Biology subjects

Mayo, C.

Publications and source records attributed to Mayo, C..

5 recordsLinked to original sources

bioRxiv2026

Quantifying Asymmetric Coevolutionary Dynamics using Normalized Phylogenetic Costs

AO_SCPLOWBSTRACTC_SCPLOWCoevolutionary studies aim to characterize associations, such as virus-host relationships, by using phylogenetic distances to quantify the topological concordance between the phylogenies of interacting taxa. However, phylogenetic distances cannot capture asymmetrical relationships that arise from differences in sampling, evolutionary rates, or characterizations between datasets. Furthermore, a lack of accurate normalization complicates the interpretation and validation of coevolutionary analyses. To address these limitations, we employed the Asymmetric Cluster Affinity and Cluster Support costs as a general framework to quantify coevolutionary patterns across multiple biological scales. We benchmarked the precision of these costs by reanalyzing a curated dataset documenting interspecies transmission frequencies across nineteen virus-host phylogenies. Our results corroborate prior findings showing that all virus families under study can cross species boundaries; however, the asymmetric costs provide a more granular representation, demonstrating that the frequency of such events varies significantly across families. We then applied the Asymmetric Cluster Support cost to quantify preferential gene segment pairings within the Bluetongue virus genome. This analysis revealed a close phylogenetic association between the outer capsid proteins VP2 and VP5, likely reflecting shared selective pressures due to their critical roles in cell entry and exit. In contrast, gene segments encoding nonstructural proteins exhibited discordant evolutionary histories relative to other segments. Finally, we demonstrated that the Asymmetric Cluster Support cost can detect coevolutionary dynamics in swine influenza A virus, identifying novel gene pairings indicative of major viral reassortment events. Overall, our approach demonstrates that normalized asymmetric phylogenetic costs accurately capture complex biological relationships and provide a robust framework for quantifying fine-scale coevolutionary dynamics in rapidly evolving pathogens.

bioinformatics↗

bioRxiv2026

Assessing the impact of host density on vector abundance and transmission scaling of Culicoides-transmitted pathogens

The spread of any pathogen depends on the dynamics of its hosts, with transmission rates typically assumed to either scale linearly with host population density (density-dependent transmission) or to be independent of it (frequency-dependent transmission). For vector-transmitted pathogens, a key determinant of transmission scaling is whether vector abundance is constant or sensitive to host abundance, with the latter being consistent with density-dependent transmission. Here, we assess whether Culicoides vector abundance increases in a manner that indicates density-dependent transmission of Culicoides-transmitted pathogens. To test this, we conducted trapping of Culicoides midges on eight livestock operations across a wide range of cattle abundances, placing traps at varying distances from the host aggregation. We used hierarchical Bayesian models to estimate the effect of host abundance on the vector-to-host ratio while accounting for differences in trapping efficacy between locations. Our results indicate a positive linear effect of host abundance on the ratio of vectors to hosts, with a posterior probability of 0.83. Median posterior values of the effect of host abundance on vector density predict a 2.3% increase (95% credible interval: -0.8, 23.2%) in the vector-to-host ratio with every 1,000 additional hosts. The weight of evidence from our study suggests that Culicoides-transmitted pathogens are likely subject to density-dependent transmission, and that transmission may be amplified in high-concentration livestock environments.

ecology↗

bioRxiv2025

Variation in Natural Infection Outcomes and Cancer Cell Release from Soft-Shell Clams (Mya arenaria) with Bivalve Transmissible Neoplasia

Bivalve transmissible neoplasias (BTNs) are leukemia-like cancers found in at least 10 bivalve species, in which the cancer cells themselves transfer from one individual to another, spreading as an unusual form of infectious disease. Before the infectious etiology was known, there were reports of lethality and outbreaks of cancer in the soft-shell clam (Mya arenaria) on the east coast of North America. Using sensitive and specific qPCR assays, we followed the progression of BTN in naturally-infected soft-shell clams from Maine, USA. We observed variable outcomes, with about half of clams (9/21) progressing to high levels of cancer and death, about half exhibiting long-term non-progression (11/21), and a single animal showing regression of cancer. We also observe a significant decrease in survival in animals that progress to >10% cancer in their hemolymph, while we see no effect on survival in clams with BTN that are long-term non-progressors. As most bivalves do not physically contact each other, and BTN cells can survive in seawater, it has been proposed that BTN is spread through release of cancer cells into the water. We used qPCR to detect BTN-specific DNA in environmental DNA (eDNA) in the tanks of animals throughout this experiment. We show that cancer cell release can be detected in tank water of most clams with >24% cancer in their hemolymph, but not below this level. Cancer cell release is variable and occurs in bursts, but above 24% detection in eDNA correlates with progression of cancer in the hemolymph. This study demonstrates both the lethality of BTN and the presence of a block to the progression of BTN in a large portion of clams in a population with enzootic disease. This also further supports the hypothesis that BTN cells transmit through seawater and provides insights into the mechanisms of the transmission dynamics.

cancer biology↗

bioRxiv2025

Larval development habitats of Culicoides midges in the western United States

Culicoides midges are vectors of bluetongue virus (BTV), an arbovirus affecting wild and domestic ruminants. Bluetongue distribution generally overlaps with vector range, so understanding the vectors ecology is necessary for predicting BTV risk. Culicoides require moist substrate for oviposition and development, and C. sonorensis, the primary vector in the western United States, is classically associated with livestock wastewater ponds. However, it is well-known that BTV can be found outside of managed livestock areas, with transmission also occurring in natural settings. To better classify development habitat for Culicoides, we conducted a broad biweekly survey of moist and wet habitats from June to September of 2022 in northern Colorado at ten sites, including large livestock operations, non-commercial domestic operations, and natural spaces. Samples were maintained in the insectary for 11 weeks and monitored for emergence of adult midges. Standing water substrates displayed higher presence and abundance of midges than running or transient habitats, though all microhabitats showed emergence. Additionally, livestock sites did not produce more midges than other site types, and in fact more midges were observed in natural spaces per sample and overall. Livestock spaces did, however, show significantly higher proportions of C. sonorensis midges, which are thought to be the most competent vectors of BTV in this region. These results suggest that development sites in natural areas may play an important role in maintaining vector populations in the western U.S. outside of previously implicated livestock operations, and that differences in larval habitat lead to differences in vector species composition.

ecology↗

bioRxiv2022

Modeling cellular co-infection and reassortment of bluetongue virus in Culicoides midges

When related segmented RNA viruses co-infect a single cell, viral reassortment can occur, potentially leading to new strains with pandemic potential. One virus capable of reassortment is bluetongue virus, which causes substantial health impacts in ruminants and is transmitted via Culicoides midges. Because midges can become co-infected by feeding on multiple different host species and remain infected for their entire life-span, there is high potential for reassortment to occur. Once a midge is co-infected, additional barriers must be crossed for a reassortant virus to emerge, such as cellular co-infection and dissemination of reassortant viruses to the salivary glands. We developed three mathematical models of within-midge bluetongue virus dynamics of increasing complexity, allowing us to explore the conditions leading to the emergence of reassortment viruses. In confronting the simplest model with published data, we estimate the average lifespan of a bluetongue virion in the midge midgut is about six hours, a key determinant of establishing a successful infection. Examination of the full model, which permits cellular co-infection and reassortment, shows that small differences in fitness of the two infecting strains may have a large impact on the frequency with which reassortant virions are observed. This is consistent with experimental co-infection studies with BTV strains with different relative fitnesses that did not produce reassortant progeny. Our models also highlight several gaps in existing data which would allow us to elucidate these dynamics in more detail, in particular the times it takes the virus to disseminate to different tissues, and measurements of viral load and reassortant frequency at different temperatures.

microbiology↗