Symptom evolution following the emergence of maize streak virus
Adérito L Monjane,
Simon Dellicour,
Penelope Hartnady,
Kehinde A Oyeniran,
Betty E Owor,
Marion Bezuidenhout,
Daphné Linderme,
Rizwan A Syed,
Lara Donaldson,
Shane Murray,
Edward P Rybicki,
Anders Kvarnheden,
Elham Yazdkhasti,
Pierre Lefeuvre,
Rémy Froissart,
Philippe Roumagnac,
Dionne N Shepherd,
Gordon W Harkins,
Marc A Suchard,
Philippe Lemey,
Arvind Varsani,
Darren P Martin
Affiliations
Adérito L Monjane
Fish Health Research Group, Norwegian Veterinary Institute, Oslo, Norway; Department of Plant Biology, Swedish University of Agricultural Sciences, Uppsala, Sweden
Department of Microbiology, Immunology and Transplantation, Rega Institute, Laboratory for Clinical and Epidemiological Virology, KU Leuven - University of Leuven, Leuven, Belgium; Spatial Epidemiology Laboratory (SpELL), Université Libre de Bruxelles, Brussels, Belgium
Penelope Hartnady
Computational Biology Division, Department of Integrative Biomedical Sciences, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Observatory, Cape Town, South Africa
Kehinde A Oyeniran
Computational Biology Division, Department of Integrative Biomedical Sciences, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Observatory, Cape Town, South Africa
Betty E Owor
Department of Agricultural Production, School of Agricultural Sciences, Makerere University, Kampala, Uganda
Marion Bezuidenhout
Molecular and Cell Biology Department, University of Cape Town, Cape Town, South Africa
Daphné Linderme
Molecular and Cell Biology Department, University of Cape Town, Cape Town, South Africa
Rizwan A Syed
Molecular and Cell Biology Department, University of Cape Town, Cape Town, South Africa
Lara Donaldson
Molecular and Cell Biology Department, University of Cape Town, Cape Town, South Africa
Shane Murray
Molecular and Cell Biology Department, University of Cape Town, Cape Town, South Africa
Edward P Rybicki
Molecular and Cell Biology Department, University of Cape Town, Cape Town, South Africa
Anders Kvarnheden
Department of Plant Biology, Swedish University of Agricultural Sciences, Uppsala, Sweden
Elham Yazdkhasti
Department of Plant Biology, Swedish University of Agricultural Sciences, Uppsala, Sweden
University of Montpellier, Centre National de la Recherche Scientifique (CNRS), Institut de recherche pour le développement (IRD), UMR 5290, Maladie Infectieuses & Vecteurs: Écologie, Génétique Évolution & Contrôle” (MIVEGEC), Montpellier, France
Molecular and Cell Biology Department, University of Cape Town, Cape Town, South Africa; Research Office, University of Cape Town, Cape Town, South Africa
Gordon W Harkins
South African Medical Research Council Bioinformatics Unit, South African National Bioinformatics Institute, University of the Western Cape, Bellville, South Africa
Marc A Suchard
Department of Biomathematics, David Geffen School of Medicine, University of California, Los Angeles, Los Angeles, United States
Philippe Lemey
Department of Microbiology, Immunology and Transplantation, Rega Institute, Laboratory for Clinical and Epidemiological Virology, KU Leuven - University of Leuven, Leuven, Belgium
The Biodesign Center for Fundamental and Applied Microbiomics, Center for Evolution and Medicine, School of Life Sciences, Arizona State University, Tempe, United States; Structural Biology Research Unit, Department of Integrative Biomedical Sciences, University of Cape Town, Cape Town, South Africa
Computational Biology Division, Department of Integrative Biomedical Sciences, Institute of Infectious Diseases and Molecular Medicine, University of Cape Town, Observatory, Cape Town, South Africa
For pathogens infecting single host species evolutionary trade-offs have previously been demonstrated between pathogen-induced mortality rates and transmission rates. It remains unclear, however, how such trade-offs impact sub-lethal pathogen-inflicted damage, and whether these trade-offs even occur in broad host-range pathogens. Here, we examine changes over the past 110 years in symptoms induced in maize by the broad host-range pathogen, maize streak virus (MSV). Specifically, we use the quantified symptom intensities of cloned MSV isolates in differentially resistant maize genotypes to phylogenetically infer ancestral symptom intensities and check for phylogenetic signal associated with these symptom intensities. We show that whereas symptoms reflecting harm to the host have remained constant or decreased, there has been an increase in how extensively MSV colonizes the cells upon which transmission vectors feed. This demonstrates an evolutionary trade-off between amounts of pathogen-inflicted harm and how effectively viruses position themselves within plants to enable onward transmission.
