Biology subjects

Grubbs, K.

Publications and source records attributed to Grubbs, K..

3 recordsLinked to original sources

bioRxiv2022

Host-driven temperature dependence of viral infection in honey bees

The temperature dependence of infection reflects changes in the performance of parasites and hosts. High temperatures (i.e., fever) often mitigate infection by favoring heat-tolerant hosts over heat-sensitive parasites. Honey bees exhibit an endothermic, colony-level temperature regulation that is exceptional among insects and favors resistance to several parasites. However, proliferation of viruses is heavily host-dependent, suggesting that viral infection could be linked to--not threatened by--optimum host function. To understand how temperature-driven changes in performance of viruses and hosts shape virus proliferation, we compared the temperature dependence of isolated viral enzyme activity, three honey bee traits, and infection of honey bee pupae. Viral enzyme activity varied by <2-fold over a >30 {degrees}C interval that spanned the temperatures typical of ectothermic insects and honey bees. In contrast, metrics of honey bee performance peaked at high ([≥] 35 {degrees}C) temperatures and were highly temperature-sensitive, with respiration varying 8-fold over a 20 {degrees}C interval and successful development requiring a narrow 8 {degrees}C temperature range. Although these results suggested that hosts would gain a relative advantage over viruses with increasing temperature, the temperature dependence of pupal infection matched that of pupal development, falling only near pupaes upper thermal limits. Our results reflect the host-dependent nature of virus proliferation, suggesting that infection is accelerated--not curtailed--by optimum host function, contradicting predictions of infection based on the relative performance of parasites and hosts, and suggesting tradeoffs between infection resistance and host survival. Despite a 98% reduction in infection at the upper end of the colony temperature range, the narrow thermal safety margin for honey bee development might preclude the effectiveness of fever for controlling viruses.

ecology↗

bioRxiv2021

Mites alight! Sunflower crop area and pollen supplementation enhance honey bee resistance to Varroa destructor

Anthropogenic landscape changes can affect parasite epidemiology in wild and agricultural animals. Honey bees are agricultural animals whose services are threatened by loss of floral resources and by parasites, most notably the invasive mite Varroa destructor. Existing mite control strategies rely heavily on chemical treatments that can adversely affect bees. Alternative, pesticide-free control methods are urgently needed to maintain effective pollination services. Many flowering plants provide nectar and pollen that enhance resistance to parasites in animals. Enrichment of landscapes with antiparasitic floral resources could therefore provide a sustainable means of parasite control in pollinators. Floral rewards of Asteraceae plants have been shown to reduce parasitic infection in diverse bee species, including honey and bumble bees. Here, we tested the effects of sunflower (Helianthus annuus) cropland and pollen supplementation on honey bee resistance to macro- and microparasites. Our results show that each doubling of sunflower crop area is associated with a 28% reduction in mite infestation intensity. Late-summer supplementation of colonies with sunflower pollen reduced mite infestation by 2.75-fold relative to an artificial pollen. Our findings suggest the potential for sunflower plantings or pollen supplements to counteract a main driver of honey bee losses worldwide.

ecology↗

bioRxiv2019

Dynamic evolution in the key honey bee pathogen Deformed wing virus

The impacts of invertebrate RNA virus population dynamics on virulence and infection outcomes are poorly understood. Deformed wing virus (DWV), the main viral pathogen of honey bees, negatively impacts bee health which can lead to colony death. Despite previous reports on the reduction of DWV diversity following the arrival of the parasitic mite Varroa destructor, the key DWV vector, we found high genetic diversity of DWV in infested United States (US) honey bee colonies. Phylogenetic analysis showed that the divergent US DWV genotypes are of monophyletic origin, which were likely generated as a result of diversification after a genetic bottleneck. To investigate the population dynamics of this divergent DWV, we designed a series of novel infectious cDNA clones corresponding to co-existing DWV genotypes, thereby devising a reverse genetic system for an invertebrate RNA virus quasispecies. Equal replication rates were observed for all clone-derived DWV variants in single infections. Surprisingly, individual clones replicated to the same high levels as their mixtures and even the parental highly diverse natural DWV population, suggesting that complementation between genotypes was not required to replicate to high levels. Mixed clone-derived infections showed a lack of strong competitive exclusion, suggesting that the DWV genotypes were adapted to co-exist. Mutational and recombination events were observed across clone progeny providing new insights into the forces that drive and constrain virus diversification. Accordingly, herein we propose a new model of Varroa-induced DWV dynamics whereby an initial selective sweep is followed by virus diversification fueled by negative frequency-dependent selection for new genotypes. This selection likely reflects the ability of rare lineages to evade host defenses, specifically antiviral RNA interference (RNAi). In support of this, we show that RNAi induced against one DWV strain is less effective against an alternate strain from the same population.\n\nAuthor SummaryVirulence of Deformed wing virus (DWV), a major pathogen of honey bees, showed a sharp and significant increase following the introduction of its vector, the mite Varroa destructor. Varroa vectoring resulted in genetic changes of DWV, including reduction of DWV diversity to nearly clonal levels in the UK and Hawaii. Contrary to the previous reports, we discovered that virulent DWV populations circulating across the Varroa-infested United States included many divergent genotypes generated following a strong bottleneck event. We designed a series of the full-length infectious cDNA clones that captured the diversity of a typical virulent DWV population from a declining Varroa-infested colony, effectively establishing first reverse genetic system for an invertebrate RNA virus quasispecies, in order to investigate interactions between the virus genotypes. We demonstrated that individual co-existing DWV genotypes and diverse natural DWV populations replicated equally well indicating that complementation between isolates was not required to enable DWV replication to high levels. Also, no obvious competitive exclusion was detected between genotypes in mixed infections suggesting DWV genotypes are adapted to co-exist to maintain overall population diversity. We suggest that introduction of Varroa resulted in an initial selective sweep of DWV diversity which was followed by DWV diversification driven by selection for new genotypes capable of evading host defenses, specifically antiviral RNA interference.

microbiology↗