Host resistance and pathogen aggressiveness are key determinants of coinfection in the wild

Abstract

Coinfection, whereby the same host is infected by more than one pathogen strain, may favor faster host exploitation rates as strains compete for the same limited resources. Hence, coinfection is expected to have major consequences for pathogen evolution, virulence, and epidemiology. Theory predicts genetic variation in host resistance and pathogen infectivity to play a key role in how coinfections are formed. The limited number of studies available has demonstrated coinfection to be a common phenomenon, but little is known about how coinfection varies in space, and what its determinants are. Our aim is to understand how variation in host resistance and pathogen infectivity and aggressiveness contribute to how coinfections are formed in the interaction between fungal pathogen Podosphaera plantaginis and Plantago lanceolata. Our phenotyping study reveals that more aggressive strains are more likely to form coinfections than less aggressive strains in the natural populations. In the natural populations most of the variation in coinfection is found at the individual plant level, and results from a common garden study confirm the prevalence of coinfection to vary significantly among host genotypes. These results show that genetic variation in both the host and pathogen populations are key determinants of coinfection in the wild.

Variable opportunities for outcrossing result in hotspots of novel genetic variation in a pathogen metapopulation

“…Finding more coinfection than would be expected by chance is in line with previous fine-scale field sampling of infections and experimental work, which show that hosts already infected with one strain of the pathogen are more likely to become infected by another strain of the same pathogen than uninfected hosts (Laine, 2011; Susi and Laine, 2017). This may be due to already infected individuals becoming more susceptible to subsequent infection, or due to strains aggregating on those hosts that are the most susceptible genotypes (Susi and Laine, 2017). Moreover, variation in host density and (micro)climatic conditions may be an important driver of infection patters in the wild (Penczykowski et al, 2018).…”

Intraspecific host variation plays a key role in virus community assembly

“…Vector preference for infected hosts 41,90 could also influence virus co-occurrence patterns. Transmission mode is often found to be critical for how pathogen communities are formed 15,40,91,92 , and reciprocally, the amount of genotypic variation within a host population may explain the abundance and composition of herbivory community present 89 .…”

Diverse and variable virus communities in wild plant populations revealed by metagenomic tools

“…An exciting avenue of future research will be to identify factors explaining the differences we observe here in virus communities among the populations. Resistance against viruses in P. lanceolata is currently unexplored, but significant genetic variation in resistance against fungal pathogens (De Nooji & van der Aa, 1987; Susi & Laine, 2015; Susi & Laine, 2017) and herbivores (Adler, Schmitt & Bowers, 1995; Barton, 2007) has been reported. Other factors driving the distribution patterns may include differences in pathogen genetic diversity (Rodriguez-Nevado, Montes & Pagan, 2017), vector dynamics (Borer et al, 2010; Hall et al, 2010), the abiotic environment (Seabloom et al, 2010) and spill over from crops (Bell & Tylianakis, 2016; Bernardo et al, 2017).…”

“…Hence, we designed primers for four virus taxa, Caulimovirus, Betapartitivirus, Enamovirus and Closterovirus . In addition, we used the PlLV detection primer pair described in Susi & Laine (2017) (Table 2). The RNA samples from each individual plant sampled in 2013 and 2015 were reverse transcribed using iScript™ cDNA Synthesis Kit (Bio-Rad Laboratories, Inc., USA) according to manufacturer’s recommendations.…”