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Emerging diseases

Overview

Sometimes, a parasite spills over from its usual host species into a novel host. When it is transmitted from individual to individual within the new host population, it has the potential to become endemic or epidemic. CIDD researchers are exploring what underlies the emergence and persistence of emerging and re-emerging diseases — from the cellular mechanisms involved in invasion of the host; to host immune responses; to the evolution of viruses by mutation, recombination and reassortment; to the spatial and social arrangement of host populations that predispose them to successful invasion.

Zoonoses and more

Many well-known emerging diseases are zoonoses — where humans are infected by an animal disease agent that does not normally depend on human hosts to complete its life cycle. West Nile Virus, rabies and Lyme Disease are all examples. CIDD researchers are investigating some zoonotic diseases (e.g. influenza, tick-borne encephalitis), as well as emerging diseases resulting from other routes of transmission:

From spillover to persistence

In most cases, a parasite challenging a host from a different species will fail to infect it. Even where a parasite does manage to infect an individual of a new species, the spillover is often a dead end for the parasite — it does not transmit adequately to new hosts. However, in some cases, the parasite transmits and persists.

CIDD researchers are investigating what makes species jumps more likely, and what enables parasites to transmit and persist in novel host populations. We are exploring variables that increase the likelihood of a spillover event resulting in persistence, including:

Controlling emerging diseases

CIDD research has implications for control of emerging diseases, particularly for strategies that attempt to:

» more on control strategies

Sample papers

Snappin KW, Holmes EC, Young DS, Bernard KA, Kramer LD & Ebel GD (2007) Declining growth rate of West Nile Virus in North America. J. Virology 81: 2531-2534

Holmes EC (2006) The evolution of viral emergence. PNAS 103: 4803-4804

Kuiken T, Holmes EC, McCauley J, Rimmelzwaan GF, Williams CS & Grenfell BT (2006). Host species barriers to influenza virus infections. Science 312: 394-397

Eppinger M, Baar B, Linz B, Raddatz G, Lanz C, Keller H, Morelli G, Gressmann H, Achtman M & Schuster SC (2006). Who ate whom? Adaptive Helicobacter genomic changes that accompanied a host jump from early humans to large felines. PLoS Genetics

Carrington CVF, Foster JE, ybus OG, Bennett SN, & Holmes EC (2005). Invasion and maintenance of dengue virus Type 2 and Type 4 in the Americas. J. Virology 79: 14680-14687

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

Shackelton LA, Parrish CR, Truyen U & Holmes EC (2005). High rate of viral evolution associated with the emergence of canine parvoviruses. Proc. Natl. Acad. Sci. USA 102: 379-384

Holmes EC & Rambaut A. (2004). Viral evolution and the emergence of SARS coronavirus. Phil. Trans. Roy. Soc. Lond. B. 359: 1059-1065.

Barnett OE, Worobey M, Holmes EC & Cooper A (2004). Detection of TT virus among chimpanzees in the wild using a noninvasive technique. J. Wildlife Diseases 40: 230-237.

Rosa R, Pugliese A, Norman R & Hudson PJ (2003). Thresholds for disease persistence in models for tick-borne infections including non-viraemic transmission, extended feeding and tick aggregation. J. Theor. Biol. 224: 359-376

Laurensen MK, Norman RA, Gilbert L, Reid HW & Hudson PJ (2003). Identifying disease reservoirs in complex systems: mountain hares as reservoirs of ticks and louping-ill virus, pathogens of red grouse. J. Anim. Ecol. 72: 177-185