Extreme heat reduces host and parasite performance in a butterfly-parasite interaction.

Environmental temperature fundamentally shapes insect physiology, fitness and interactions with parasites. Differential climate warming effects on host versus parasite biology could exacerbate or inhibit parasite transmission, with far-reaching implications for pollination services, biocontrol and human health. Here, we experimentally test how controlled temperatures influence multiple components of host and parasite fitness in monarch butterflies (Danaus plexippus) and their protozoan parasites Ophryocystis elektroscirrha. Using five constant-temperature treatments spanning 18-34°C, we measured monarch development, survival, size, immune function and parasite infection status and intensity. Monarch size and survival declined sharply at the hottest temperature (34°C), as did infection probability, suggesting that extreme heat decreases both host and parasite performance. The lack of infection at 34°C was not due to greater host immunity or faster host development but could instead reflect the thermal limits of parasite invasion and within-host replication. In the context of ongoing climate change, temperature increases above current thermal maxima could reduce the fitness of both monarchs and their parasites, with lower infection rates potentially balancing negative impacts of extreme heat on future monarch abundance and distribution.

Effects of food supplementation and helminth removal on space use and spatial overlap in wild rodent populations.

Animal space use and spatial overlap can have important consequences for population-level processes such as social interactions and pathogen transmission. Identifying how environmental variability and inter-individual variation affect spatial patterns and in turn influence interactions in animal populations is a priority for the study of animal behaviour and disease ecology. Environmental food availability and macroparasite infection are common drivers of variation, but there are few experimental studies investigating how they affect spatial patterns of wildlife. Bank voles (Clethrionomys glareolus) are a tractable study system to investigate spatial patterns of wildlife and are amenable to experimental manipulations. We conducted a replicated, factorial field experiment in which we provided supplementary food and removed helminths in vole populations in natural forest habitat and monitored vole space use and spatial overlap using capture-mark-recapture methods. Using network analysis, we quantified vole space use and spatial overlap. We compared the effects of food supplementation and helminth removal and investigated the impacts of season, sex and reproductive status on space use and spatial overlap. We found that food supplementation decreased vole space use while helminth removal increased space use. Space use also varied by sex, reproductive status and season. Spatial overlap was similar between treatments despite up to threefold differences in population size. By quantifying the spatial effects of food availability and macroparasite infection on wildlife populations, we demonstrate the potential for space use and population density to trade-off and maintain consistent spatial overlap in wildlife populations. This has important implications for spatial processes in wildlife including pathogen transmission.

Habitat Specialization by Wildlife Reduces Pathogen Spread in Urbanizing Landscapes.

AbstractUrban areas are expanding globally with far-reaching ecological consequences, including for wildlife-pathogen interactions. Wildlife show tremendous variation in their responses to urbanization; even within a single population, some individuals can specialize on urban or natural habitat types. This specialization could alter pathogen impacts on host populations via changes to wildlife movement and aggregation. Here, we build a mechanistic model to explore how habitat specialization in urban landscapes affects interactions between a mobile host population and a density-dependent specialist pathogen that confers no immunity. We model movement on a network of resource-stable urban sites and resource-fluctuating natural sites, where hosts are urban specialists, natural specialists, or generalists that use both patch types. We find that for generalists, natural and partially urban landscapes produce the highest infection prevalence and mortality, driven by high movement rates at natural sites and high densities at urban sites. However, habitat specialization protects hosts from these negative effects of partially urban landscapes by limiting movement between patch types. These findings suggest that habitat specialization can benefit populations by reducing infectious disease transmission, but by reducing movement between habitat types it could also carry the cost of reducing other movement-related ecosystem functions, such as seed dispersal and pollination.

Light pollution affects West Nile virus exposure risk across Florida.

Emerging infectious diseases (EIDs) present global health threats, and their emergences are often linked to anthropogenic change. Artificial light at night (ALAN) is one form of anthropogenic change that spans beyond urban boundaries and may be relevant to EIDs through its influence on the behaviour and physiology of hosts and/or vectors. Although West Nile virus (WNV) emergence has been described as peri-urban, we hypothesized that exposure risk could also be influenced by ALAN in particular, which is testable by comparing the effects of ALAN on prevalence while controlling for other aspects of urbanization. By modelling WNV exposure among sentinel chickens in Florida, we found strong support for a nonlinear relationship between ALAN and WNV exposure risk in chickens with peak WNV risk occurring at low ALAN levels. Although our goal was not to discern how ALAN affected WNV relative to other factors, effects of ALAN on WNV exposure were stronger than other known drivers of risk (i.e. impervious surface, human population density). Ambient temperature in the month prior to sampling, but no other considered variables, strongly influenced WNV risk. These results indicate that ALAN may contribute to spatio-temporal changes in WNV risk, justifying future investigations of ALAN on other vector-borne parasites.

Host and parasite thermal ecology jointly determine the effect of climate warming on epidemic dynamics.

Host-parasite systems have intricately coupled life cycles, but each interactor can respond differently to changes in environmental variables like temperature. Although vital to predicting how parasitism will respond to climate change, thermal responses of both host and parasite in key traits affecting infection dynamics have rarely been quantified. Through temperature-controlled experiments on an ectothermic host-parasite system, we demonstrate an offset in the thermal optima for survival of infected and uninfected hosts and parasite production. We combine experimentally derived thermal performance curves with field data on seasonal host abundance and parasite prevalence to parameterize an epidemiological model and forecast the dynamical responses to plausible future climate-warming scenarios. In warming scenarios within the coastal southeastern United States, the model predicts sharp declines in parasite prevalence, with local parasite extinction occurring with as little as 2 °C warming. The northern portion of the parasite's current range could experience local increases in transmission, but assuming no thermal adaptation of the parasite, we find no evidence that the parasite will expand its range northward under warming. This work exemplifies that some host populations may experience reduced parasitism in a warming world and highlights the need to measure host and parasite thermal performance to predict infection responses to climate change.

Reactivation of latent infections with migration shapes population-level disease dynamics.

Annual migration is common across animal taxa and can dramatically shape the spatial and temporal patterns of infectious disease. Although migration can decrease infection prevalence in some contexts, these energetically costly long-distance movements can also have immunosuppressive effects that may interact with transmission processes in complex ways. Here, we develop a mechanistic model for the reactivation of latent infections driven by physiological changes or energetic costs associated with migration (i.e. 'migratory relapse') and its effects on disease dynamics. We determine conditions under which migratory relapse can amplify or reduce infection prevalence across pathogen and host traits (e.g. infectious periods, virulence, overwinter survival, timing of relapse) and transmission phenologies. We show that relapse at either the start or end of migration can dramatically increase prevalence across the annual cycle and may be crucial for maintaining pathogens with low transmissibility and short infectious periods in migratory populations. Conversely, relapse at the start of migration can reduce the prevalence of highly virulent pathogens by amplifying culling of infected hosts during costly migration, especially for highly transmissible pathogens and those transmitted during migration or the breeding season. Our study provides a mechanistic foundation for understanding the spatio-temporal patterns of relapsing infections in migratory hosts, with implications for zoonotic surveillance and understanding how infection patterns will respond to shifts in migratory propensity associated with environmental change. Further, our work suggests incorporating within-host processes into population-level models of pathogen transmission may be crucial for reconciling the range of migration-infection relationships observed across migratory species.

Antarctic Penguins as Reservoirs of Diversity for Avian Avulaviruses.

Wild birds harbor a huge diversity of avian avulaviruses (formerly avian paramyxoviruses). Antarctic penguin species have been screened for avian avulaviruses since the 1980s and, as such, are known hosts of these viruses. In this study, we screened three penguin species from the South Shetland Islands and the Antarctic Peninsula for avian avulaviruses. We show that Adelie penguins (Pygoscelis adeliae) are hosts for four different avian avulavirus species, the recently described avian avulaviruses 17 to 19 and avian avulavirus 10-like, never before isolated in Antarctica. A total of 24 viruses were isolated and sequenced; avian avulavirus 17 was the most common, and phylogenetic analysis demonstrated patterns of occurrence, with different genetic clusters corresponding to penguin age and location. Following infection in specific-pathogen-free (SPF) chickens, all four avian avulavirus species were shed from the oral cavity for up to 7 days postinfection. There was limited shedding from the cloaca in a proportion of infected chickens, and all but one bird seroconverted by day 21. No clinical signs were observed. Taken together, we propose that penguin species, including Antarctic penguins, may be the central reservoir for a diversity of avian avulavirus species and that these viruses have the potential to infect other avian hosts.IMPORTANCE Approximately 99% of all viruses are still to be described, and in our changing world, any one of these unknown viruses could potentially expand their host range and cause epidemic disease in wildlife, agricultural animals, or humans. Avian avulavirus 1 causes outbreaks in wild birds and poultry and is thus well described. However, for many avulavirus species, only a single specimen has been described, and their viral ecology and epidemiology are unknown. Through the detection of avian avulaviruses in penguins from Antarctica, we have been able to expand upon our understanding of three avian avulavirus species (avian avulaviruses 17 to 19) and report a potentially novel avulavirus species. Importantly, we show that penguins appear to play a key role in the epidemiology of avian avulaviruses, and we encourage additional sampling of this avian group.

Movement rules determine nomadic species' responses to resource supplementation and degradation.

In environments that vary unpredictably, many animals are nomadic, moving in an irregular pattern that differs from year to year. Exploring the mechanisms of nomadic movement is needed to understand how animals survive in highly variable environments, and to predict behavioural and population responses to environmental change. We developed a network model to identify plausible mechanisms of nomadic animal movement by comparing the performance of multiple movement rules along a continuum from nomadism to residency. Using simulations and analytical results, we explored how different types of habitat modifications (that augment or decrease resource availability) might affect the abundance and movement rates of animals following each of these rules. Movement rules for which departure from patches depended on resource availability and/or competition performed almost equally well and better than residency or uninformed movement under most conditions, even though animals using each rule moved at substantially different rates. Habitat modifications that stabilized resources, either by resource supplementation or degradation, eroded the benefits of informed nomadic movements, particularly for movements based on resource availability alone. These results suggest that simple movement rules can explain nomadic animal movements and determine species' responses to environmental change. In particular, landscape stabilization and supplementation might be useful strategies for promoting populations of resident animals, but would be less beneficial for managing highly mobile species, many of which are threatened by habitat disruption and changes in climate.

Landscape-level toxicant exposure mediates infection impacts on wildlife populations.

Anthropogenic landscape modification such as urbanization can expose wildlife to toxicants, with profound behavioural and health effects. Toxicant exposure can alter the local transmission of wildlife diseases by reducing survival or altering immune defence. However, predicting the impacts of pathogens on wildlife across their ranges is complicated by heterogeneity in toxicant exposure across the landscape, especially if toxicants alter wildlife movement from toxicant-contaminated to uncontaminated habitats. We developed a mechanistic model to explore how toxicant effects on host health and movement propensity influence range-wide pathogen transmission, and zoonotic exposure risk, as an increasing fraction of the landscape is toxicant-contaminated. When toxicant-contaminated habitat is scarce on the landscape, costs to movement and survival from toxicant exposure can trap infected animals in contaminated habitat and reduce landscape-level transmission. Increasing the proportion of contaminated habitat causes host population declines from combined effects of toxicants and infection. The onset of host declines precedes an increase in the density of infected hosts in contaminated habitat and thus may serve as an early warning of increasing potential for zoonotic spillover in urbanizing landscapes. These results highlight how sublethal effects of toxicants can determine pathogen impacts on wildlife populations that may not manifest until landscape contamination is widespread.

Multiple transmission routes sustain high prevalence of a virulent parasite in a butterfly host.

Understanding factors that allow highly virulent parasites to reach high infection prevalence in host populations is important for managing infection risks to human and wildlife health. Multiple transmission routes have been proposed as one mechanism by which virulent pathogens can achieve high prevalence, underscoring the need to investigate this hypothesis through an integrated modelling-empirical framework. Here, we examine a harmful specialist protozoan infecting monarch butterflies that commonly reaches high prevalence (50-100%) in resident populations. We integrate field and modelling work to show that a combination of three empirically-supported transmission routes (vertical, adult transfer and environmental transmission) can produce and sustain high infection prevalence in this system. Although horizontal transmission is necessary for parasite invasion, most new infections post-establishment arise from vertical transmission. Our study predicts that multiple transmission routes, coupled with high parasite virulence, can reduce resident host abundance by up to 50%, suggesting that the protozoan could contribute to declines of North American monarchs.

Light pollution increases West Nile virus competence of a ubiquitous passerine reservoir species.

Among the many anthropogenic changes that impact humans and wildlife, one of the most pervasive but least understood is light pollution. Although detrimental physiological and behavioural effects resulting from exposure to light at night are widely appreciated, the impacts of light pollution on infectious disease risk have not been studied. Here, we demonstrate that artificial light at night (ALAN) extends the infectious-to-vector period of the house sparrow (Passer domesticus), an urban-dwelling avian reservoir host of West Nile virus (WNV). Sparrows exposed to ALAN maintained transmissible viral titres for 2 days longer than controls but did not experience greater WNV-induced mortality during this window. Transcriptionally, ALAN altered the expression of gene regulatory networks including key hubs (OASL, PLBD1 and TRAP1) and effector genes known to affect WNV dissemination (SOCS). Despite mounting anti-viral immune responses earlier, transcriptomic signatures indicated that ALAN-exposed individuals probably experienced pathogen-induced damage and immunopathology, potentially due to evasion of immune effectors. A simple mathematical modelling exercise indicated that ALAN-induced increases of host infectious-to-vector period could increase WNV outbreak potential by approximately 41%. ALAN probably affects other host and vector traits relevant to transmission, and additional research is needed to advise the management of zoonotic diseases in light-polluted areas.

On the relationship between body condition and parasite infection in wildlife: a review and meta-analysis.

Body condition metrics are widely used to infer animal health and to assess costs of parasite infection. Since parasites harm their hosts, ecologists might expect negative relationships between infection and condition in wildlife, but this assumption is challenged by studies showing positive or null condition-infection relationships. Here, we outline common condition metrics used by ecologists in studies of parasitism, and consider mechanisms that cause negative, positive, and null condition-infection relationships in wildlife systems. We then perform a meta-analysis of 553 condition-infection relationships from 187 peer-reviewed studies of animal hosts, analysing observational and experimental records separately, and noting whether authors measured binary infection status or intensity. Our analysis finds substantial heterogeneity in the strength and direction of condition-infection relationships, a small, negative average effect size that is stronger in experimental studies, and evidence for publication bias towards negative relationships. The strongest predictors of variation in study outcomes are host thermoregulation and the methods used to evaluate body condition. We recommend that studies aiming to assess parasite impacts on body condition should consider host-parasite biology, choose condition measures that can change during the course of infection, and employ longitudinal surveys or manipulate infection status when feasible.

Host Dispersal Responses to Resource Supplementation Determine Pathogen Spread in Wildlife Metapopulations.

Many wildlife species occupy landscapes that vary in the distribution, abundance, and quality of food resources. Increasingly, urbanized and agricultural habitats provide supplemental food resources that can have profound consequences for host distributions, movement patterns, and pathogen exposure. Understanding how host and pathogen dispersal across landscapes is affected by the spatial extent of food-supplemented habitats is therefore important for predicting the consequences for pathogen spread and impacts on host occupancy. Here we develop a generalizable metapopulation model to understand how the relative abundance of provisioned habitats across the landscape and how the host dispersal responses to provisioning and infection influence patch occupancy by hosts and their pathogens. We find that pathogen invasion and landscape-level infection prevalence are greatest when provisioning increases patch attractiveness and disperser production and when infection has minimal costs on dispersal success. Alternatively, if provisioning promotes site fidelity or reduces disperser production, increasing the fraction of food-supplemented habitats can reduce landscape-scale infection prevalence and minimize disease-induced declines in host occupancy. This work highlights the importance of considering how resources and infection jointly influence host dispersal for predicting how changing resource distributions influence the spread of infectious diseases.

Migratory behaviour predicts greater parasite diversity in ungulates.

Long-distance animal movements can increase exposure to diverse parasites, but can also reduce infection risk through escape from contaminated habitats or culling of infected individuals. These mechanisms have been demonstrated within and between populations in single-host/single-parasite interactions, but how long-distance movement behaviours shape parasite diversity and prevalence across host taxa is largely unknown. Using a comparative approach, we analyse the parasite communities of 93 migratory, nomadic and resident ungulate species. We find that migrants have higher parasite species richness than residents or nomads, even after considering other factors known to influence parasite diversity, such as body size and host geographical range area. Further analyses support a novel 'environmental tracking' hypothesis, whereby migration allows parasites to experience environments favourable to transmission year-round. In addition, the social aggregation and large group sizes that facilitate migration might increase infection risk for migrants. By contrast, we find little support for previously proposed hypotheses, including migratory escape and culling, in explaining the relationship between host movement and parasitism in mammals at this cross-species scale. Our findings, which support mechanistic links between long-distance movement and increased parasite richness at the species level, could help predict the effects of future environmental change on parasitism in migratory animals.

Pandemic Seasonal H1N1 Reassortants Recovered from Patient Material Display a Phenotype Similar to That of the Seasonal Parent.

UNLABELLED: We have previously shown that 11 patients became naturally coinfected with seasonal H1N1 (A/H1N1) and pandemic H1N1 (pdm/H1N1) during the Southern hemisphere winter of 2009 in New Zealand. Reassortment of influenza A viruses is readily observed during coinfection of host animals and in vitro; however, reports of reassortment occurring naturally in humans are rare. Using clinical specimen material, we show reassortment between the two coinfecting viruses occurred with high likelihood directly in one of the previously identified patients. Despite the lack of spread of these reassortants in the community, we did not find them to be attenuated in several model systems for viral replication and virus transmission: multistep growth curves in differentiated human bronchial epithelial cells revealed no growth deficiency in six recovered reassortants compared to A/H1N1 and pdm/H1N1 isolates. Two reassortant viruses were assessed in ferrets and showed transmission to aerosol contacts. This study demonstrates that influenza virus reassortants can arise in naturally coinfected patients. IMPORTANCE: Reassortment of influenza A viruses is an important driver of virus evolution, but little has been done to address humans as hosts for the generation of novel influenza viruses. We show here that multiple reassortant viruses were generated during natural coinfection of a patient with pandemic H1N1 (2009) and seasonal H1N1 influenza A viruses. Though apparently fit in model systems, these reassortants did not become established in the wider population, presumably due to herd immunity against their seasonal H1 antigen.

Competition-mediated feedbacks in experimental multispecies epizootics.

Competition structures ecological communities and alters host-pathogen interactions. In environmentally transmitted pathogens, an infection-resistant competitor may influence infection dynamics in a susceptible species through the negative impacts of competition (e.g., by reducing host density or causing nutritional stress that increases susceptibility to infection) and/or the positive impacts of reducing transmission efficiency (e.g., by removing environmental pathogen stages). Thus, a non-susceptible competitor may enhance, reduce, or have no net effect on susceptible host density and infection prevalence. Here, we couple an epidemiological model with experimental epidemics to test how resource competition with a non-susceptible competitor (Daphnia pulicaria) influences fungal microparasite (Metschnikowia bicuspidata) infection dynamics in a susceptible host species (D. dentifera). Our model and experiments suggest that competitor density can mediate the direction and magnitude of the effect of competition on infection dynamics, with a peak in infection prevalence occurring at intermediate competitor densities. At low densities, the non-susceptible competitor D. pulicaria may reduce infection prevalence in the susceptible host by removing fungal spores from the environment through feeding. However, when competitor density is increased and resources become limiting, D. pulicaria negatively impacts the susceptible host by increasing susceptible host feeding rates, and therefore fungal spore intake, and further by reducing susceptible host population size as it is driven toward competitive exclusion. In conclusion, these results show that a tradeoff between the competitor as a consumer of pathogen, which serves to reduce epidemic size, and as a modifier of susceptible host foraging ecology, which influences infection rates, may alternately enhance or dampen the magnitude of local epidemics.

'Candidatus Tenderia electrophaga', an uncultivated electroautotroph from a biocathode enrichment.

Biocathode communities are of interest for a variety of applications, including electrosynthesis, bioremediation, and biosensors, yet much remains to be understood about the biological processes that occur to enable these communities to grow. One major difficulty in understanding these communities is that the critical autotrophic organisms are difficult to cultivate. An uncultivated, electroautotrophic bacterium previously identified as an uncultivated member of the family Chromatiaceae appears to be a key organism in an autotrophic biocathode microbial community. Metagenomic, metaproteomic and metatranscriptomic characterization of this community indicates that there is likely a single organism that utilizes electrons from the cathode to fix CO2, yet this organism has not been obtained in pure culture. Fluorescence in situ hybridization reveals that the organism grows as rod-shaped cells approximately 1.8 × 0.6 µm, and forms large clumps on the cathode. The genomic DNA G+C content was 59.2 mol%. Here we identify the key features of this organism and propose 'Candidatus Tenderia electrophaga', within the Gammaproteobacteria on the basis of low nucleotide and predicted protein sequence identity to known members of the orders Chromatiales and Thiotrichales.

The response of migratory populations to phenological change: a Migratory Flow Network modelling approach.

Declines in migratory species have been linked to anthropogenic climate change through phenological mismatch, which arises due to asynchronies between the timing of life-history events (such as migration) and the phenology of available resources. Long-distance migratory species may be particularly vulnerable to phenological change in their breeding ranges, since the timing of migration departure is based on environmental cues at distant non-breeding sites. Migrants may, however, be able to adjust migration speed en route to the breeding grounds, and thus, ability of migrants to update their timing of migration may depend critically on stopover frequency during migration; however, understanding how migratory strategy influences population dynamics is hindered by a lack of predictive models explicitly linking habitat quality to demography and movement patterns throughout the migratory cycle. Here, we present a novel modelling framework, the Migratory Flow Network (MFN), in which the seasonally varying attractiveness of breeding, winter and stopover regions drives the direction and timing of migration based on a simple general flux law. We use the MFN to investigate how populations respond to shifts in breeding site phenology based on their frequency of stopover and ability to detect and adapt to these changes. With perfect knowledge of advancing phenology, 'jump' migrants (low-frequency stopover) require more adaptation for populations to recover than 'hop' and 'skip' (high or medium frequency stopover) migrants. If adaptation depends on proximity, hop and skip migrants' populations can recover but jump migrants cannot adjust and decline severely. These results highlight the importance of understanding migratory strategies and maintaining high-quality stopover habitat to buffer migratory populations from climate-induced mismatch. We discuss how MFNs could be applied to diverse migratory taxa and highlight the potential of MFNs as a tool for exploring how migrants respond to other environmental changes such as habitat loss.

Discovery and complete genome sequence of a novel circovirus-like virus in the endangered rowi kiwi, Apteryx rowi.

Circoviruses are circular, non-enveloped, single-stranded DNA viruses around 2000 nucleotides (nt) in length and include the pathogenic species, Porcine circovirus 1 and Beak and feather disease virus, capable of causing significant morbidity and mortality. This group of viruses may be robust to degradation by external environments, and avian circoviruses are known to move between closely related hosts. Using a de novo metagenomic approach, followed by confirmatory PCR, we identify for the first time a circular Rep-encoding single-stranded (CRESS) DNA virus in New Zealand kiwi, Apteryx spp., derived from faecal matter of the rowi kiwi (A. rowi) showing signs of verminous dermatitis. The entire 2085 nt genome was cloned and sequenced and contains both capsid and replicase genes, as well as a conserved 9 nt motif. Phylogenetic analyses place it within Circoviridae, adjacent to other environmental CRESS-DNA viruses, and most closely related to badger circovirus-like virus (Meles meles circovirus-like virus). As the rowi is the most critically endangered kiwi, it is vital to understand the role of rowi kiwi circovirus-like virus as a possible pathogen and also any potential cross-species transmission.

Discovery of novel virus sequences in an isolated and threatened bat species, the New Zealand lesser short-tailed bat (Mystacina tuberculata).

Bats harbour a diverse array of viruses, including significant human pathogens. Extensive metagenomic studies of material from bats, in particular guano, have revealed a large number of novel or divergent viral taxa that were previously unknown. New Zealand has only two extant indigenous terrestrial mammals, which are both bats, Mystacina tuberculata (the lesser short-tailed bat) and Chalinolobus tuberculatus (the long-tailed bat). Until the human introduction of exotic mammals, these species had been isolated from all other terrestrial mammals for over 1 million years (potentially over 16 million years for M. tuberculata). Four bat guano samples were collected from M. tuberculata roosts on the isolated offshore island of Whenua hou (Codfish Island) in New Zealand. Metagenomic analysis revealed that this species still hosts a plethora of divergent viruses. Whilst the majority of viruses detected were likely to be of dietary origin, some putative vertebrate virus sequences were identified. Papillomavirus, polyomavirus, calicivirus and hepevirus were found in the metagenomic data and subsequently confirmed using independent PCR assays and sequencing. The new hepevirus and calicivirus sequences may represent new genera within these viral families. Our findings may provide an insight into the origins of viral families, given their detection in an isolated host species.