Formal kinetics of H1N1 epidemic

<p>Abstract</p> <p>Background</p> <p>The formal kinetics of the H1N1 epidemic seems to take the form of an exponential curve. There is a good correlation between this theoretical model and epidemiological data on the number of H1N1-infected people. But this formal model leads to paradoxes about the dates when everyone becomes infected: in Mexico this will happen after one year, then in the rest of the world.</p> <p>Further implications of the formal model</p> <p>The general limitations of this formal kinetics model are discussed. More detailed modeling is examined and the implications are examined in the light of currently available data. The evidence indicates that not more than 10% of the population is initially resistant to the H1N1 virus.</p> <p>Conclusion</p> <p>We are probably only at the initial stage of development of the H1N1 epidemic. Increasing the number of H1N1-resistant people in future (e.g. due to vaccination) may influence the dynamics of epidemic development. At present, the development of the epidemic depends only on the number of people in the population who are initially resistant to the virus.</p

A comprehensive probabilistic analysis of SIR-type epidemiological models based on full randomized Discrete-Time Markov Chain formulation with applications

[EN] This paper provides a comprehensive probabilistic analysis of a full randomization of approximate SIR-type epidemiological models based on discrete-time Markov chain formulation. The randomization is performed by assuming that all input data (initial conditions, the contagion, and recovering rates involved in the transition matrix) are random variables instead of deterministic constants. In the first part of the paper, we determine explicit expressions for the so called first probability density function of each subpopulation identified as the corresponding states of the Markov chain (susceptible, infected, and recovered) in terms of the probability density function of each input random variable. Afterwards, we obtain the probability density functions of the times until a given proportion of the population remains susceptible, infected, and recovered, respectively. The theoretical analysis is completed by computing explicit expressions of important randomized epidemiological quantities, namely, the basic reproduction number, the effective reproduction number, and the herd immunity threshold. The study is conducted under very general assumptions and taking extensive advantage of the random variable transformation technique. The second part of the paper is devoted to apply our theoretical findings to describe the dynamics of the pandemic influenza in Egypt using simulated data excerpted from the literature. The simulations are complemented with valuable information, which is seldom displayed in epidemiological models. In spite of the nonlinear mathematical nature of SIR epidemiological model, our results show a strong agreement with the approximation via an appropriate randomized Markov chain. A justification in this regard is discussed.Spanish Ministerio de Economia y Competitividad, Grant/Award Number: MTM2017-89664-P; Generalitat Valenciana, Grant/Award Number: APOSTD/2019/128; Ministerio de Economia y Competitividad, Grant/Award Number: MTM2017-89664-PCortés, J.; El-Labany, S.; Navarro-Quiles, A.; Selim, MM.; Slama, H. (2020). A comprehensive probabilistic analysis of SIR-type epidemiological models based on full randomized Discrete-Time Markov Chain formulation with applications. Mathematical Methods in the Applied Sciences. 43(14):8204-8222. https://doi.org/10.1002/mma.6482S820482224314Hamra, G., MacLehose, R., & Richardson, D. (2013). Markov Chain Monte Carlo: an introduction for epidemiologists. International Journal of Epidemiology, 42(2), 627-634. doi:10.1093/ije/dyt043Becker, N. (1981). A General Chain Binomial Model for Infectious Diseases. Biometrics, 37(2), 251. doi:10.2307/2530415Allen, L. J. S. (2010). An Introduction to Stochastic Processes with Applications to Biology. doi:10.1201/b12537Hethcote, H. W. (2000). The Mathematics of Infectious Diseases. SIAM Review, 42(4), 599-653. doi:10.1137/s0036144500371907Brauer, F., & Castillo-Chávez, C. (2001). Mathematical Models in Population Biology and Epidemiology. Texts in Applied Mathematics. doi:10.1007/978-1-4757-3516-1Cortés, J.-C., Navarro-Quiles, A., Romero, J.-V., & Roselló, M.-D. (2018). Some results about randomized binary Markov chains: theory, computing and applications. International Journal of Computer Mathematics, 97(1-2), 141-156. doi:10.1080/00207160.2018.1440290Cortés, J.-C., Navarro-Quiles, A., Romero, J.-V., & Roselló, M.-D. (2017). Randomizing the parameters of a Markov chain to model the stroke disease: A technical generalization of established computational methodologies towards improving real applications. Journal of Computational and Applied Mathematics, 324, 225-240. doi:10.1016/j.cam.2017.04.040Casabán, M.-C., Cortés, J.-C., Romero, J.-V., & Roselló, M.-D. (2015). Probabilistic solution of random SI-type epidemiological models using the Random Variable Transformation technique. Communications in Nonlinear Science and Numerical Simulation, 24(1-3), 86-97. doi:10.1016/j.cnsns.2014.12.016Casabán, M.-C., Cortés, J.-C., Navarro-Quiles, A., Romero, J.-V., Roselló, M.-D., & Villanueva, R.-J. (2016). A comprehensive probabilistic solution of random SIS-type epidemiological models using the random variable transformation technique. Communications in Nonlinear Science and Numerical Simulation, 32, 199-210. doi:10.1016/j.cnsns.2015.08.009Slama, H., Hussein, A., El-Bedwhey, N. A., & Selim, M. M. (2019). An approximate probabilistic solution of a random SIR-type epidemiological model using RVT technique. Applied Mathematics and Computation, 361, 144-156. doi:10.1016/j.amc.2019.05.019Slama, H., El-Bedwhey, N. A., El-Depsy, A., & Selim, M. M. (2017). Solution of the finite Milne problem in stochastic media with RVT Technique. The European Physical Journal Plus, 132(12). doi:10.1140/epjp/i2017-11763-6Kegan, B., & West, R. W. (2005). Modeling the simple epidemic with deterministic differential equations and random initial conditions. Mathematical Biosciences, 195(2), 179-193. doi:10.1016/j.mbs.2005.02.004Dorini, F. A., Cecconello, M. S., & Dorini, L. B. (2016). On the logistic equation subject to uncertainties in the environmental carrying capacity and initial population density. Communications in Nonlinear Science and Numerical Simulation, 33, 160-173. doi:10.1016/j.cnsns.2015.09.009Van den Driessche, P. (2017). Reproduction numbers of infectious disease models. Infectious Disease Modelling, 2(3), 288-303. doi:10.1016/j.idm.2017.06.002Heffernan, J. ., Smith, R. ., & Wahl, L. . (2005). Perspectives on the basic reproductive ratio. Journal of The Royal Society Interface, 2(4), 281-293. doi:10.1098/rsif.2005.0042Khalil, K. M., Abdel-Aziz, M., Nazmy, T. T., & Salem, A.-B. M. (2012). An Agent-Based Modeling for Pandemic Influenza in Egypt. Intelligent Systems Reference Library, 205-218. doi:10.1007/978-3-642-25755-1_1

Theoretical size distribution of fossil taxa: analysis of a null model

BACKGROUND: This article deals with the theoretical size distribution (of number of sub-taxa) of a fossil taxon arising from a simple null model of macroevolution. MODEL: New species arise through speciations occurring independently and at random at a fixed probability rate, while extinctions either occur independently and at random (background extinctions) or cataclysmically. In addition new genera are assumed to arise through speciations of a very radical nature, again assumed to occur independently and at random at a fixed probability rate. CONCLUSION: The size distributions of the pioneering genus (following a cataclysm) and of derived genera are determined. Also the distribution of the number of genera is considered along with a comparison of the probability of a monospecific genus with that of a monogeneric family

How big is an outbreak likely to be? Methods for epidemic final-size calculation

Epidemic models have become a routinely used tool to inform policy on infectious disease. A particular interest at the moment is the use of computationally intensive inference to parametrize these models. In this context, numerical efficiency is critically important. We consider methods for evaluating the probability mass function of the total number of infections over the course of a stochastic epidemic, with a focus on homogeneous finite populations, but also considering heterogeneous and large populations. Relevant methods are reviewed critically, with existing and novel extensions also presented. We provide code in Matlab and a systematic comparison of numerical efficiency.Thomas House, Joshua V. Ross and David Sir

Transition probabilities for general birth-death processes with applications in ecology, genetics, and evolution

A birth-death process is a continuous-time Markov chain that counts the number of particles in a system over time. In the general process with $n$ current particles, a new particle is born with instantaneous rate $\lambda_n$ and a particle dies with instantaneous rate $\mu_n$. Currently no robust and efficient method exists to evaluate the finite-time transition probabilities in a general birth-death process with arbitrary birth and death rates. In this paper, we first revisit the theory of continued fractions to obtain expressions for the Laplace transforms of these transition probabilities and make explicit an important derivation connecting transition probabilities and continued fractions. We then develop an efficient algorithm for computing these probabilities that analyzes the error associated with approximations in the method. We demonstrate that this error-controlled method agrees with known solutions and outperforms previous approaches to computing these probabilities. Finally, we apply our novel method to several important problems in ecology, evolution, and genetics

Susceptibility sets and the final outcome of collective Reed–Frost epidemics

This paper is concerned with exact results for the final outcome of stochastic SIR (susceptible → infective → recovered) epidemics among a closed, finite and homogeneously mixing population. The factorial moments of the number of initial susceptibles who ultimately avoid infection by such an epidemic are shown to be intimately related to the concept of a susceptibility set. This connection leads to simple, probabilistically illuminating proofs of exact results concerning the total size and severity of collective Reed–Frost epidemic processes, in terms of Gontcharoff polynomials, first obtained in a series of papers by Claude Lef`evre and Philippe Picard. The proofs extend easily to include general final state random variables defined on SIR epidemics, and also to multitype epidemics

Dynamics of multi-stage infections on networks

This paper investigates the dynamics of infectious diseases with a nonexponentially distributed infectious period. This is achieved by considering a multistage infection model on networks. Using pairwise approximation with a standard closure, a number of important characteristics of disease dynamics are derived analytically, including the final size of an epidemic and a threshold for epidemic outbreaks, and it is shown how these quantities depend on disease characteristics, as well as the number of disease stages. Stochastic simulations of dynamics on networks are performed and compared to output of pairwise models for several realistic examples of infectious diseases to illustrate the role played by the number of stages in the disease dynamics. These results show that a higher number of disease stages results in faster epidemic outbreaks with a higher peak prevalence and a larger final size of the epidemic. The agreement between the pairwise and simulation models is excellent in the cases we consider

Theoretical basis to measure the impact of short-lasting control of an infectious disease on the epidemic peak

Background. While many pandemic preparedness plans have promoted disease control effort to lower and delay an epidemic peak, analytical methods for determining the required control effort and making statistical inferences have yet to be sought. As a first step to address this issue, we present a theoretical basis on which to assess the impact of an early intervention on the epidemic peak, employing a simple epidemic model. Methods. We focus on estimating the impact of an early control effort (e.g. unsuccessful containment), assuming that the transmission rate abruptly increases when control is discontinued. We provide analytical expressions for magnitude and time of the epidemic peak, employing approximate logistic and logarithmic-form solutions for the latter. Empirical influenza data (H1N1-2009) in Japan are analyzed to estimate the effect of the summer holiday period in lowering and delaying the peak in 2009. Results. Our model estimates that the epidemic peak of the 2009 pandemic was delayed for 21 days due to summer holiday. Decline in peak appears to be a nonlinear function of control-associated reduction in the reproduction number. Peak delay is shown to critically depend on the fraction of initially immune individuals. Conclusions. The proposed modeling approaches offer methodological avenues to assess empirical data and to objectively estimate required control effort to lower and delay an epidemic peak. Analytical findings support a critical need to conduct population-wide serological survey as a prior requirement for estimating the time of peak. © 2011 Omori and Nishiura; licensee BioMed Central Ltd.published_or_final_versio