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A well-known characteristic of pandemics such as COVID-19 is the high level of transmission heterogeneity in the infection spread: not all infected individuals spread the disease at the same rate and some individuals (superspreaders) are responsible for most of the infections. To quantify this phenomenon requires the analysis of the effect of the variance and higher moments of the infection distribution. Working in the framework of stochastic branching processes, we derive an approximate analytical formula for the probability of an outbreak in the high variance regime of the infection distribution, verify it numerically and analyze its regime of validity in various examples. We show that it is possible for an outbreak not to occur in the high variance regime even when the basic reproduction number $R_0$ is larger than one and discuss the implications of our results for COVID-19 and other pandemics.
Infectious diseases are caused by pathogenic microorganisms and can spread through different ways. Mathematical models and computational simulation have been used extensively to investigate the transmission and spread of infectious diseases. In other
There are often multiple diseases with cross immunity competing for vaccination resources. Here we investigate the optimal vaccination program in a two-layer Susceptible-Infected-Removed (SIR) model, where two diseases with cross immunity spread in t
Covid-19 has caused hundred of thousands of deaths and an economic damage amounting to trillions of dollars, creating a desire for the rapid development of vaccine. Once available, vaccine is gradually produced, evoking the question on how to distrib
We extend the classical SIR model of infectious disease spread to account for time dependence in the parameters, which also include diffusivities. The temporal dependence accounts for the changing characteristics of testing, quarantine and treatment
We model and calculate the fraction of infected population necessary to reach herd immunity, taking into account the heterogeneity in infectiousness and susceptibility, as well as the correlation between those two parameters. We show that these cause