No Arabic abstract
Epidemic models are useful tools in the fight against infectious diseases, as they allow policy makers to test and compare various strategies to limit disease transmission while mitigating collateral damage on the economy. Epidemic models that are more faithful to the microscopic details of disease transmission can offer more reliable projections, which in turn can lead to more reliable control strategies. For example, many epidemic models describe disease progression via a series of artificial stages or compartments (e.g. exposed, activated, infectious, etc.) but an epidemic model that explicitly tracks time since infection (TSI) can provide a more precise description. At present, epidemic models with compartments are more common than TSI models , largely due to higher computational cost and complexity typically associated with TSI models. Here, however, we show that with the right discretization scheme a TSI model is not much more difficult to solve than a comparment model with three or four stages for the infected class. We also provide a new perspective for adding stages to a TSI model in a way that decouples the disease transmission dynamics from the residence time distributions at each stage. These results are also generalized for age-structured TSI models in an appendix. Finally, as proof-of-principle for the efficiency of the proposed numerical methods, we provide calculations for optimal epidemic control by non-pharmaceutical intervention. Many of the tools described in this report are available through the software package pyross
We study the early stages of viral infection, and the distribution of times to obtain a persistent infection. The virus population proliferates by entering and reproducing inside a target cell until a sufficient number of new virus particles are released via a burst, with a given burst size distribution, which results in the death of the infected cell. Starting with a 2D model describing the joint dynamics of the virus and infected cell populations, we analyze the corresponding master equation using the probability generating function formalism. Exploiting time-scale separation between the virus and infected cell dynamics, the 2D model can be cast into an effective 1D model. To this end, we solve the 1D model analytically for a particular choice of burst size distribution. In the general case, we solve the model numerically by performing extensive Monte-Carlo simulations, and demonstrate the equivalence between the 2D and 1D models by measuring the Kullback-Leibler divergence between the corresponding distributions. Importantly, we find that the distribution of infection times is highly skewed with a fat exponential right tail. This indicates that there is non-negligible portion of individuals with an infection time, significantly longer than the mean, which may have implications on when HIV tests should be performed.
We present an efficient and flexible method for computing likelihoods of phenotypic traits on a phylogeny. The method does not resort to Monte-Carlo computation but instead blends Felsensteins discrete character pruning algorithm with methods for numerical quadrature. It is not limited to Gaussian models and adapts readily to model uncertainty in the observed trait values. We demonstrate the framework by developing efficient algorithms for likelihood calculation and ancestral state reconstruction under Wrights threshold model, applying our methods to a dataset of trait data for extrafloral nectaries (EFNs) across a phylogeny of 839 Labales species.
Quantifying the attack ratio of disease is key to epidemiological inference and Public Health planning. For multi-serotype pathogens, however, different levels of serotype-specific immunity make it difficult to assess the population at risk. In this paper we propose a Bayesian method for estimation of the attack ratio of an epidemic and the initial fraction of susceptibles using aggregated incidence data. We derive the probability distribution of the effective reproductive number, R t , and use MCMC to obtain posterior distributions of the parameters of a single-strain SIR transmission model with time-varying force of infection. Our method is showcased in a data set consisting of 18 years of dengue incidence in the city of Rio de Janeiro, Brazil. We demonstrate that it is possible to learn about the initial fraction of susceptibles and the attack ratio even in the absence of serotype specific data. On the other hand, the information provided by this approach is limited, stressing the need for detailed serological surveys to characterise the distribution of serotype-specific immunity in the population.
Recent work has found that the behavior of an individual can be altered when infected by a parasite. Here we explore the question: under what conditions, in principle, can a general parasitic infection control system-wide social behaviors? We analyze fixed points and hysteresis effects under the Master Equation, with transitions between two behaviors given two different subpopulations, healthy vs. parasitically-infected, within a population which is kept fixed overall. The key model choices are: (i) the internal opinion of infected humans may differ from that of the healthy population, (ii) the extent that interaction drives behavioral changes may also differ, and (iii) indirect interactions are most important. We find that the socio-configuration can be controlled by the parasitically-infected population, under some conditions, even if the healthy population is the majority and of opposite opinion.
In this paper, we introduce a novel modeling framework for incorporating fear of infection and frustration with social distancing into disease dynamics. We show that the resulting SEIR behavior-perception model has three principal modes of qualitative behavior---no outbreak, controlled outbreak, and uncontrolled outbreak. We also demonstrate that the model can produce transient and sustained waves of infection consistent with secondary outbreaks. We fit the model to cumulative COVID-19 case and mortality data from several regions. Our analysis suggests that regions which experience a significant decline after the first wave of infection, such as Canada and Israel, are more likely to contain secondary waves of infection, whereas regions which only achieve moderate success in mitigating the diseases spread initially, such as the United States, are likely to experience substantial secondary waves or uncontrolled outbreaks.