Abstract
The pathogen and parasite community that inhabits every free-living organism can control host vital rates including lifespan and reproductive output. To date, however, there have been few experiments examining pathogen community assembly replicated at large-enough spatial scales to inform our understanding of pathogen dynamics in natural systems. Pathogen community assembly may be driven by neutral stochastic colonization and extinction events or by niche differentiation that constrains pathogen distributions to particular environmental conditions, hosts, or vectors.Here, we present results from a regionally-replicated experiment investigating the community of barley and cereal yellow dwarf viruses (B/CYDV's) in over 5000 experimentally planted individuals of six grass species along a 700 km latitudinal gradient along the Pacific coast of North America (USA) in response to experimentally manipulated nitrogen and phosphorus supplies. The composition of the virus community varied predictably among hosts and across nutrient-addition treatments, indicating niche differentiation among virus species. There were some concordant responses among the viral species. For example, the prevalence of most viral species increased consistently with perennial grass cover, leading to a 60% increase in the richness of the viral community within individual hosts (i.e., coinfection) in perennial-dominated plots. Furthermore, infection rates of the six host species in the field were highly correlated with vector preferences assessed in laboratory trials. Our results reveal the importance of niche differentiation in structuring virus assemblages. Virus species distributions reflected a combination of local host community composition, host species-specific vector preferences, and virus responses to host nutrition. In addition, our results suggest that heterogeneity among host species in their capacity to attract vectors or support pathogens between growing seasons can lead to positive covariation among virus species.
Highlights
The study of host-pathogen interactions has focused on three components essential to the completion of a pathogen lifecycle forming the ‘disease triangle’: an infectious microbe, a host, and a favorable environment [1,2,3]
Coinfection by multiple pathogens can increase the severity of disease, as is the case for humans infected by multiple strains of human immunodeficiency virus (HIV), HIV and malaria, or the hepatitis C virus and the trematode Schistosoma mansonii [30,31,32,33]
Among the 10 pairwise combinations of virus species, the highest correlations were between the S. avenae vectored viruses, BYDV-MAV and BYDV-PAV, (r = 0.56, p,0.001) and the R. padi vectored viruses, BYDV-PAV and CYDV-RPV, (r = 0.43, p,0.001)
Summary
The study of host-pathogen interactions has focused on three components essential to the completion of a pathogen lifecycle forming the ‘disease triangle’: an infectious microbe, a host, and a favorable environment [1,2,3]. While many studies have probed the interactions among the vertices of the disease triangle (e.g., [1,2,3,4,5,6,7,8,9,10,11,12,13,14,15,16]), investigations of the larger ecological context in which host-pathogenenvironment interactions occur, including the interactions among multiple microbial species infecting the same host, multiple species in a host community, and the impact of multiple abiotic parameters have generally been observational or limited in spatial scope [17,18,19,20,21]. Despite the importance of interactions among pathogens within a host, we know relatively little about the assembly of pathogen communities in natural systems, and we know of no field experiments that have been replicated at scales large enough to inform our understanding of how the biotic and abiotic context interact to mediate the natural assembly of pathogen communities in multi-host systems
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