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Interactions among parasite species coinfecting the same host individual can have far reaching consequences for parasite ecology and evolution. How these within-host interactions affect epidemics may depend on two non-exclusive mechanisms: parasite growth and reproduction within hosts, and parasite transmission between hosts. Yet, how these two mechanisms operate under coinfection, and how sensitive they are to the composition of the coinfecting parasite community, remains poorly understood. Here, we test the hypothesis that the relationship between within- and between-host transmission of the fungal pathogen, Phomopsis subordinaria, is affected by co-occurring parasites infecting the host plant, Plantago lanceolata. We conducted a field experiment manipulating the parasite community of transmission source plants, then tracked P. subordinaria within-host transmission, as well as between-host transmission to naïve recipient plants. We find that coinfection with the powdery mildew pathogen, Podosphaera plantaginis, causes increased between-host transmission of P. subordinaria by affecting the number of infected flower stalks in the source plants, resulting from altered auto-infection. In contrast, coinfection with viruses did not have an effect on either within- or between-host transmission. We then analyzed data on the occurrence of P. subordinaria in 2018 and the powdery mildew in a multi-year survey data set from natural host populations to test whether the positive association predicted by our experimental results is evident in field epidemiological data. Consistent with our experimental findings, we observed a positive association in the occurrence of P. subordinaria and historical powdery mildew persistence. Jointly, our experimental and epidemiological results suggest that within- and between-host transmission of P. subordinaria depends on the identity of coinfecting parasites, with potentially far-reaching effects on disease dynamics and parasite co-occurrence patterns in wild populations. [ABSTRACT FROM AUTHOR]

While the negative effects that pathogens have on their hosts are well-documented in humans and agricultural systems, direct evidence of pathogen-driven impacts in wild host populations is scarce and mixed. Here, to determine how the strength of pathogen-imposed selection depends on spatial structure, we analyze growth rates across approximately 4000 host populations of a perennial plant through time coupled with data on pathogen presence-absence. We find that infection decreases growth more in the isolated than well-connected host populations. Our inoculation study reveals isolated populations to be highly susceptible to disease while connected host populations support the highest levels of resistance diversity, regardless of their disease history. A spatial eco-evolutionary model predicts that non-linearity in the costs to resistance may be critical in determining this pattern. Overall, evolutionary feedbacks define the ecological impacts of disease in spatially structured systems with host gene flow being more important than disease history in determining the outcome. The ecological and evolutionary impacts of disease vary in spatially structured populations. Here, the authors study ~4000 populations of Plantago lanceolata and find that resistance evolution depends on both disease history and population structure, with isolated populations more susceptible to fungal disease. [ABSTRACT FROM AUTHOR]

The discovery and full-genome sequences of two isolates of a fourth capulavirus species are reported. The viruses were discovered during a viral metagenomics survey of uncultivated Plantago lanceolata plants in the Åland archipelago of south western Finland. The newly discovered viruses apparently produce no symptoms in P. lanceolata. They have a genome organization that is very similar to that of the three known capulavirus species and additionally share between 62.9 and 67.1% genome-wide sequence identity with the isolates of these species. It is therefore proposed that these viruses be assigned to a new capulavirus species named ' Plantago lanceolata latent virus'. [ABSTRACT FROM AUTHOR]

In recent years the potential for evolutionary change to drive ecological dynamics, and vice versa, has been widely recognized. However, the convincing examples of eco-evolutionary dynamics mainly stem from highly artificial experimental systems, with conspicuously few examples contributed by field systems. While rarely considered in the eco-evolutionary literature, the gene-for-gene hypothesis inherently recognizes the tight link between evolutionary and ecological dynamics. The boom-and-bust dynamics of some agricultural pathogens are an extreme demonstration of this. In this perspective, we place plant-pathogen systems in a spatial eco-evolutionary framework, which recognizes that ecology and evolution are tightly linked, take place at the same time scale and are strongly influenced by spatial structure. Specifically, we: i) exemplify how the ecological process of dispersal modifies rapid local coevolutionary dynamics and thereby shapes spatial variation in resistance, infectivity, and local adaptation; and ii) illustrate how the outcome of coevolution (spatial distribution in resistance, infectivity and local adaptation) drives ecological metapopulation processes. Overall, we conclude that both agricultural and wild pathosystems provide a unique illustration of the high relevance of spatial eco-evolutionary feedback in understanding species interactions. [ABSTRACT FROM AUTHOR]

Infection by multiple pathogens of the same host is ubiquitous in both natural and managed habitats. While intraspecific variation in disease resistance is known to affect pathogen occurrence, how differences among host genotypes affect the assembly of pathogen communities remains untested. In our experiment using cloned replicates of naive Plantago lanceolata plants as sentinels during a seasonal virus epidemic, we find non-random co-occurrence patterns of five focal viruses. Using joint species distribution modelling, we attribute the non-random virus occurrence patterns primarily to differences among host genotypes and local population context. Our results show that intraspecific variation among host genotypes may play a large, previously unquantified role in pathogen community structure. The factors that determine whether pathogens co-occur in a host are poorly understood, especially for plant viruses. Here the authors conduct field experiments with the plant Plantago lanceolata and its viruses, showing that viral co-occurrences are driven predominantly by environmental context and host genotype rather than viral interactions. [ABSTRACT FROM AUTHOR]