recent models suggest that this could be due to the heterogeneity of the target populations susceptibility. We study a computer malware ecosystem exhibiting spread mechanisms resembling those of biological systems while offering details unavailable for human epidemics. Rather than comparing models, we directly estimate reach from a new and vastly more complete data from a parallel domain, that offers superior details and insight as concerns biological outbreaks. We find a highly heterogeneous distribution of computer susceptibilities, with nearly all outbreaks initially over-affecting the tail of the distribution, then collapsing quickly once this tail is depleted. This mechanism restricts the correlation between an epidemics initial growth rate and its total reach, thus preventing the majority of epidemics, including initially fast-growing outbreaks, from reaching a macroscopic fraction of the population. The few pervasive malwares distinguish themselves early on via the following key trait: they avoid infecting the tail, while preferentially targeting computers unaffected by typical malware.
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Epidemic spreading has been studied for a long time and most of them are focused on the growing aspect of a single epidemic outbreak. Recently, we extended the study to the case of recurrent epidemics (Sci. Rep. {bf 5}, 16010 (2015)) but limited only to a single network. We here report from the real data of coupled regions or cities that the recurrent epidemics in two coupled networks are closely related to each other and can show either synchronized outbreak phase where outbreaks occur simultaneously in both networks or mixed outbreak phase where outbreaks occur in one network but do not in another one. To reveal the underlying mechanism, we present a two-layered network model of coupled recurrent epidemics to reproduce the synchronized and mixed outbreak phases. We show that the synchronized outbreak phase is preferred to be triggered in two coupled networks with the same average degree while the mixed outbreak phase is preferred for the case with different average degrees. Further, we show that the coupling between the two layers is preferred to suppress the mixed outbreak phase but enhance the synchronized outbreak phase. A theoretical analysis based on microscopic Markov-chain approach is presented to explain the numerical results. This finding opens a new window for studying the recurrent epidemics in multi-layered networks.
The ongoing COVID-19 pandemic is being responded with various methods, applying vaccines, experimental treatment options, total lockdowns or partial curfews. Weekend curfews is one of the methods to reduce the amount of infected persons and this method is practically applied in some countries such as Turkey. In this study, the effect of weekend curfews on reducing the spread of a contagious disease, such as COVID-19, is modeled using a Monte Carlo algorithm with a hybrid lattice model. In the simulation setup, a fictional country with three towns and 26,610 citizens were used as a model. Results indicate that applying a weekend curfew reduces the active cases significantly and is one of the efficient ways to fight the epidemic. The results also show that applying personal precautions such as social distancing is important for reducing the number of cases and deaths.
We develop a minimalist compartmental model to study the impact of mobility restrictions in Italy during the Covid-19 outbreak. We show that an early lockdown shifts the epidemic in time, while that beyond a critical value of the lockdown strength, the epidemic tend to restart after lifting the restrictions. As a consequence, specific mitigation strategies must be introduced. We characterize the relative importance of different broad strategies by accounting for two fundamental sources of heterogeneity, i.e. geography and demography. First, we consider Italian regions as separate administrative entities, in which social interactions between age classs occur. Due to the sparsity of the inter-regional mobility matrix, once started the epidemics tend to develop independently across areas, justifying the adoption of solutions specific to individual regions or to clusters of regions. Second, we show that social contacts between age classes play a fundamental role and that measures which take into account the age structure of the population can provide a significant contribution to mitigate the rebound effects. Our model is general, and while it does not analyze specific mitigation strategies, it highlights the relevance of some key parameters on non-pharmaceutical mitigation mechanisms for the epidemics.
We describe the population-based SEIR (susceptible, exposed, infected, removed) model developed by the Irish Epidemiological Modelling Advisory Group (IEMAG), which advises the Irish government on COVID-19 responses. The model assumes a time-varying effective contact rate (equivalently, a time-varying reproduction number) to model the effect of non-pharmaceutical interventions. A crucial technical challenge in applying such models is their accurate calibration to observed data, e.g., to the daily number of confirmed new cases, as the past history of the disease strongly affects predictions of future scenarios. We demonstrate an approach based on inversion of the SEIR equations in conjunction with statistical modelling and spline-fitting of the data, to produce a robust methodology for calibration of a wide class of models of this type.
The software program BAMM has been widely used to study the dynamics of speciation, extinction, and phenotypic evolution on phylogenetic trees. The program implements a model-based clustering algorithm to identify clades that share common macroevolutionary rate dynamics and to estimate rate parameters. A recent simulation study published in Evolution (2017) by Meyer and Wiens (M&W) claimed that (i) simple (MS) estimators of diversification rates perform much better than BAMM, and (ii) evolutionary rates inferred with BAMM are weakly correlated with the true rates in the generating model. I demonstrate that their assessment suffers from two major conceptual errors that invalidate both primary conclusions. These statistical considerations are not specific to BAMM and apply to all methods for estimating parameters from empirical data where the true grouping structure of the data is unknown. First, M&Ws comparisons between BAMM and MS estimators suffer from false equivalency because the MS estimators are given perfect prior knowledge of the locations of rate shifts on the simulated phylogenies. BAMM is given no such information and must simultaneously estimate the number and location of rate shifts from the data, thus resulting in a massive degrees-of-freedom advantage for the MS estimators.When both methods are given equivalent information, BAMM dramatically outperforms the MS estimators. Second, M&Ws experimental design is unable to assess parameter reliability because their analyses conflate small effect sizes across treatment groups with error in parameter estimates. Nearly all model-based frameworks for partitioning data are susceptible to the statistical mistakes in M&W, including popular clustering algorithms in population genetics, phylogenetics, and comparative methods.
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