Bats and rodents are recognized to host a great diversity of viruses and several important viral zoonoses, but how this viral diversity is structured and how viruses are connected, shared and distributed among host networks is not well understood. To address this gap in knowledge, we compared the associative capacity of the host–virus networks in rodents and bats with the identification of those viruses with zoonotic potential. A virus database, detected by molecular methods, was constructed in the two taxonomic groups. We compiled 5,484 records: 825 in rodents and 4,659 in bats. We identified a total of 173 and 166 viruses, of which 53 and 40 are zoonotic viruses, in rodents and bats, respectively. Based on a network theory, a non‐directed bipartite host–virus network was built for each group. Subsequently, the networks were collapsed to represent the connections among hosts and viruses. We identified both discrete and connected communities. We observed a greater degree of connectivity in bat viruses and more discrete communities in rodents. The Coronaviridae recorded in bats have the highest values of degree, betweenness and closeness centralities. In rodents, higher degree positions were distributed homogeneously between viruses and hosts. At least in our database, a higher proportion of rodent viruses were zoonotic. Rodents should thus not be underestimated as important reservoirs of zoonotic disease. We found that viruses were more frequently shared among bats than in rodents. Network theory can reveal some macroecological patterns and identify risks that were previously unrecognized. For example, we found that parvovirus in megabats and Gbagroube virus in rodents may represent a zoonotic risk due to the proximity to humans and other zoonotic viruses. We propose that epidemiological surveillance programmes should consider the connectivity of network actors as a measure of the risks of dispersion and transmission.

One of the main goals of community ecology is to measure the relative importance of environmental filters to understand patterns of species distribution at different temporal and spatial scales. Likewise, the identification of factors that shape symbiont metacommunity structures is important in disease ecology because resulting structures drive disease transmission. We tested the hypothesis that distributions of virus species and viral families from rodents and bats are defined by shared responses to host phylogeny and host functional characteristics, shaping the viral metacommunity structures at four spatial scales (Continental, Biogeographical, Zoogeographical, and Regional). The contribution of host phylogeny and host traits to the metacommunity of viruses at each spatial scale was calculated using a redundant analysis of canonical ordering (RDA). For rodents, at American Continental scale the coherence of viral species metacommunity increased while the spatial scale decreased and Quasi-Clementsian structures were observed. This pattern suggests a restricted distribution of viruses through their hosts, while in the Big Mass (Europe, Africa, and Asia), the coherence decreased as spatial scale decreased. Viral species metacommunities associated with bats was dominated by random structures along all spatial scales. We suggest that this random pattern is a result of the presence of viruses with high occupancy range such as rabies (73%) and coronavirus (27%), that disrupt such structures. At viral family scale, viral metacommunities associated with bats showed coherent structures, with the emergence of Quasi-Clementsian and Checkerboard structures. RDA analysis indicates that the assemblage of viral diversity associated with rodents and bats responds to phylogenetic and functional characteristics, which alternate between spatial scales. Several of these variations could be subject to the spatial scale, in spite of this, we could identify patterns at macro ecological scale. The application of metacommunity theory at symbiont scales is particularly useful for large-scale ecological analysis. Understanding the rules of host-virus association can be useful to take better decisions in epidemiological surveillance, control and even predictions of viral distribution and dissemination.

A great deal of effort has been invested in trying to understand the distribution and function of the different biota at multiple scales, with the aim of predicting community assembly rules and the consequences of their complex interactions (Cavender-Bares et al., 2009). Developing such an understanding has important implications in the case of viral disease dynamics and outbreak occurrence, as it would provide us with useful tools for inferring both the causes and consequences of viral distributions, as well as aiding the decision-making process in the prevention, monitoring, and control of infectious diseases (Pedersen & Fenton, 2006). However, in the case of communities of symbionts (organisms associated with other organisms, generally parasites) comparatively little is known about their assembly processes. In this case, it is evident that host characteristics could act as strong filters on the assembly of pathogen communities