Abstract
BackgroundStandard epidemiological theory claims that in structured populations competition between multiple pathogen strains is a deterministic process which is mediated by the basic reproduction number () of the individual strains. A new theory based on analysis, simulation and empirical study challenges this predictor of success.Principal FindingsWe show that the quantity is a valid predictor in structured populations only when size is infinite. In this article we show that when population size is finite the dynamics of infection by multi-strain pathogens is a stochastic process whose outcome can be predicted by evolutionary entropy, S, an information theoretic measure which describes the uncertainty in the infectious age of an infected parent of a randomly chosen new infective. Evolutionary entropy characterises the demographic stability or robustness of the population of infectives. This statistical parameter determines the duration of infection and thus provides a quantitative index of the pathogenicity of a strain. Standard epidemiological theory based on as a measure of selective advantage is the limit as the population size tends to infinity of the entropic selection theory. The standard model is an approximation to the entropic selection theory whose validity increases with population size.ConclusionAn epidemiological analysis based on entropy is shown to explain empirical observations regarding the emergence of less pathogenic strains of human influenza during the antigenic drift phase. Furthermore, we exploit the entropy perspective to discuss certain epidemiological patterns of the current H1N1 swine 'flu outbreak.
Highlights
Recent years have seen an apparent acceleration in the rate of emergence of new infectious disease pathogens in the human population [1]
An epidemiological analysis based on entropy is shown to explain empirical observations regarding the emergence of less pathogenic strains of human influenza during the antigenic drift phase
The argument is that a larger R0 results in a faster rate of infection of susceptibles thereby driving competitor pathogen strains with lower R0 to extinction
Summary
Recent years have seen an apparent acceleration in the rate of emergence of new infectious disease pathogens in the human population [1]. Some of these have their origins in animal (wild or domesticated) reservoirs [2,3,4], and the years since 2003 have witnessed the appearance of SARS [5,6] and swine flu [7]. In recent months the emergence of a swine ‘flu (H1N1 2009) with human-to-human transmission capability has re-focussed attention on this issue [7,13] Likewise, studies, such of those of Creanza et al [14] who used a computational analysis of viral nucleotide and amino acid sequence data collected during seasonal ’flu epidemics show how diversity declines over the course of an epidemic. A new theory based on analysis, simulation and empirical study challenges this predictor of success
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