Biology subjects

Longdon, B.

Publications and source records attributed to Longdon, B..

18 recordsLinked to original sources

bioRxiv2026

Examining interactions between the microbiome and viral infection across Drosophila species

Microbiomes can influence the outcomes of virus infection, while viral infections can disrupt microbiome composition. These reciprocal interactions may contribute to patterns of host susceptibility, but it remains unclear whether microbiome-virus interactions are consistent across host species, or whether host evolutionary relationships influence microbiome variation and its association with viral susceptibility. Here, we investigate interactions between bacterial microbiomes and Drosophila C virus (DCV) infection across 32 Drosophilidae host species, using experimental infections and 16S rRNA amplicon sequencing. Using phylogenetic mixed models, we tested for phylogenetic structure in microbiome diversity and composition, and whether specific bacterial taxa were associated with among-species variation in viral load. Drosophilidae microbiomes were consistently dominated by a small number of bacterial genera and showed limited phylogenetic structuring. DCV infection was associated with a small reduction in bacterial richness, but microbiome composition was only weakly affected by wounding or infection and largely dominated by within-species variation. However, specific taxa were associated with large differences in viral replication, including reduced DCV load in flies harbouring Streptococcus before infection or Bacillus during infection. These results suggest that, at least in the conditions used in this study, microbiome composition may not generate strong, generalisable host phylogenetic patterns in virus susceptibility.

evolutionary biology↗

bioRxiv2026

Drosophila-virus genotype interactions dominate transmission, virulence and load, eroding additive fitness variance

Host-parasite coevolution is expected to generate strong selection for susceptibility and infectivity that has the potential to erode genetic variation. Despite this, natural populations often retain extensive genetic variation in these traits. Negative frequency-dependent selection could explain the maintenance of variation since it results in genotype-by-genotype interactions on fitness that, unlike additive genetic variance among hosts and pathogens, is masked from selection and so can remain cryptic. Here we combine coevolutionary modelling with large-scale experimental infection assays to quantify how host-pathogen interactions structure fitness variance in a vertically transmitted virus system, Drosophila melanogaster and sigma virus. Simulations show that coevolution typically erodes additive genetic variance in host and pathogen fitness, concentrating variance in host-virus interaction terms. Consistent with these predictions, experiments spanning 90 host-virus genotype combinations reveal that transmission, viral load and virulence are overwhelmingly governed by host-virus genetic interactions rather than host or virus main (i.e., additive) effects. As a result, neither host resistance alleles nor viral genotypes confer consistently higher fitness across genetic backgrounds. Interactions tend to be sex-specific, further limiting heritable fitness variation. Our results demonstrate that coevolution can substantially mask heritable genetic variation from selection by rendering fitness context dependent. This extensive cryptic genetic variation may be revealed either when ecological or evolutionary conditions shift, or when the process of coevolution itself alters the direction of selection. This demonstrates the need to account for genotype-specific interactions when forecasting evolutionary responses.

evolutionary biology↗

bioRxiv2026

Bacterial phylogeny explains variation in virulence but not phage efficacy in vivo

The continuing emergence of antimicrobial resistance (AMR) poses one of the most urgent threats to public health in the 21st century, causing [~]1.2 million deaths per year. A promising alternative to traditional antimicrobials is phage therapy, which has proved effective in the treatment of antimicrobial-resistant infections, including methicillin-resistant Staphylococcus aureus (MRSA). However, considerable variation in the outcome of phage therapy remains, with phage that show high efficacy in vitro often showing little to no effect when applied in vivo. To allow for the efficient clinical use of phage, it is vital to understand how both bacterial virulence and phage efficacy vary in vivo and determine how well in vitro and in vivo measures of phage efficacy correlate. Here, we infected 4,968 Galleria mellonella larvae with 64 phylogenetically diverse Staphylococcaceae isolates, both with and without co-inoculation of the bacteriophage ISP, and recorded mortality and melanisation over 24 hours. We found that bacterial virulence varied among Staphylococcaceae strains, and that a large proportion of this variation could be explained by the evolutionary relationships between bacteria. These results indicate that pathogen phylogeny may be a useful tool for explaining variation in both the severity of clinical infections and the virulence of novel emerging pathogens. The addition of phage significantly improved the survival of G. mellonella larvae, with an average 15.2% increase in endpoint survival and 10.1% reduction in endpoint melanisation across Staphylococcaceae strains. Phage efficacy in vivo showed phylogenetic repeatability, but no detectable phylogenetic heritability across bacteria species, in contrast to previous in vitro studies of phage infections. Concurrently, we found no evidence of a correlation between in vivo and in vitro measures of phage efficacy across bacterial isolates, demonstrating that environment plays a major role in determining the outcomes of bacteria-phage interactions. This highlights that caution should be used when extrapolating from in vitro measures of phage efficacy to select phages for therapeutic uses.

microbiology↗

bioRxiv2025

Life history and infection susceptibility parameters of Drosophila species reared on a common diet

The fruit fly Drosophila is a powerful model organism for many biological questions. While Drosophila melanogaster has been the most widely used species owing to its versatile genetic tools, comparative studies also take advantage of the rich evolutionary, ecological, and behavioural diversity of Drosophilidae. This model system has only benefitted from the sequencing of hundreds of genomes assembled to chromosome level, and rich array of publicly-available datasets. However, labs that typically use just D. melanogaster can have difficulties adopting other species into their experiments due to unique dietary needs and care regimens. While dedicated research groups can rear dozens of fly species, this often requires preparing a variety of food media, which can be logistically taxing. In this study, we report an agar food recipe that we have used to rear >70 species of Drosophilidae (Prop recipe). This list includes ecological specialists such as D. sechellia, major pest species including D. suzukii, cactophiles, slime flux feeders, detritivores, and even mushroom-feeding species of the Quinaria and Testacea groups. This food recipe uses only standard powdered ingredients and molasses, and is already in use by one commercial transgenic injection provider. We provide life history parameters for dozens of species reared on this recipe, including comparisons in a subset of species across a variety of diets, finding fly fitness to be comparable or better on the Prop recipe among tested species. We further provide comparative data for 42 species after systemic infection by Acetobacter bacteria. However, unexpectedly, we found a striking interaction of diet and the microbiota that impacts susceptibility to infection in species-specific fashion. Our results suggest certain experiment types may be impacted by diet due to the microbiome that the diet itself supports. By providing rearing advice, life history parameters, and this infection dataset and experience, we hope to enable researchers to take advantage of the diversity of Drosophila as a model system for evolutionary research.

evolutionary biology↗

bioRxiv2025

Effect of the microbiome on pathogen susceptibility across four Drosophilidae species

The microbiota has been shown to play an important role in host susceptibility to infections in some hosts. However, less is known about whether microbiota-mediated effects are consistent across host species, as our understanding of such interactions may be affected by publication bias. Following on from a large study of 36 species of Drosophilidae challenged with four bacterial pathogens, we identified two candidate host species that might have protective microbiome based on low susceptibility and high abundance of the culturable microbiota; we selected two other host species for comparison. We tested whether germ-reduced flies, and flies with a natural or re-constituted microbiome, varied in their susceptibility to systemic infection with two bacterial pathogens (Providencia rettgeri and Staphylococcus aureus) and one viral pathogen (Drosophila C Virus). The composition and abundance of the bacterial microbiota varied between species and microbiome treatments. We found an overall interaction between host species and pathogen type, confirming previous work that host species vary in their susceptibility in a pathogen-specific manner. Similarly, we found that microbiome treatments had differing effects on host survival among host species, although effect sizes tended to be small. In D. putrida individuals with manipulated microbiomes showed increased susceptibility to all pathogens tested; in other hosts altered susceptibility was pathogen dependent. While there are always challenges to manipulating microbiomes, especially across multiple host species, our results indicate that host microbiota may play limited roles on survival in systemic infection in these four species. This work demonstrates that caution is required when generalising about the potential beneficial impact of microbiomes.

microbiology↗

bioRxiv2024

Positive correlations in susceptibility to a diverse panel of viruses across host species

Our ability to predict the emergence of novel viruses relies on there being generalisable patterns in the susceptibilities of hosts to novel infections. Studies investigating variation in susceptibility among host species have consistently shown that closely related hosts share similar susceptibilities to a given virus. However, the extent to which such phylogenetic patterns of susceptibility are correlated amongst diverse sets of viruses is unclear. Here, we investigate phylogenetic correlations in susceptibility among Drosophilidae hosts to a panel of eleven different invertebrate viruses, comprising seven unique virus species, six unique families, and both RNA and DNA viruses. The susceptibility of hosts to each pair of viruses tested was either positively correlated across host species or did not show evidence of correlation. No negative correlations, indicative of evolutionary trade-offs in host susceptibility to different viruses, were detected between any virus pairs. The strength of correlations were generally higher in viruses of the same species and family, consistent with virus phylogenetic patterns in host infectivity. Our results suggest that generalised host susceptibility can result in positive correlations, even between highly diverged viruses, while specialised interactions with individual viruses cause a stepwise decrease in correlation strength between viruses from the within-species, to the within-family, to the across-family level.

evolutionary biology↗

bioRxiv2024

Varying phylogenetic signal to four bacterial pathogens across species of Drosophilidae

Bacterial infections are one of the major sources threatening public health. Pathogen host shifts - where a pathogen jumps from one host species to another - are important sources of emerging infectious diseases. However, compared to viruses, we know relatively little about the factors that determine whether a bacteria can infect a novel host, such as how host phylogenetics constrains variation in pathogen-host range and the link between host phylogeny and the infectivity and virulence of a pathogen. Here, we experimentally examined susceptibility to bacterial infections using a panel of 36 Drosophilidae species and four pathogens (Providencia rettgeri, Pseudomonas entomophila, Enterococcus faecalis, Staphylococcus aureus). The outcomes of infection differed greatly among pathogens and across host species. The host phylogeny explains a considerable amount of variation in susceptibility, with the greatest phylogenetic signal for P. rettgeri infection, explaining 94% of the variation in mortality. Positive correlations were observed between mortality and bacterial load for three out of the four pathogens. Correlations in susceptibility between the four pathogens were positive but largely non-significant, suggesting susceptibility is mostly pathogen-specific. These results suggest that susceptibility to bacterial pathogens may be predicted by the host phylogeny, but the effect may vary in magnitude between different bacteria.

evolutionary biology↗

bioRxiv2022

Investigating the outcomes of virus coinfection within and across host species

Interactions between coinfecting pathogens have the potential to alter the course of infection and can act as a source of phenotypic variation in susceptibility between hosts. This phenotypic variation may influence the evolution of host-pathogen interactions within host species and interfere with patterns in the outcomes of infection across host species. Here, we examine experimental coinfections of two Cripaviruses - Cricket Paralysis Virus (CrPV), and Drosophila C Virus (DCV) -across a panel of 25 Drosophila melanogaster inbred lines and 47 Drosophilidae host species. We find that interactions between these viruses alter viral loads across D. melanogaster genotypes, with a ~3 fold increase in the viral load of DCV and a ~2.5 fold decrease in CrPV in coinfection compared to single infection, but we find little evidence of a host genetic basis for these effects. Across host species, we find no evidence of systematic changes in susceptibility during coinfection, with no interaction between DCV and CrPV detected in the majority of host species. These results suggest that phenotypic variation in coinfection interactions within host species can occur independently of natural host genetic variation in susceptibility, and that patterns of susceptibility across host species to single infections can be robust to the added complexity of coinfection.

evolutionary biology↗

bioRxiv2022

The host phylogeny determines viral infectivity and replication across Staphylococcus host species

Genetic similarity between eukaryotic host species is an important determinant of the outcome of virus host shifts, where a pathogen infects a novel host species. However, it is less clear if this is the case for prokaryotes where anti-virus defences can be transmitted by horizontal gene transfer and evolve rapidly. Understanding the patterns and determinants of cross-species transmissions may provide insights into the processes underlying pathogen emergence. Here, we measure the susceptibility of 64 strains of Staphylococcus bacteria (48 strains of S. aureus and 16 non-aureus species) to the bacteriophage ISP, which is currently under investigation for use in phage therapy. Using three methods - plaque assays, optical density (OD) assays, and quantitative (q)PCR - we find that the host phylogeny explains a large proportion of the variation in susceptibility to ISP across the host panel. These patterns were consistent in models of only S. aureus strains and models with a single representative from each Staphylococcus species, suggesting that these phylogenetic effects are conserved both within and among host species. We find positive correlations between susceptibility assessed using a binary measure of plaque assay, OD, and qPCR, but not between the continuous component of plaque assay and any other method, suggesting that plaque assays alone may be inadequate to assess host range. Together, our results demonstrate the ability of bacterial host evolutionary relatedness to explain differences in susceptibility to phage infection, with implications for the development of ISP both as a phage therapy treatment and as an experimental system for the study of virus host shifts.

evolutionary biology↗

bioRxiv2022

Sex and tissue differences in virus susceptibility across species

Species vary in their susceptibility to pathogens, and this can alter the ability of a pathogen to infect a novel host. However, many factors can generate heterogeneity in infection outcomes, obscuring our ability to understand pathogen emergence. Such heterogeneities can alter the consistency of responses across individuals and host species. For example, sexual dimorphism in susceptibility means males are often intrinsically more susceptible than females (although this can vary by host and pathogen). Further, we know little about whether the tissues infected by a pathogen in one host are the same in another species, and how this relates to the harm a pathogen does to its host. Here, we first take a comparative approach to examine sex differences in susceptibility across 31 species of Drosophilidae infected with Drosophila C Virus (DCV). We found a strong positive inter-specific correlation in viral load between males and females, with a close to 1:1 relationship, suggesting that susceptibility to DCV across species is not sex specific. Next, we made comparisons of the tissue tropism of DCV across seven species of fly. We found differences in viral load between the tissues of the seven host species, but no evidence of tissues showing different patterns of susceptibility in different host species. We conclude that, in this system, patterns of viral infectivity across host species are robust between males and females, and susceptibility in a given host is general across tissue types.

evolutionary biology↗

bioRxiv2021

DrosoPhyla: genomic resources for drosophilid phylogeny and systematics

The vinegar fly Drosophila melanogaster is a pivotal model for invertebrate development, genetics, physiology, neuroscience, and disease. The whole family Drosophilidae, which contains over 4000 species, offers a plethora of cases for comparative and evolutionary studies. Despite a long history of phylogenetic inference, many relationships remain unresolved among the groups and genera in the Drosophilidae. To clarify these relationships, we first developed a set of new genomic markers and assembled a multilocus data set of 17 genes from 704 species of Drosophilidae. We then inferred well-supported group and species trees for this family. Additionally, we were able to determine the phylogenetic position of some previously unplaced species. These results establish a new framework for investigating the evolution of traits in fruit flies, as well as valuable resources for systematics.

evolutionary biology↗

bioRxiv2021

Virus relatedness predicts susceptibility in novel host species

Virus host shifts are a major source of outbreaks and emerging infectious diseases, and predicting the outcome of novel host and virus interactions remains a key challenge for virus research. The evolutionary relationships between host species can explain variation in transmission rates, virulence, and virus community composition between hosts, but the potential for different viruses to interact with host species effects has yet to be established. Here, we measure correlations in viral load of four Cripavirus isolates across experimental infections of 45 Drosophilidae host species. We find positive correlations between every pair of viruses tested, suggesting that broadly susceptible host clades could act as reservoirs and donors for certain types of viruses. Additionally, we find evidence of genotype-by-genotype interactions between viruses and host species, highlighting the importance of both host and virus traits in determining the outcome of virus host shifts. More closely related viruses tended to be more strongly correlated, providing tentative evidence that virus evolutionary relatedness may be a useful proxy for determining the likelihood of novel virus emergence, which warrants further research. Impact SummaryMany new infectious diseases are caused by viruses jumping into novel host species. Estimating the probability that jumps will occur, what the characteristics of new viruses will be, and how they are likely to evolve after jumping to new host species are major challenges. To solve these challenges, we require a detailed understanding of the interactions between different viruses and hosts, or metrics that can capture some of the variation in these interactions. Previous studies have shown that the evolutionary relationships between host species can be used to predict traits of infections in different hosts, including transmission rates and the damage caused by infection. However, the potential for different viruses to influence the patterns of these host species effects has yet to be determined. Here, we use four viruses of insects in experimental infections across 45 different fruit fly host species to begin to answer this question. We find similarities in the patterns of replication and persistence between all four viruses, suggesting susceptible groups of related hosts could act as reservoirs and donors for certain types of virus. However, we also find evidence that different virus genotypes interact in different ways with some host species. Viruses that were more closely related tended to behave in similar ways, and so we suggest that virus evolutionary relatedness may prove to be a useful metric for predicting the traits of novel infections and should be explored further in future studies.

evolutionary biology↗

bioRxiv2020

Diet has no effect on susceptibility to an RNA virus across host species

The likelihood of a successful host shift of a parasite to a novel host species can be influenced by environmental factors that can act on both the host and parasite. Changes in nutritional resource availability have been shown to alter pathogen susceptibility and the outcome of infection in a range of systems. Here we examined how dietary protein to carbohydrate altered susceptibility in a large cross infection experiment. We infected 27 species of Drosophilidae with an RNA virus on three food types of differing protein to carbohydrate ratios. We then measured how viral load and mortality across species was affected by changes in diet. We found that changes in the protein:carbohydrate in the diet did not alter the outcomes of infection, with strong positive inter-species correlations in both viral load and mortality across diets, suggesting no species by diet interaction. Mortality and viral load were strongly positively correlated, and this association was consistent across diets. This suggests changes in diet may give consistent outcomes across host species, and may not be universally important in determining host susceptibility to pathogens. Twitter summaryNo role of host diet in susceptibility to a novel viral pathogen across host species Impact StatementA successful host shift of a parasite from one susceptible species to a novel host can be influenced by many ecological factors. Changes in host diet can alter the immune response and outcomes of host-parasite interactions and could potentially alter the outcome of a virus host shift. To investigate, we infected 27 species of Drosophilidae with an RNA virus (DCV) across three food types with differing protein to carbohydrate ratios. We then looked at pathogen loads and survival of infected hosts compared to uninfected controls. Changes in the ratio of protein to carbohydrate did not alter susceptibility to DCV across host species.

evolutionary biology↗

bioRxiv2019

Short-term evolution under copper stress increases probability of plasmid uptake

Understanding plasmid transfer dynamics remains a key knowledge gap in the mitigation of antibiotic resistance gene spread. Direct effects of exposure to stressors on plasmid uptake are well monitored. However, it remains untested whether evolution of strains under stress conditions modulates subsequent plasmid uptake. Here, we evolved a compost derived microbial community for six weeks under copper stress and non-exposed control conditions. We then tested the ability of isolated clones from both treatments to take up the broad host range plasmid pKJK5 from an E.coli donor strain. Clones pre-adapted to copper displayed a significantly increased probability to be permissive towards the plasmid compared to those isolated from the control treatment. Further, increased phylogenetic distance to the donor strain was significantly and negatively correlated with plasmid uptake probabilities across both treatments.

microbiology↗

bioRxiv2018

Host-pathogen coevolution increases genetic variation in susceptibility to infection

It is common to find considerable genetic variation in susceptibility to infection in natural populations. We have investigated whether natural selection increases this variation by testing whether host populations show more genetic variation in susceptibility to pathogens that they naturally encounter than novel pathogens. In a large cross-infection experiment involving four species of Drosophila and four host-specific viruses, we always found greater genetic variation in susceptibility to viruses that had coevolved with their host. We went on to examine the genetic architecture of resistance in one host species, finding that there are more major-effect genetic variants in coevolved host-parasite interactions. We conclude that selection by pathogens increases genetic variation in host susceptibility, and much of this effect is caused by the occurrence of major-effect resistance polymorphisms within populations.

evolutionary biology↗

bioRxiv2018

Changes in temperature alter susceptibility to a virus following a host shift

Host shifts - where a pathogen jumps between different host species - are an important source of emerging infectious disease. With ongoing climate change there is an increasing need to understand the effect changes in temperature may have on emerging infectious disease. We investigated whether species susceptibilities change with temperature and ask if susceptibility is greatest at different temperatures in different species. We infected 45 species of Drosophilidae with an RNA virus and measured how viral load changes with temperature. We found the host phylogeny explained a large proportion of the variation in viral load at each temperature, with strong phylogenetic correlations between viral loads across temperature. The variance in viral load increased with temperature, whilst the mean viral load did not, such that as temperature increased the most susceptible species become more susceptible, and the least susceptible less so. We found no significant relationship between a species susceptibility across temperatures and proxies for thermal optima; critical thermal maximum and minimum or basal metabolic rate. These results suggest that whilst the rank order of species susceptibilities can remain the same with changes in temperature, the likelihood of host shifts into a given species may increase or decrease.\n\nAuthor SummaryEmerging infectious diseases are often the result of a host shift, where a pathogen jumps from one host species into another. Understanding the factors underlying host shifts is a major goal for infectious disease researchers. This effort has been further complicated by the fact that host-parasite interactions are now taking place in a period of unprecedented global climatic warming. Here, we ask how host shifts are affected by temperature by carrying out experimental infections using an RNA virus across a wide range of related species, at three different temperatures. We find that as temperature increases the most susceptible species become more susceptible, and the least susceptible less so. This has important consequences for our understanding of host shift events in a changing climate, and suggests that temperature changes may affect the likelihood of a host shift into certain species.

evolutionary biology↗

bioRxiv2017

Host shifts result in parallel genetic changes when viruses adapt to closely related species

Host shifts, where a pathogen invades and establishes in a new host species, are a major source of emerging infectious diseases. They frequently occur between related host species and often rely on the pathogen evolving adaptations that increase their fitness in the novel host species. To investigate genetic changes in novel hosts, we experimentally evolved replicate lineages of an RNA virus (Drosophila C Virus) in 19 different species of Drosophilidae and deep sequenced the viral genomes. We found a strong pattern of parallel evolution, where viral lineages from the same host were genetically more similar to each other than to lineages from other host species. When we compared viruses that had evolved in different host species, we found that parallel genetic changes were more likely to occur if the two host species were closely related. This suggests that when a virus adapts to one host it might also become better adapted to closely related host species. This may explain in part why host shifts tend to occur between related species, and may mean that when a new pathogen appears in a given species, closely related species may become vulnerable to the new disease.

evolutionary biology↗

bioRxiv2016

Vertically transmitted rhabdoviruses are found across three insect families and have dynamic interactions with their hosts

A small number of free-living viruses have been found to be obligately vertically transmitted, but it remains uncertain how widespread vertically transmitted viruses are and how quickly they can spread through host populations. Recent metagenomic studies have found several insects to be infected with sigma viruses (Rhabdoviridae). Here, we report that sigma viruses that infect Mediterranean fruit flies (Ceratitis capitata), Drosophila immigrans, and speckled wood butterflies (Pararge aegeria) are all vertically transmitted. We find patterns of vertical transmission that are consistent with those seen in Drosophila sigma viruses, with high rates of maternal transmission, and lower rates of paternal transmission. This mode of transmission allows them to spread rapidly in populations, and using viral sequence data we found the viruses in D. immigrans and C. capitata had both recently swept through host populations. The viruses were common in nature, with mean prevalences of 12% in C. capitata, 38% in D. immigrans and 74% in P. aegeria. We conclude that vertically transmitted rhabdoviruses may be widespread in insects, and that these viruses can have dynamic interactions with their hosts.

evolutionary biology↗