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Viruses are omnipresent, yet the knowledge on drivers of viral prevalence in wild host populations is often limited. Biotic factors, such as sympatric managed host species, as well as abiotic factors, such as climatic variables, are likely to impact viral prevalence. Managed and wild bees, which harbor several multi-host viruses with a mostly fecal–oral between-species transmission route, provide an excellent system with which to test for the impact of biotic and abiotic factors on viral prevalence in wild host populations. Here we show on a continental scale that the prevalence of three broad host viruses: the AKI-complex ( Acute bee paralysis virus , Kashmir bee virus and Israeli acute paralysis virus ), Deformed wing virus , and Slow bee paralysis virus in wild bee populations (bumble bees and solitary bees) is positively related to viral prevalence of sympatric honey bees as well as being impacted by climatic variables. The former highlights the need for good beekeeping practices, including Varroa destructor management to reduce honey bee viral infection and hive placement. Furthermore, we found that viral prevalence in wild bees is at its lowest at the extreme ends of both temperature and precipitation ranges. Under predicted climate change, the frequency of extremes in precipitation and temperature will continue to increase and may hence impact viral prevalence in wild bee communities.

Honey bee colony health has received considerable attention in recent years, with many studies highlighting multifactorial issues contributing to colony losses. Disease and weather are consistently highlighted as primary drivers of colony loss, yet little is understood about how they interact. Here, we combined disease records from government honey bee health inspections with meteorological data from the CEDA to identify how weather impacts EFB, AFB, CBP, varroosis, chalkbrood and sacbrood. Using R-INLA, we determined how different meteorological variables influenced disease prevalence and disease risk. Temperature caused an increase in the risk of both varroosis and sacbrood, but overall, the weather had a varying effect on the six honey bee diseases. The risk of disease was also spatially varied and was impacted by the meteorological variables. These results are an important step in identifying the impacts of climate change on honey bees and honey bee diseases.

Most pathogens are embedded in complex communities composed of multiple interacting hosts, but we are still learning how community-level factors, such as host diversity, abundance, and composition, contribute to pathogen spread for many host–pathogen systems. Evaluating relationships among multiple pathogens and hosts may clarify whether particular host or pathogen traits consistently drive links between community factors and pathogen prevalence. Pollinators are a good system to test how community composition influences pathogen spread because pollinator communities are extremely variable and contain several multi-host pathogens transmitted on shared floral resources. We conducted a field survey of four pollinator species to test the prevalence of three RNAviruses (deformed wing virus, black queen cell virus, and sacbrood virus) among pollinator communities with variable species richness, abundance, and composition. All three viruses showed a similar pattern of prevalence among hosts. Apis mellifera and Bombus impatiens had significantly higher viral prevalence than Lasioglossum spp. and Eucera pruinosa. In each species, lower virus prevalence was most strongly linked with greater pollinator community species richness. In contrast, pollinator abundance, species-specific pollinator abundance, and community composition were not associated with virus prevalence. Our results support a consistent dilution effect for multiple viruses and host species. Pollinators in species-rich communities had lower viral prevalence than pollinators from species-poor communities, when accounting for differences in pollinator abundance. Species-rich communities likely had lower viral prevalence because species-rich communities contained more native bee species likely to be poor viral hosts than species-poor communities, and all communities contained the highly competent hosts A. mellifera and B. impatiens. Interestingly, the strength of the dilution effect was not consistent among hosts. Instead, host species with low viral prevalence exhibited weaker dilution effects compared to hosts with high viral prevalence. Therefore, host species susceptibility and competence for each virus may contribute to variation in the strength of dilution effects. This study expands biodiversity–disease studies to the pollinator–virus system, finding consistent evidence of the dilution effect among multiple similar pathogens that infect “replicate” host communities.

The parasitic mite Varroa destructor is a leading cause of mortality for Western honey bee ( Apis mellifera ) colonies around the globe. We sought to confirm the presence and likely introduction of only one V. destructor haplotype in New Zealand, and describe the viral community within both V. destructor mites and the bees that they parasitise. A 1232 bp fragment from mitochondrial gene regions suggests the likely introduction of only one V. destructor haplotype to New Zealand. Seventeen viruses were found in bees. The most prevalent and abundant was the Deformed wing virus A (DWV-A) strain, which explained 95.0% of the variation in the viral community of bees. Black queen cell virus , Sacbrood virus , and Varroa destructor virus 2 (VDV-2) played secondary roles. DWV-B and the Israeli acute paralysis virus appeared absent from New Zealand. Ten viruses were observed in V. destructor , with > 99.9% of viral reads from DWV-A and VDV-2. Substantially more variation in viral loads was observed in bees compared to mites. Where high levels of VDV-2 occurred in mites, reduced DWV-A occurred in both the mites and the bees co-occurring within the same hive. Where there were high loads of DWV-A in mites, there were typically high viral loads in bees.

Efforts to improve honey bee colony health continue due to persistent high loss rates. A major focus in this area is Deformed wing virus (DWV), a key driver of colony loss. The application of modern molecular techniques has characterized the DWV genome and its high mutational rate that enables the formation of diverse quasi-species populations capable of evading host immune responses, while other work has led to the development of DWV clones suitable for sequence-specific tracking of viral dynamics. In this work we combine knowledge of these efforts to track the mutational progression in a DWV clone surrounding an area of low nucleotide diversity and compare it to its wild-type source. We achieve this through amplicon sequencing of the structural viral protein, VP2, after incubation across three generations and multiple host genetic sources. Inocula were injected into pupae, allowed to replicate, then extracted for a further two generations of injections. For the final injection generation, recipient pupae were injected with preparations from either the same genetic source or cross-fostered from other colonies. Overall, we compared the mean number and type of mutations, their proportional abundance in the read pool, and specific locations across strains. Sequencing results indicate a limited number of mutational hotspots, which were driven by silent mutations in the final injection generation of the wild-type strains. No significant differences were found among other mutation types, cross-fostering status, or interactions with host genetics. This work is an initial attempt at examining viral dynamics in a cloned system across multiple generations and treatment groups. The results provide valuable insights, which may further enhance our understanding of viral dynamics and potentially improve future honey bee therapeutics.

The worldwide dispersal of the ectoparasitic mite Varroa destructor from its Asian origins has fundamentally transformed the relationship of the honey bee ( Apis mellifera ) with several of its viruses, via changes in transmission and/or host immunosuppression. The extent to which honey bee-virus relationships change after Varroa invasion is poorly understood for most viruses, in part because there are few places in the world with several geographically close but completely isolated honey bee populations that either have, or have not, been exposed long-term to Varroa , allowing for separate ecological, epidemiological, and adaptive relationships to develop between honey bees and their viruses, in relation to the mite’s presence or absence. The Azores is one such place, as it contains islands with and without the mite. Here, we combined qPCR with meta-amplicon deep sequencing to uncover the relationship between Varroa presence, and the prevalence, load, diversity, and phylogeographic structure of eight honey bee viruses screened across the archipelago. Four viruses were not detected on any island (ABPV-Acute bee paralysis virus, KBV-Kashmir bee virus, IAPV-Israeli acute bee paralysis virus, BeeMLV-Bee macula-like virus); one (SBV-Sacbrood virus) was detected only on mite-infested islands; one (CBPV-Chronic bee paralysis virus) occurred on some islands, and two (BQCV-Black queen cell virus, LSV-Lake Sinai virus,) were present on every single island. This multi-virus screening builds upon a parallel survey of Deformed wing virus (DWV) strains that uncovered a remarkably heterogeneous viral landscape featuring Varroa -infested islands dominated by DWV-A and -B, Varroa -free islands naïve to DWV, and a refuge of the rare DWV-C dominating the easternmost Varroa -free islands. While all four detected viruses investigated here were affected by Varroa for one or two parameters (usually prevalence and/or the Richness component of ASV diversity), the strongest effect was observed for the multi-strain LSV. Varroa unambiguously led to elevated prevalence, load, and diversity (Richness and Shannon Index) of LSV, with these results largely shaped by LSV-2, a major LSV strain. Unprecedented insights into the mite-virus relationship were further gained from implementing a phylogeographic approach. In addition to enabling the identification of a novel LSV strain that dominated the unique viral landscape of the easternmost islands, this approach, in combination with the recovered diversity patterns, strongly suggests that Varroa is driving the evolutionary change of LSV in the Azores. This study greatly advances the current understanding of the effect of Varroa on the epidemiology and adaptive evolution of these less-studied viruses, whose relationship with Varroa has thus far been poorly defined.

Transmission routes impact pathogen virulence and genetics, therefore comprehensive knowledge of these routes and their contribution to pathogen circulation is essential for understanding host–pathogen interactions and designing control strategies. Deformed wing virus (DWV), a principal viral pathogen of honey bees associated with increased honey bee mortality and colony losses, became highly virulent with the spread of its vector, the ectoparasitic mite Varroa destructor . Reproduction of Varroa mites occurs in capped brood cells and mite-infested pupae from these cells usually have high levels of DWV. The removal of mite-infested pupae by worker bees, Varroa Sensitive Hygiene (VSH), leads to cannibalization of pupae with high DWV loads, thereby offering an alternative route for virus transmission. We used genetically tagged DWV to investigate virus transmission to and between worker bees following pupal cannibalisation under experimental conditions. We demonstrated that cannibalization of DWV-infected pupae resulted in high levels of this virus in worker bees and that the acquired virus was then transmitted between bees via trophallaxis, allowing circulation of Varroa -vectored DWV variants without the mites. Despite the known benefits of hygienic behaviour, it is possible that higher levels of VSH activity may result in increased transmission of DWV via cannibalism and trophallaxis.

The worldwide population of western honey bees (Apis mellifera) is under pressure from habitat loss, environmental stress, and pathogens, particularly viruses that cause lethal epidemics. Deformed wing virus (DWV) from the family Iflaviridae, together with its vector, the mite Varroa destructor, is likely the major threat to the world’s honey bees. However, lack of knowledge of the atomic structures of iflaviruses has hindered the development of effective treatments against them. Here, we present the virion structures of DWV determined to a resolution of 3.1 Å using cryo-electron microscopy and 3.8 Å by X-ray crystallography. The C-terminal extension of capsid protein VP3 folds into a globular protruding (P) domain, exposed on the virion surface. The P domain contains an Asp-His-Ser catalytic triad that is, together with five residues that are spatially close, conserved among iflaviruses. These residues may participate in receptor binding or provide the protease, lipase, or esterase activity required for entry of the virus into a host cell. Furthermore, nucleotides of the DWV RNA genome interact with VP3 subunits. The capsid protein residues involved in the RNA binding are conserved among honey bee iflaviruses, suggesting a putative role of the genome in stabilizing the virion or facilitating capsid assembly. Identifying the RNA-binding and putative catalytic sites within the DWV virion structure enables future analyses of how DWV and other iflaviruses infect insect cells and also opens up possibilities for the development of antiviral treatments.

Interspecies transmission of RNA viruses is a major concern for human and animal health. However, host-range, transmission routes and especially the possible impact of these viruses on alternative hosts are often poorly understood. Here, we investigated the role of the labyrinth spider, Agelena labyrinthica , as a potential alternative host of viruses commonly known from western honey bees, Apis mellifera . Field-collected spiders were screened for Acute bee paralysis virus (ABPV), Black queen cell virus, Chronic bee paralysis virus, Deformed wing virus type A and B (DWV-B), Israeli acute paralysis virus, Lake Sinai virus and Sacbrood virus. In a laboratory experiment, labyrinth spiders were fed with ABPV and DWV-B infected honey bees or virus free control food. Our results show that natural infections of A . labyrinthica with these viruses are common in the field, as 62.5% of the samples were positive for at least one virus, supporting their wide host range. For DWV-B, the laboratory data indicate that foodborne transmission occurs and that high virus titres may reduce cocoon building, which would be the first report of clinical symptoms of DWV in Araneae. Since cocoons are tokens of fitness, virus transmission from honey bees might affect spider populations, which would constitute a concern for nature conservation.

Previously unknown pathogens often emerge from primary ecosystems, but there is little knowledge on the mechanisms of emergence. Most studies analyzing the influence of land-use change on pathogen emergence focus on a single host–pathogen system and often observe contradictory effects. Here, we studied virus diversity and prevalence patterns in natural and disturbed ecosystems using a multi-host and multi-taxa approach. Mosquitoes sampled along a disturbance gradient in Côte d’Ivoire were tested by generic RT-PCR assays established for all major arbovirus and insect-specific virus taxa including novel viruses previously discovered in these samples based on cell culture isolates enabling an unbiased and comprehensive approach. The taxonomic composition of detected viruses was characterized and viral infection rates according to habitat and host were analyzed. We detected 331 viral sequences pertaining to 34 novel and 15 previously identified viruses of the families Flavi -, Rhabdo -, Reo -, Toga -, Mesoni - and Iflaviridae and the order Bunyavirales . Highest host and virus diversity was observed in pristine and intermediately disturbed habitats. The majority of the 49 viruses was detected with low prevalence. However, nine viruses were found frequently across different habitats of which five viruses increased in prevalence towards disturbed habitats, in congruence with the dilution effect hypothesis. These viruses were mainly associated with one specific mosquito species ( Culex nebulosus ), which increased in relative abundance from pristine (3%) to disturbed habitats (38%). Interestingly, the observed increased prevalence of these five viruses in disturbed habitats was not caused by higher host infection rates but by increased host abundance, an effect tentatively named abundance effect. Our data show that host species composition is critical for virus abundance. Environmental changes that lead to an uneven host community composition and to more individuals of a single species are a key driver of virus emergence.