TitleNon-random biodiversity loss underlies predictable increases in viral disease prevalence.
Publication TypeJournal Article
Year of Publication2014
AuthorsLacroix, C, Jolles, AE, Seabloom, EW, Power, AG, Mitchell, CE, Borer, ET
JournalJ R Soc Interface
Volume11
Issue92
Pagination20130947
Date Published2014 Mar 06
ISSN1742-5662
KeywordsAnimals, Aphids, Biodiversity, British Columbia, California, Fertility, Host-Pathogen Interactions, Insect Vectors, Linear Models, Luteovirus, Oregon, Plant Diseases, Poaceae, Prevalence
Abstract

Disease dilution (reduced disease prevalence with increasing biodiversity) has been described for many different pathogens. Although the mechanisms causing this phenomenon remain unclear, the disassembly of communities to predictable subsets of species, which can be caused by changing climate, land use or invasive species, underlies one important hypothesis. In this case, infection prevalence could reflect the competence of the remaining hosts. To test this hypothesis, we measured local host species abundance and prevalence of four generalist aphid-vectored pathogens (barley and cereal yellow dwarf viruses) in a ubiquitous annual grass host at 10 sites spanning 2000 km along the North American West Coast. In laboratory and field trials, we measured viral infection as well as aphid fecundity and feeding preference on several host species. Virus prevalence increased as local host richness declined. Community disassembly was non-random: ubiquitous hosts dominating species-poor assemblages were among the most competent for vector production and virus transmission. This suggests that non-random biodiversity loss led to increased virus prevalence. Because diversity loss is occurring globally in response to anthropogenic changes, such work can inform medical, agricultural and veterinary disease research by providing insights into the dynamics of pathogens nested within a complex web of environmental forces.

DOI10.1098/rsif.2013.0947
Alternate JournalJ R Soc Interface
PubMed ID24352672
PubMed Central IDPMC3899862