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Evolution and virulence

Overview

We study the evolution of parasites and pathogens (including those which jump to novel host species, causing emerging disease), and how this affects their pathogenicity and virulence. We are also investigating coevolution between hosts and disease agents, and between interacting parasites and pathogens of different strains and species. Findings are relevant to disease surveillance and control policies.

Characterizing evolution

CIDD researchers are:

We mostly focus on:

Identifying gene function and expression

Once genetic differences between related microorganisms have been identified, we are looking in more detail at some of them to investigate the function and expression of particular genes. This can enable us to identify the genes involved in virulence and the circumstances under which they are expressed. For instance, Schuster and colleagues are investigating the bacterium Wolinella succinogenes which is non-pathogenic to its bovine host, but contains genes identified as virulence factors in related species (e.g. Campylobacter jejuni).

Investigating coevolution

Hosts and pathogens can exert powerful selective pressures on each other. CIDD researchers are investigating coevolution of hosts and disease agents in a variety of systems. For example:

Next step phylodynamics

Information about patterns, mechanisms and causes of evolution is at the core of the emerging discipline of phylodynamics, which is being pioneered by CIDD researchers.

Study systems include

Influenza (Grenfell, Holmes)

Rabbit Haemorrhagic Disease Virus (Hudson)

A wide variety of other RNA viruses including dengue and lyssaviruses (Holmes)

Myxoma (Cattadori, Holmes, Hudson, Schuster)

Campylobacteraceae (Schuster)

Helicobacteraceae (Schuster)

Bordetella (Bjørnstad, Harvill)

Sample papers

Chen R & Holmes EC (2007) Avian influenza virus exhibits rapid evolutionary dynamics. Molecular Biology and Evolution 23: 2336-2341.

Poss M, Adoine A, Ross HA, Terwee JA, VandeWoude S & Rodrigo A (2007) Recombination in feline lentiviral genomes following experimental cross-species infection. Virology 359: 146-151.

Koelle K, Cobey S, Grenfell B & Pascual M (2006) Epochal evolution shapes the phylodynamics of influenza A (H3N2) in humans. Science 314: 1898-1903

Nelson MI, Simonsen L, Viboud C, Miller MA, Taylor J, St. George K, Griesemer SB, Ghedin E, Sengamalay NA, Spiro DJ, Volkov I, Grenfell BT, Lipman DJ, Taubenberger JK & Holmes EC. Stochastic processes are key determinants of short-term evolution in Influenza A Virus. PLoS Pathogens 2(11): e125

Luis AD & Hudson PJ (2006). Hibernation patterns in mammals: a role for bacterial growth?. Funct. Ecol. 20: 471

Zhang C, Mammen MP, Chinnawirotpisan P, Klungthong C, Rodpradit P, Monkongdee P, Nimmannitya S, Kalayanarooj S & Holmes EC (2005) Clade replacements in Dengue virus serotypes 1 and 3 are associated with changing serotype prevalence J. Virology 79: 15123-15130

Bjørnstad ON & Harvill ET (2005). Evolution and emergence of Bordetella in humans. Trends Microbiol. 13: 355-359

Holmes EC, Ghedin E, Miller N, Taylor J, Bao Y, St George K, Grenfell BT, Salzberg SL, Fraser CM, Lipman DJ & Taubenberger JK (2005). Whole-genome analysis of human influenza A virus reveals multiple persistent lineages and reassortment among recent H3N2 viruses. PLOS Biology 3(9)

Boots M, Hudson PJ & Sasaki A (2004). Large shifts in pathogen virulence relate to host population structure. Science 303: 842-844.