Integration of community ecology with disease biology is viewed as a promising avenue for uncovering determinants of pathogen diversity, and for predicting disease risks. Plant-infecting viruses represent a vastly underestimated component of biodiversity with potentially important ecological and evolutionary roles. We performed hierarchal spatial analysis of wild plant populations to characterise the diversity and coexistence structure of within-host virus communities, and their predictors. Our results show that these virus communities are characterised by single infections of few, dominating virus taxa as well as diverse, non-random coinfections. Using a novel graphical modelling framework we demonstrate that after accounting for environmental heterogeneity at the level of both individual host plants and populations, most virus co-occurrence patterns can be attributed to virus-virus associations. Moreover, we show that conditioning variables changed virus association networks especially through their indirect effects. This highlights a previously underestimated mechanism of how human-driven environmental change can influence disease risks.

The trade-off between within-host infection load and transmission to new hosts is predicted to constrain pathogen evolution, and to maintain polymorphism in pathogen populations. The life-history stages and their correlations that underpin infection development may change under coinfection with other parasites as they compete for the same limited host resources. Cross-kingdom interactions are common among pathogens in both natural and cultivated systems yet their impact on disease ecology and evolution are rarely studied. Host plant Plantago lanceolata is naturally infected by both Phompopsis subordinaria, a seed killing fungus, as well as Plantago lanceolata latent virus (PlLV) in the Åland Islands, SW Finland. We performed an inoculation assay to test whether coinfection with PlLV affects performance of two P. subordinaria strains, and the correlation between within-host infection load and transmission potential. The strains differed in the measured life-history traits and their correlations. Moreover, we found that under virus coinfection, within-host infection load of P. subordinaria was lower but transmission potential was higher compared to strains under single infection. The negative correlation between within-host infection load and transmission potential detected under single infection became positive under coinfection with PlLV. In wild populations, within-host infection load was positively associated with within-population disease prevalence. Jointly, our results suggest that the trade-off between within-host infection load and transmission may be strain specific, and that the pathogen life-history that underpin epidemics may change depending on the diversity of infection, generating variation in disease dynamics.