Phylodynamics of Infectious Disease Epidemics

  • Erik M Volz
    Department of Epidemiology , University of Michigan, Ann Arbor, Michigan 48109
  • Sergei L Kosakovsky Pond
    Department of Medicine, University of California , La Jolla, California 92093
  • Melissa J Ward
    School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JR , United Kingdom and
  • Andrew J Leigh Brown
    School of Biological Sciences, University of Edinburgh, Edinburgh EH9 3JR , United Kingdom and
  • Simon D W Frost
    Department of Veterinary Medicine, University of Cambridge , Cambridge CB3 0ES, United Kingdom

抄録

<jats:title>Abstract</jats:title><jats:p>We present a formalism for unifying the inference of population size from genetic sequences and mathematical models of infectious disease in populations. Virus phylogenies have been used in many recent studies to infer properties of epidemics. These approaches rely on coalescent models that may not be appropriate for infectious diseases. We account for phylogenetic patterns of viruses in susceptible–infected (SI), susceptible–infected–susceptible (SIS), and susceptible–infected–recovered (SIR) models of infectious disease, and our approach may be a viable alternative to demographic models used to reconstruct epidemic dynamics. The method allows epidemiological parameters, such as the reproductive number, to be estimated directly from viral sequence data. We also describe patterns of phylogenetic clustering that are often construed as arising from a short chain of transmissions. Our model reproduces the moments of the distribution of phylogenetic cluster sizes and may therefore serve as a null hypothesis for cluster sizes under simple epidemiological models. We examine a small cross-sectional sample of human immunodeficiency (HIV)-1 sequences collected in the United States and compare our results to standard estimates of effective population size. Estimated prevalence is consistent with estimates of effective population size and the known history of the HIV epidemic. While our model accurately estimates prevalence during exponential growth, we find that periods of decline are harder to identify.</jats:p>

収録刊行物

  • Genetics

    Genetics 183 (4), 1421-1430, 2009-12-01

    Oxford University Press (OUP)

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