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      Effect of Biodiversity Changes in Disease Risk: Exploring Disease Emergence in a Plant-Virus System

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          Abstract

          The effect of biodiversity on the ability of parasites to infect their host and cause disease (i.e. disease risk) is a major question in pathology, which is central to understand the emergence of infectious diseases, and to develop strategies for their management. Two hypotheses, which can be considered as extremes of a continuum, relate biodiversity to disease risk: One states that biodiversity is positively correlated with disease risk (Amplification Effect), and the second predicts a negative correlation between biodiversity and disease risk (Dilution Effect). Which of them applies better to different host-parasite systems is still a source of debate, due to limited experimental or empirical data. This is especially the case for viral diseases of plants. To address this subject, we have monitored for three years the prevalence of several viruses, and virus-associated symptoms, in populations of wild pepper (chiltepin) under different levels of human management. For each population, we also measured the habitat species diversity, host plant genetic diversity and host plant density. Results indicate that disease and infection risk increased with the level of human management, which was associated with decreased species diversity and host genetic diversity, and with increased host plant density. Importantly, species diversity of the habitat was the primary predictor of disease risk for wild chiltepin populations. This changed in managed populations where host genetic diversity was the primary predictor. Host density was generally a poorer predictor of disease and infection risk. These results support the dilution effect hypothesis, and underline the relevance of different ecological factors in determining disease/infection risk in host plant populations under different levels of anthropic influence. These results are relevant for managing plant diseases and for establishing conservation policies for endangered plant species.

          Author Summary

          Biodiversity has been proposed as a major ecological factor determining disease prevalence. However, the relationship between biodiversity and disease risk remains underexplored. Few studies focus on host-virus systems and, particularly on plant viruses. To address this subject the prevalence of virus infection and disease symptoms was monitored in wild-pepper (chiltepin) populations under different levels of human management. For these populations, species diversity, host genetic diversity and host plant density were determined. Higher levels of human management resulted in increased disease and virus infection risk, which was associated with decreased habitat species diversity and host genetic diversity, and with increased host plant density. More specifically, for wild chiltepin populations, species diversity of the habitat was the primary predictor of disease risk; and host genetic diversity was the primary predictor in managed populations, with host density being generally a poorer predictor of disease risk. These results support a dilution effect of biodiversity on disease risk, and underline the relevance of different ecological factors in determining disease risk in wild and in human-managed habitats.

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          Most cited references52

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          Social and environmental risk factors in the emergence of infectious diseases

          Fifty years ago, the age-old scourge of infectious disease was receding in the developed world in response to improved public health measures, while the advent of antibiotics, better vaccines, insecticides and improved surveillance held the promise of eradicating residual problems. By the late twentieth century, however, an increase in the emergence and re-emergence of infectious diseases was evident in many parts of the world. This upturn looms as the fourth major transition in human–microbe relationships since the advent of agriculture around 10,000 years ago. About 30 new diseases have been identified, including Legionnaires' disease, human immunodeficiency virus (HIV)/acquired immune deficiency syndrome (AIDS), hepatitis C, bovine spongiform encephalopathy (BSE)/variant Creutzfeldt-Jakob disease (vCJD), Nipah virus, several viral hemorrhagic fevers and, most recently, severe acute respiratory syndrome (SARS) and avian influenza. The emergence of these diseases, and resurgence of old ones like tuberculosis and cholera, reflects various changes in human ecology: rural-to-urban migration resulting in high-density peri-urban slums; increasing long-distance mobility and trade; the social disruption of war and conflict; changes in personal behavior; and, increasingly, human-induced global changes, including widespread forest clearance and climate change. Political ignorance, denial and obduracy (as with HIV/AIDS) further compound the risks. The use and misuse of medical technology also pose risks, such as drug-resistant microbes and contaminated equipment or biological medicines. A better understanding of the evolving social dynamics of emerging infectious diseases ought to help us to anticipate and hopefully ameliorate current and future risks.
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            Effects of plant species richness on invasion dynamics, disease outbreaks, insect abundances and diversity

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              A single determinant dominates the rate of yeast protein evolution.

              A gene's rate of sequence evolution is among the most fundamental evolutionary quantities in common use, but what determines evolutionary rates has remained unclear. Here, we carry out the first combined analysis of seven predictors (gene expression level, dispensability, protein abundance, codon adaptation index, gene length, number of protein-protein interactions, and the gene's centrality in the interaction network) previously reported to have independent influences on protein evolutionary rates. Strikingly, our analysis reveals a single dominant variable linked to the number of translation events which explains 40-fold more variation in evolutionary rate than any other, suggesting that protein evolutionary rate has a single major determinant among the seven predictors. The dominant variable explains nearly half the variation in the rate of synonymous and protein evolution. We show that the two most commonly used methods to disentangle the determinants of evolutionary rate, partial correlation analysis and ordinary multivariate regression, produce misleading or spurious results when applied to noisy biological data. We overcome these difficulties by employing principal component regression, a multivariate regression of evolutionary rate against the principal components of the predictor variables. Our results support the hypothesis that translational selection governs the rate of synonymous and protein sequence evolution in yeast.
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                Author and article information

                Contributors
                Role: Editor
                Journal
                PLoS Pathog
                PLoS Pathog
                plos
                plospath
                PLoS Pathogens
                Public Library of Science (San Francisco, USA )
                1553-7366
                1553-7374
                July 2012
                July 2012
                5 July 2012
                : 8
                : 7
                : e1002796
                Affiliations
                [1 ]Centro de Biotecnología y Genómica de Plantas (UPM-INIA), and E.T.S.I. Agrónomos, Campus de Montegancedo, Universidad Politécnica de Madrid, Pozuelo de Alarcón, Madrid, Spain
                [2 ]Departamento de Ecología Evolutiva, Instituto de Ecología, Universidad Nacional Autónoma de México, Ciudad de México, México
                University of California Riverside, United States of America
                Author notes

                Conceived and designed the experiments: FGA. Performed the experiments: PGJ MRU. Analyzed the data: IP AF FGA. Wrote the paper: IP AML AF DP FGA. Collected field data: PGJ AML DP FGA.

                Article
                PPATHOGENS-D-11-02622
                10.1371/journal.ppat.1002796
                3390404
                22792068
                90a3349c-b115-43b2-bc0a-2f87ef836f8c
                Pagán et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
                History
                : 24 November 2011
                : 25 May 2012
                Page count
                Pages: 12
                Categories
                Research Article
                Biology
                Ecology
                Biodiversity
                Microbiology
                Host-Pathogen Interaction
                Virology

                Infectious disease & Microbiology
                Infectious disease & Microbiology

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