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Browse SpaceDr Jonathan M. Read
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Read the University of Liverpool press release. I am a lecturer in infectious disease epidemiology, within the Epidemiology and Public Health group of the School of Veterinary Science, and am affiliated with the National Center for Zoonosis Research. My research interests include the transmission of infectious diseases and the evolutionary pressures acting on pathogens, at a variety of spatial and temporal scales (see below for more information). A substantial part of this interest lies in understanding transmission upon contact networks, measuring social contact networks and patterns, and understanding the behvaioural responses of people to infections. I will be the Programme Director for the Veterinary Infection and Disease Control MSc from autumn 2008 onwards. Keywords Grants Awarded
Current PhD students
Teaching
Collaborators
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Contact Details.Epidemiology & Public Health, |
Presentations and achievements
- 2009-, Honorary Research Fellow, University of Warwick.
- 1991, awarded the Shell Environmental Prize for my undergraduate dissertation under the supervision of Dr Richard Law.
- 2006, presented a poster of my work on disease evolution on networks at the House of Commons as part of SET for Europe and National Science Week.
- see here for list of invited presentations and others.
Publications
- Eames, K.T.D., Read, J.M., Edmunds, W.J. (2009) Epidemic prediction and control in weighted networks. Epidemics 1, 70-76. DOI: 10.1016/j.epidem.2008.12.001
- Read, J.M., Eames, K.T.D., Edmunds, W.J. (2008) Dynamic social networks and the implications for the spread of infectious disease. Journal of the Royal Society Interface 5(26), 957-1118.
- Eames, K.T.D., Read J.M. (2008) Networks in epidemology. Lecture Notes in Computer Science (including subseries Lecture Notes in Artificial Intelligence and Lecture Notes in Bioinformatics) 5151 LNCS, pp. 79-90
- Read, J.M. & Keeling, M.J. (2007). Stochasticity generates an evolutionary instability for infectious disease. Ecology Letters 10, 818-827.
- Read, J.M. & Keeling, M.J. (2006). Disease evolution across a range of spatio-temporal scales. Theoretical Population Biology 70, 210-213.
- Read, J.M. & Keeling, M.J. (2003). Disease evolution on networks: the role of contact structure. Proc. Roy. Soc. Lond. B 270, 699-708.
- Keeling, M.J., Jiggins, F.M. & Read, J.M. (2003). The invasion and coexistence of competing Wolbachia strains. Heredity 91, 382-388
- Read, J.M., Birch, C.P.D. & Milne, J. (2002). HeathMod: a model of the impact of seasonal grazing by sheep on upland heaths dominated by Calluna vulgaris (heather). Biological Conservation 105, 279-292.
- Lingjærde, O.C., Stenseth, N.C., Kristoffersen , A.B., Smith, R.H., Moe , S.J., Read, J.M., Daniels, S., & Simkiss, K. (2002). Exploring the density-dependent structure of blowfly populations by nonparametric additive modeling. Ecology 82, 2645-2658.
Research Interests
Contact networks
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The spread of diseases which require close-contact between individuals for transmission is ultimately dictated by the way individuals behave. How they interact provides the infection with opportunities for transmission. Different diseases that have different transmission modes (e.g. fomite, airborne, water-borne, vector-borne or sexually transmitted) could, therefore, have very transmission networks with very different structures and very different patterns of disease spread. Relatively little is known about the structure of infection networks, and many mathematical models of epidemics are forced, by necessity, to make strong assumptions about how individuals mix. Arguably, the structure of sexual partner networks and the spread of sexually transmitted infections is the most studied type of transmission network. Much of my current research is directed to quantifying and understanding the structure of human social and animal interaction networks, through direct or proxy measurements. The aim is to better understand the transmission process, the opportunities for disease transmission, and to develop better and more precise control or mitigation strategies. |
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Disease evolution
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Social interactions between individuals and their movements are very different today compared to hundreds of years ago. Undoubtedly this affects the way disease spreads through communities and populations, but does it also exert an evolutionary force on the transmission characteristic of pathogens? The threat posed by avian influenza, and recent experience with the spread of SARS, have highlighted our vulnerability to mutating pathogens. It is important to understand whether such emerging diseases are an evolutionary response to substantial changes in social and movement patterns over recent decades, or represent temporary lineages that do not persist. The number and frequency of interactions between hosts necessarily determines the potential routes of transmission available to an infection, within a host population. Explicit models of the spread of a pathogen on a host population contact network, and the random mutation of pathogen characteristics as it proliferates, enable us to describe the long-term evolutionary pressure exerted by the structure of a host population on pathogen transmission and survival. Adaptation of the host population structure by the infecting pathogen is one of the surprising results to arise from this work. |
Within-host dynamics and between-host transmission
The nature of the interaction between a pathogen and its host's immune system has dramatic consequences, not only for the fate of the pathogen within the host, but also on the transmission (or not) of the pathogen to other hosts. This has implications at the population-scale of spread and ultimately evolution of the pathogen species. Additionally, all pathogen mutation takes place within the host, not as it transfers to other host which is how disease evolution is typically modelled. Consequently I am really interested in developing a general model of host-pathogen interaction, and pathogen mutation and transmission.
Control of pathogens
The threat of covert release of infectious pathogens by terrorists and the emergence of novel zoonotic and human diseases present healthcare authorities with difficult tests of management policies, and the appropriate and proportionate response to the allocation of resources. From a disease control perspective it is of fundamental importance to identify when an epidemic may be best controlled using targeted response (e.g. contact tracing and quarantining of individuals) compared to a blanket response (such as mass vaccination, or culling in the case of livestock diseases).
Using an explicit network of contacts (assumed to be representative of the UK population), Matt Keeling and I developed a model of covert smallpox release and infection within a reltaively small population, for the Health Protection Agency in 2003. We applied various control options (quarantine, contact tracing and mass vaccination) to identify the ideal control strategy for a given situation. We found network structure to have a profound influence on the appropriate response to such outbreaks.
Previous life
From 2001 until 2007 I was post-doc with Matt Keeling at the University of Warwick, before that I was at the University of Cambridge as a post-doc in Bryan Grenfell's group, again working with Matt Keeling; this was working on models of evolutionary and infectious disease epidemiology. Prior to this I was to be found studying the long-term dynamics of blowfly populations (University of Leicester), the grazing management of upland heather moors (Macauley Institute, Aberdeen), and modelling above- and below-ground competition between plants (PhD, Stirling University).
Other stuff
I struggle with rocks and light. It passes the time.
