Biology subjects

Johnson, N.

Publications and source records attributed to Johnson, N..

At least 19 recordsLinked to original sources

bioRxiv2026

Cohesin residence time gates 3D genome response to histone hyperacetylation

Cohesin-mediated loop extrusion and chromatin state-dependent compartmentalization are major drivers of three-dimensional (3D) genome organization. Although epigenomic perturbations are widely assumed to reshape chromatin architecture, the mechanisms that determine how changes in chromatin state are translated into structural reorganization remain poorly understood. Here, we identify cohesin residence time as a key regulator of the genomes architectural response to histone hyperacetylation induced by histone deacetylase inhibition (HDACi). Acute depletion of RAD21 or CTCF weakens chromatin loops but preserves HDACi-induced changes in compartmentalization, contact-scaling behavior, and loop density. In contrast, perturbation of cohesin loading or release produces opposing effects: NIPBL depletion sensitizes and amplifies architectural responses to HDACi, whereas WAPL loss renders the genome largely refractory to HDACi-induced remodeling, suppressing changes in compartments and loop density while stabilizing CTCF-anchored loops. These distinct architectural outcomes occur despite comparable levels of HDACi-induced histone hyperacetylation across genotypes, indicating that differential epigenomic input is not responsible for the observed effects. Together, our findings demonstrate that dynamic cohesin turnover, rather than cohesin chromatin association alone, governs whether epigenomic perturbations are converted into higher-order genome reorganization. These results establish cohesin residence time as a molecular gate linking chromatin state to 3D genome architecture and reveal a previously unrecognized principle underlying chromatin architecture plasticity.

genomics↗

bioRxiv2026

First Usutu virus detections in wild birds in Scotland, 2025

In summer 2025, several Eurasian Blackbird (Turdus merula) deaths were reported on the Isle of Arran in Scotland. Initial investigation included post-mortem examination, where no diagnosis was achieved. Following Orthoflavivirus and avian paramyxovirus testing, Usutu virus RNA was detected in two Blackbirds by reverse transcription-PCR. Phylogenetic analysis identified Usutu virus Africa 3.2 lineage which clustered closely with existing UK detections, indicating geographic expansion rather than a new incursion. Subsequent surveillance confirmed the presence of several potential mosquito vector species.

microbiology↗

bioRxiv2026

Functional assignment of Golgi-associated vesicle tethers to specific membrane recycling pathways

During maturation of a Golgi cisterna, multiple vesicular transport pathways recycle resident Golgi proteins. Recycling vesicles are captured by Golgi-associated tethers. To assign individual tethers to specific recycling pathways in Saccharomyces cerevisiae, we examined tether arrival and departure using kinetic mapping, and we examined tether function using an ectopic tether localization assay. Those approaches yielded mutually consistent results. Our analysis focused on two coiled coil golgin tethers and the multi-subunit tether GARP. At an intermediate stage of cisternal maturation, the golgin Sgm1 tethers proteins that follow an intra-Golgi recycling pathway dependent on COPI. At a late stage of cisternal maturation, GARP and the golgin Imh1 tether trans- Golgi network (TGN) proteins that follow an intra-Golgi recycling pathway dependent on the AP-1 and Ent5 clathrin adaptors. This involvement of GARP in intra-Golgi recycling had not previously been documented. Imh1 also tethers proteins that recycle from prevacuolar endosome compartments to the TGN. Our findings contribute to an integrated model of Golgi membrane traffic.

cell biology↗

bioRxiv2026

Rhomboid protease RHBDL2 is a calcium-activated suppressor of EGFR signalling in keratinocytes.

Signalling via the epidermal growth factor receptor (EGFR) is indispensable for morphogenesis and tissue homeostasis. It is activated by extracellular ligands, typically released from transmembrane precursors by proteolysis. Ligand shedding activity is provided by the conserved rhomboid intramembrane serine proteases in Drosophila, but by the unrelated ADAM family metalloproteases in mammals, leaving the functions of mammalian non-mitochondrial rhomboids underexplored. Using quantitative proteomics, we show that EGFR is the main endogenous substrate of the human rhomboid protease RHBDL2 in keratinocytes. By shedding the EGFR ectodomain, thus producing a decoy receptor, RHBDL2 suppresses EGFR signalling, limiting cell migration and invasion. Conspicuously, RHBDL2 activity is upregulated by elevated intracellular calcium concentration, a condition typical for keratinocyte differentiation. These effects are recapitulated in primary human keratinocytes, and human skin equivalents deficient in RHBDL2 display incomplete differentiation and are morphologically disordered compared to wild type cells. We propose that context-specific fine-tuning of EGFR signalling and sensitivity to cross-talk from other signalling pathways could be important and hitherto overlooked roles of rhomboid proteases in mammals.

cell biology↗

bioRxiv2026

Repeated and widespread introduction of a mosquito-borne virus, but wildlife impact remains localised in urban area

Mosquito-borne viruses are emerging in new regions with increasing regularity. Shifting climatic envelopes, especially in temperate regions, and altered enzootic cycles are changing likelihoods of persistence, meaning new approaches are required to predict and monitor establishment. Usutu virus (USUV) is a mosquito-borne viral zoonosis, which was first recorded in the United Kingdom in wild birds and mosquitoes in 2020. By developing a multidisciplinary approach, incorporating enhanced passive and active surveillance of wild birds, we discovered previously unrecorded introductions and identified USUV persistence and geographic expansion. By combining molecular and serological testing with citizen science derived datasets, we show an associated marked decline in a common, widespread, and highly susceptible host species (Eurasian Blackbird, Turdus merula). However, the clearest continuous signal of host population decline remains localised to a large urban area, despite the much wider virus distribution. This may be a consequence of an urban heat island effect and associated increase in length of the mosquito active season. Our results indicate that the establishment and impact of future mosquito-borne pathogens in temperate zones, anticipated under climate change, may first be most apparent in urban areas. Consequently, enhanced surveillance efforts in urban areas could provide an efficient mechanism for detecting novel pathogen emergence. The epidemiology of emerging vector-borne diseases, especially in temperate areas, depends on the interplay between climate, land-use and available hosts; therefore, considering each in isolation will not be sufficient to reliably inform surveillance or response planning.

ecology↗

bioRxiv2026

PRDX6 Modulates Immune Checkpoint Inhibitor Response by Antagonizing Ferroptosis Induced By HDAC Inhibitors

Therapeutic resistance limits the efficacy of histone deacetylase (HDAC) inhibitors and immune checkpoint therapies in cancer. While HDAC inhibitors can induce ferroptosis, tumor cells often evade this cell death via antioxidant defenses. Here we identify peroxiredoxin 6 (PRDX6) as a critical modulator of resistance to HDAC inhibitor largazole by suppressing ferroptosis through its phospholipase A2 activity and maintaining GPX4 expression. Using genome-wide CRISPR activation screening, biochemical assays, and syngeneic tumor models, we show that PRDX6 depletion enhances largazole-induced lipid peroxidation, ferroptotic stress, and reshapes the tumor microenvironment to promote T-cell infiltration and inflammatory cytokine release. Importantly, combining PRDX6 knockdown with HDAC inhibition potentiates anti-PD-L1 immunotherapy efficacy and prolongs survival in vivo. These findings reveal PRDX6 as a redox gatekeeper linking ferroptosis resistance to immune evasion and suggest that co-targeting PRDX6 and HDAC pathways may improve responses to cancer immunotherapy.

cancer biology↗

bioRxiv2026

Epidural Thin Film Implants of Polymerized Curcumin Downregulate Inflammatory Markers and Improve Functional Recovery After Spinal Cord Injury in Mice

Spinal cord injury (SCI) is a notoriously intractable medical problem for which there is no neuroprotective pharmacotherapy, despite four decades of clinical trials on systemically administered small molecules that target plausible injury mechanisms. The shared failure mode of those trials is delivery: oxidative and inflammatory injury evolves locally at the lesion site over days to weeks, a timescale that far exceeds the half-life of systemically administered drugs. Furthermore, systemically administered drugs often cannot be dosed at high enough levels to achieve efficacious concentrations locally at the lesion site, without off-target effects. In this study, we show the first example of a locally implantable drug depot that exerts long-lasting activity at the lesion site. We demonstrate in vivo efficacy of a poly(pro-drug) thin film deployed locally, to address delivery problem in SCI. The films are composed of a copolyester in which curcumin, a potent natural antioxidant, is incorporated as a backbone repeat unit alongside poly(ethylene glycol) sebacate segments. The soft, thin film ([~]100 {micro}m) is employed as an epidural implant that quenches reactive oxygen species on-contact and can sustain activity for over two months, which is orders of magnitude longer than free curcumin (half-life of [~]10 min in buffer). A single epidural P50 film, placed on the exposed dura immediately after a moderate-to-severe T9 contusion in mice, produced a statistically significant improvement in Basso Mouse Scale locomotor recovery at 14 days post-injury, relative to a non-antioxidant control polymer of same architecture. The film preserved myelinated white matter, attenuated reactive gliosis (GFAP, Iba1), and produced coherent downregulation of neuroinflammatory gene-expression programs. These effects were spatially restricted to tissue rostral to the lesion, consistent with on-contact, locally confined polymer activity. Because curcumin is covalently enchained within the polymer itself, rather than blended as a payload in a carrier matrix, release is governed by backbone hydrolysis and the architecture can generalize to other phenolic bioactives, potentially establishing epidural poly(pro-drug) thin films as a mechanistically grounded, surgical platform for sustained local pharmacotherapy of CNS injury.

bioengineering↗

bioRxiv2025

A unified genetic perturbation language for human cellular programming

Evolution simultaneously and combinatorially explores complex genetic changes across perturbation classes, including gene knockouts, knockdowns, overexpression, and the creation of new genes from existing domains. Separate technologies are capable of genetic perturbations at scale in human cells, but these methods are largely mutually incompatible. Here we present CRISPR-All, a unified genetic perturbation language for programming of any major type of genetic perturbation simultaneously, in any combination, at genome scale, in primary human cells. This is enabled by a standardized molecular architecture for each major perturbation class, development of a functional syntax for combining arbitrary numbers of elements across classes, and linkage to unique single cell compatible barcodes. To facilitate use, CRISPR-All converts high level descriptions of desired complex genetic changes into a single DNA sequence that can rewire genomic programs within a cell. Using the CRISPR-All language allowed for head-to-head functional comparisons across perturbation types in a comprehensive analysis of all previously identified genetic enhancements of human CAR-T cells. Combining CRISPR-All programs with single cell RNA sequencing revealed a greater diversity of phenotypic states, including improved functional performance, only accessible through distinct perturbation classes. Finally, CRISPR-All combinatorial genome scale screening of up to four distinct perturbations simultaneously revealed additive functional improvements in human T cells accessible only through iterative multiplexing of modifications across perturbation classes. CRISPR-All enables exploration of a combinatorial genetic perturbation space, which may be impactful for biological and clinical applications.

genetics↗

bioRxiv2025

COPI-dependent intra-Golgi recycling at an intermediate stageof cisternal maturation

The traffic pathways that recycle resident Golgi proteins during cisternal maturation are not completely defined. We addressed this challenge using the yeast Saccharomyces cerevisiae, in which maturation of individual cisternae can be visualized directly. A new assay captures a specific population of Golgi-derived vesicles at the bud neck, thereby revealing which resident Golgi proteins are carried as cargo in those vesicles. This method supplies evidence for at least three classes of intra-Golgi vesicles with different cargo compositions. Consistent with our previously published data, one class of vesicles mediates a late pathway of intra-Golgi recycling with the aid of the AP-1 and Ent5 clathrin adaptors, and a second class of vesicles mediates an early pathway of intra-Golgi recycling with the aid of the COPI vesicle coat. Here, we identify another COPI-dependent pathway of intra-Golgi recycling and show that it operates kinetically between the two previously known pathways. Thus, intra-Golgi recycling is mediated by multiple COPI-dependent pathways followed by a clathrin-dependent pathway.

cell biology↗

bioRxiv2025

Detection of West Nile Virus via Retrospective Mosquito Arbovirus Surveillance in the United Kingdom

In March 2025, as part of on-going enhanced surveillance for mosquito-borne Orthoflaviviruses, West Nile virus (WNV) RNA was detected in two pools of female Aedes vexans collected in July 2023 in Nottinghamshire, England. Viral RNA detection was achieved via reverse transcription-qPCR. Sequencing and subsequent phylogenetic analysis of a 402 bp fragment indicated that the detections clustered with WNV lineage 1a. The exact origin of this virus remains unclear, but this finding indicates a historic WNV presence in the United Kingdom (UK). Surveillance has not provided evidence of further viral transmission to date.

molecular biology↗

bioRxiv2025

Impact of temperature on vector competence of Culex pipiens molestus: implications for Usutu virus transmission in temperate regions

IntroductionUsutu virus (USUV) has been detected annually in the southeast of England since 2020. USUV RNA has been identified in wild birds and mosquito populations, and exposure of captive birds to USUV at Zoological Society of London (ZSL) has also been confirmed. Since its first detection in London, USUVs distribution has expanded across the South East, highlighting a need to understand the transmission dynamics of this virus in the UK. The primary vectors of USUV in the UK are likely Culex pipiens mosquitoes. Two biotypes have been identified, the bird-feeding Cx. pipiens pipiens and Cx. pipiens molestus which shows no restriction in host preference. The latter may play an important role in transmitting USUV from birds to humans. MethodsA laboratory colony of Cx. pipiens molestus mosquitoes were orally infected with the London strain of USUV and, incubated at 22 {degrees}C, 20 {degrees}C and 18{degrees} C for up to 28 days. Body samples and mosquito saliva samples were collected and analysed using a quantitative real-time reverse transcription PCR to determine infection and transmission potential, respectively. ResultsUSUV RNA was detected in all sample times at all temperatures assessed; with the highest temperature (22 {degrees}C) showing the greatest proportion of saliva and body positive samples. At this temperature, there was also an eight-fold increase in the relative viral copy number in the mosquito bodies, which was unobserved at other experimental temperatures. When a more sensitive PCR assay was used at the lowest experimental temperature used (18 {degrees}C) USUV RNA was present in the mosquito saliva and body samples for longer and showed a greater proportion of positive samples when compared to 20 {degrees}C. ConclusionThis study has demonstrated that Cx. pipiens molestus may be able to transmit USUV at 22 {degrees}C. Active replication of USUV was identified in the mosquito bodies at 22 {degrees}C but could not be demonstrated at lower temperatures, suggesting that 20 {degrees}C to 22 {degrees}C may be an important temperature threshold in USUV replication and transmission. Utilisation of a more sensitive assay for the lower experimental temperatures revealed that USUV was detectable at 18 {degrees}C. Therefore, when conducting infection studies on temperate mosquito-borne viruses, it is important to consider assay sensitivity.

molecular biology↗

bioRxiv2025

Single-Cell Epigenomics Uncovers Heterochromatin Instability and Transcription Factor Dysfunction during Mouse Brain Aging

The mechanisms regulating transcriptional changes in brain aging remain poorly understood. Here, we use single-cell epigenomics to profile chromatin accessibility and gene expression across eight brain regions in the mouse brain at 2, 9, and 18 months of age. In addition to a significant decline in progenitor cell populations involved in neurogenesis and myelination, we observed widespread and concordant changes of transcription and chromatin accessibility during aging in glial and neuronal cell types. These alterations are accompanied by dysregulation of master transcription factors and a shift toward stress-responsive programs driven by AP-1, indicating a progressive loss of cell identity with aging. We also identify region- and cell-type-specific heterochromatin decay, characterized by increased accessibility at H3K9me3-marked domains, activation of transposable elements, and upregulation of long non-coding RNAs, particularly in glutamatergic neurons. Together, these results reveal age-related disruption of heterochromatin maintenance and transcriptional programs, identify vulnerable brain regions and cell types, and pinpoint key molecular pathways altered in brain aging. HighlightsO_LISingle-cell multimodal profiling across eight brain regions reveals coordinated chromatin and transcriptional shifts during aging C_LIO_LIAge-related depletion of progenitor cells coincides with dysregulation of key developmental transcription factors C_LIO_LICell identity maintenance is compromised with the decline of master transcription factors C_LIO_LIHeterochromatin destabilization accompanied by activation of AP-1, transposable elements, pseudogene families, and long non-coding RNAs C_LI

genomics↗

bioRxiv2025

Cell-type-specific transposable element demethylation and TAD remodeling in the aging mouse brain

Aging is a major risk factor for neurodegenerative diseases, yet underlying epigenetic mechanisms remain unclear. Here, we generated a comprehensive single-nucleus cell atlas of brain aging across multiple brain regions, comprising 132,551 single-cell methylomes and 72,666 joint chromatin conformation-methylome nuclei. Integration with companion transcriptomic and chromatin accessibility data yielded a cross-modality taxonomy of 36 major cell types. We observed that age-related methylation changes were more pronounced in non-neuronal cells. Transposable element methylation alone distinguished age groups, showing cell-type-specific genome-wide demethylation. Chromatin conformation analysis demonstrated age-related increases in TAD boundary strength with enhanced accessibility at CTCF binding sites. Spatial transcriptomics across 895,296 cells revealed regional heterogeneity during aging within identical cell types. Finally, we developed novel deep-learning models that accurately predict age-related gene expression changes using multi-modal epigenetic features, providing mechanistic insights into gene regulation. This dataset advances our understanding of brain aging and offers potential translational applications. HighlightsO_LISingle-cell multi-omic profiling maps the epigenetic and spatial transcriptomic landscape of brain aging across multiple regions. C_LIO_LICell-type-specific genome-wide demethylation of retrotransposable elements correlates with increased chromatin accessibility and expression. C_LIO_LIElevated TAD boundary strength emerges as a unique marker of brain aging associated with CTCF gaining accessibility. C_LIO_LIA novel deep-learning model reveals the significance of epigenetic features on age-related transcriptomic changes across genes. C_LI

genomics↗

bioRxiv2025

Predicting West Nile Virus risk across Europe for the current and future conditions

Vector-borne diseases have significant impacts on animal and human health globally, and these impacts are likely to increase in the future due to environmental and climate change. Understanding where to target surveillance and control measures to mitigate the impacts of emerging vector-borne diseases can be challenging when pathogens or disease is absent. In this study, we utilise a species distribution modelling approach previously applied to the UK to predict areas at higher risk of mosquito-borne disease across Europe, using West Nile Virus (WNV) as a case study. WNV is an Orthoflavivirus that is naturally transmitted between Culex mosquitoes and a range of avian species. However, it can spread to hosts such as humans and horses where it has the potential to lead to severe illness and mortality. Suitability predictions for Culex (Cx. pipiens and Cx. modestus) and avian hosts (mainly Passerine species) are made across Europe to determine potential risk of WNV circulation and establishment. These maps are then combined with information on human and horse density to determine risk to human and equine health. The resulting risk maps reveal that across Europe, there are areas of higher and lower risk that are predominantly driven by vector suitability as avian hosts are widespread. These predictions are projected into the future in 2100 using best- and worst-case Shared Socioeconomic Pathways (SSP1 and SSP5 respectively) to determine how risk may change over time, revealing that some areas see an increase in suitability for both vectors and hosts leading to higher risk (e.g., central England and northern Belgium) whilst other areas see a decline in suitability and consequently lower WNV risk (e.g., northern Italy and western Germany). Overall, this work will improve understanding of mosquito-borne disease risk in changing environments and demonstrates how species distribution modelling can be used to aid contingency preparedness by highlighting areas at higher risk of emerging disease.

pathology↗

bioRxiv2024

APC coordinates GSK3 phosphorylation of SETD8 to suppress colorectal cancer

Colorectal cancer (CRC) is the second-leading cause of cancer-related deaths with increasing incidence globally. Mutations in the tumor suppressor APC initiate CRC at least in part by preventing the GSK3 kinase from phosphorylating {beta}-CATENIN, leading to its constitutive stabilization and transactivation of mitogenic target genes. While the importance of {beta}-CATENIN phosphorylation by GSK3 is well-established, APC regulation of GSK3 activity upon other targets with potential oncogenic relevance are not understood. Here, we identify the H4K20 methyltransferase SETD8 as target of APC-coordinated GSK3 phosphorylation in the intestinal epithelium. We found that phosphorylation by GSK3 restrains the oncogenic activity of SETD8, with loss of phosphorylation sensitizing mice to oncogenic insults. Mechanistically, phosphorylation alters the role of SETD8 in transcriptional regulation, most notably by preventing it from activating oncogenic YAP signaling and a fetal-like transcriptional program. These results underscore the importance of SETD8 in CRC and represent a novel {beta}-CATENIN -independent oncogenic consequence of APC loss. SignificanceGSK3 is thought to restrain colorectal cancer primarily by phosphorylation of {beta}-CATENIN. We show that GSK3 also phosphorylates SETD8, preventing SETD8 activation of oncogenic programs including YAP-driven fetal-like gene expression.

cancer biology↗

bioRxiv2024

Using correlative and mechanistic species distribution models to predict vector-borne disease risk for the current and future environmental and climatic change: a case study of West Nile Virus in the UK.

Globally, vector-borne diseases have significant impacts on both animal and human health, and these are predicted to increase with the effects of climate change. Understanding the drivers of such diseases can help inform surveillance and control measures to minimise risks both now and in the future. In this study, we illustrate a generalised approach for assessing disease risk combining species distribution models of vector and wildlife hosts with data on livestock and human populations using the potential emergence of West Nile Virus (WNV) in the UK as a case study. Currently absent in the UK, WNV is an orthoflavivirus with a natural transmission cycle between Culex mosquitos (Cx. pipiens and Cx. modestus) and birds. It can spread into non-target hosts (e.g., equids, humans) via mosquito bites where it can cause febrile disease with encephalitis and mortality in severe cases. We compared six correlative species distribution models and selected the most appropriate for each vector based on a selection of performance measures and compared this to mechanistic species distribution models and known distributions. We then combined these with correlative species distribution models of representative avian hosts, equines, and human population data to predict risk of WNV occurrence. Our findings highlighted areas at greater risk of WNV due to higher habitat suitability for both avian hosts and vectors, and considered how this risk could change by 2100 under a best-case Shared Socioeconomic Pathway (SSP1) and worst-case (SSP5) future climate scenario. Generally, WNV risk in the future was found to increase in south-eastern UK and decrease further north. Overall, this paper presents how current and future vector distributions can be modelled and combined with projected host distributions to predict areas at greater risk of novel diseases. This is important for policy decision making and contingency preparedness to enable adaptation to changing environments and the resulting shifts in vector-borne diseases that are predicted to occur.

ecology↗

bioRxiv2024

Genetic Manipulation of Caveolin-1 in the Mouse Model of Marfan Syndrome Associated Aortic Root Aneurysm: Effects on Endothelial and Smooth Muscle Function

Marfan Syndrome (MFS) is a systemic connective tissue disorder caused by mutations in the gene encoding for the large glycoprotein Fibrillin-1 (Fbn1), leading to wide-spectrum clinical manifestations, with the most life-threatening being aortic root aneurysm. MFS aortic aneurysm is known to be associated with reduced endothelial nitric oxide synthase (eNOS)-mediated nitric oxide (NO) production. Previous studies have shown that caveolin-1 (Cav1), a coat protein of caveolae structure on the plasma membrane, acts as a negative regulator of eNOS activity. This suggests that Cav1 may play a role in the development of aortic root aneurysm in MFS by modulating eNOS activity. In this study, we investigated the role of Cav1 in regulating aortic smooth muscle and endothelial function, aortic wall elasticity, and wall strength by generating MFS mice (FBN1+/Cys1041Gly) lacking Cav1 gene expression (MFS/Cav1KO). Our data show that ablation of the Cav1 gene results in a significant decrease in aortic smooth muscle contraction in response to the vasoconstricting agent phenylephrine seemingly due to a marked increase in NO production within the aortic wall. We also showed that acetylcholine-induced vasorelaxation was increased in MFS/Cav1KO mice potentially through the endothelial nitric oxide-dependent mechanism, further confirming inhibitory role of Cav1 on endothelial NO production. In addition, aortic wall elastin fiber structure and strength were markedly improved in male MFS/Cav1KO mice. This study demonstrates the regulatory role of Cav1 during the development of aortic root aneurysm in MFS mice through its effects on smooth muscle and endothelial functions in an NO-dependent manner.

physiology↗

bioRxiv2024

UK mosquitoes are competent to transmit Usutu virus at native temperatures

Usutu virus (USUV) is an emerging zoonotic virus transmitted primarily by Culex mosquitoes. Since its introduction into Europe from Africa during the late 20th century, it has caused mortality within populations of passerine birds and captive owls, and can on occasion lead to disease in humans. USUV was first detected in the UK in 2020 and has become endemic, having been detected in either birds and/or mosquitoes every subsequent year. Importantly, the vector competence of indigenous mosquitoes for the circulating UK (London) USUV strain at representative regional temperatures is still to be elucidated. This study assessed the vector competence of five field-caught mosquito species/biotypes, Culex pipiens biotype molestus, Culex pipiens biotype pipiens, Culex torrentium, Culiseta annulata and Aedes detritus for the London USUV strain, with infection rates (IR) and transmission rates (TR) evaluated between 7 to 28 days post-infection. Infection and transmission were observed in all species/biotypes aside from Ae. detritus and Cx. torrentium. For Cx. pipiens biotype molestus, transmission potential suggests these populations should be monitored further for their role in transmission to humans. Furthermore, both Cx. pipiens biotype pipiens and Cs. annulata were shown to be competent vectors at 19{degrees}C indicating the potential for geographical spread of the virus to other UK regions.

ecology↗