Available studentships

All scholarships come with UKRI stipend (currently £20,780 per annnum), UK fees and research costs for 4 years. A small number of international fee waivers will be available. 

In order to be eligible to apply for the necessary security clearance, applicants for projects with Dstl must be a UK national, currently resident in the UK, and have resided in the UK continuously for the past five year. Applicants for projects including laboratory work at APHA, UKHSA or Pirbright Institute must be currently resident in the UK and have at least three years continuous UK residency. All residency requirements must be fulfilled by 23 January 2026 to be eligible. 

Counter Terrorist Check (CTC) clearance is required prior to commencing work at all the above laboratories. Candidates need to ensure that they are eligible for security clearance. It is up to each person applying for a studentship to ensure they meet the residency criteria. Please contact the supervisors of your chosen project if you have any questions. 

You will have the ambition, motivation and scientific curiosity to research new approaches to combatting infectious diseases in the themes of:

• Detection, prevention and intervention
• Microbial evolution and drug resistance
• Understanding disease spread
• Infection and cellular biology. 

You will have or expect to have an MSc, and/or a first or upper second honours degree in a relevant subject. We welcome applications from graduates of all universities, and from candidates already in work, or returning after a career break.

Note: Lab experience is desirable but not essential as all successful applicants will be trained in basic lab skills where applicable.

Find out more about postgraduate research:

1. What to expect from a PhD in Biosciences
2. Life after a PhD

Equity, diversity and inclusion

All partners in Wessex One Health are committed to EDI and want to ensure that researchers from a diverse population are attracted into our programme. We welcome and will provide support for applicants from underrepresented groups, to help build a research community that reflects our society. 

Please apply by submitting an application form and completing our EDI survey. 

Prospective students are asked to select and rank four projects from those available below and if invited for interview they must  contact prospective supervisors ahead of interview.

• Submission deadline: Midnight Friday 23 January 2026
• Shortlisting: by 13 February 2026
• Online interviews: Online, week beginning 3 March 2026

For further information on the programme or application process, email WOH@surrey.ac.uk. 

For further information on individual projects, email supervisors, their email addresses can be found in the projects listed below. 

Apply now

Application form   EDI survey 

For more information view: Q&As from the Wessex One Health Doctoral Programme Webinar (PDF).

Theme(s): Understanding disease spread, detection, prevention and intervention

Lead partner: University of Exeter 
Supervisor: 

• EIvana Gudelj: i.gudelj@exeter.ac.uk  
• Adilia Warris: a.warris@exeter.ac.uk 

Joint partner: DSTL 
Supervisor: Richard Thomas, Rjthomas@mail.dstl.gov.uk 

Project Summary

Aspergillus fumigatus is an environmentally ubiquitous mould found in soil, water, organic debris and decaying vegetation. While harmless to most, it is a leading cause of life-threatening infections in vulnerable patients. The World Health Organisation has listed A. fumigatus as the 4th highest priority fungal pathogen, reflecting its critical importance for global health. Invasive aspergillosis is associated with mortality rates of up to 50% in immunocompromised individuals, with hundreds of thousands of severe cases reported worldwide each year.

To design effective preventative measures, we need to understand precisely where and how infections are acquired. A crucial step in this process is determining how fungal spores leave natural and man-made surfaces to become airborne, a process known as particle resuspension.

Recent advances in resuspension modelling by our project partners at the Defence Science and Technology Laboratory (DSTL) provide powerful tools to predict how hazardous particles enter the atmosphere. However, these models remain difficult to parameterise under realistic environmental conditions.

This PhD project will exploit the Global Meteorological Simulator, a new state-of-the-art facility at the University of Exeter that can replicate complex weather patterns under controlled laboratory settings. By combining this unique experimental platform with advanced microbiology, high-speed imaging and innovative data interpretation, the project will quantify resuspension rates of A. fumigatus spores across diverse environmental factors (e.g. wind, rainfall) and terrains (vegetation, water, concrete).

The outcomes will provide, for the first time, a mechanistic understanding of how Aspergillus spores disperse in the environment, enabling improvement of predictive models and inform strategies to reduce human exposure. This multidisciplinary studentship offers the opportunity to work at the intersection of medical mycology, environmental microbiology, aerosol science and cutting-edge simulation, contributing directly to tackling one of the world’s most urgent fungal threats.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

Application form   EDI survey 

Theme(s): Microbial Evolution and Drug Resistance; Understanding Disease Spread; Infection and Cellular Biology; Detection, Prevention and Intervention.

Lead partner: University of Exeter 
Supervisor: Orly Razgour, O.Razgour@exeter.ac.uk

Joint partner: The Pirbright Institute 
Supervisor: 

• Duncan Wilson: Duncan.Wilson@exeter.ac.uk
• Saeed Farjami: Saeed.Farjami@pirbright.ac.uk
• Simon Gubbins: simon.gubbins@pirbright.ac.uk

Project Summary

Fungal infections are now responsible for 2.5 million deaths annually (PMID: 38224705). Certain fungi, such as Histoplasma, cause disease in specific geographic regions—these are known as the “endemic mycoses.” Due to their often-non-specific clinical presentations, accurate diagnosis and effective treatment rely heavily on understanding both the current and potential geographic distribution of these pathogens.

We have developed a novel ecosystem–vector transmission model in which Histoplasma cycles between acidic soil environments and bat hosts. While bats are recognised reservoirs of Histoplasma, the specific African bat species that harbour the fungus remain unidentified.

This PhD will collect and analyse microbial DNA from a diverse range of South African bat species to address the following objectives:

(i) Identify key hosts of Histoplasma and the environmental conditions associated with high pathogen load.

(ii) Characterise the gut mycobiome and microbiome and the interactions with pathogen load.

(iii) Model changes to the distribution of key Histoplasma hosts and risk of disease spread.

This project will integrate Histoplasma-specific qPCR and metabarcoding to detect both the target fungus and the broader fungal and bacterial community within each host with ecological niche modelling to map current distributions and project shifts under future climate scenarios. This will enable us to identify both present and emerging regions at risk for Histoplasma infection. 

The University of Exeter and Pirbright Institute offer unparalleled environments for this research, bringing together world-leading expertise in medical mycology, ecological modelling and epidemiology. The Doctoral Researcher will receive interdisciplinary training in molecular biology, microbiology, ecology, epidemiology and modelling.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

Application form   EDI survey 

Theme(s): Infection and cellular biology

Lead partner: University of Exeter 
Supervisor: Professor Adilia Warris, a.warris@exeter.ac.uk

Joint partner: UKHSA 
Supervisor: Professor Andy Borman, andy.borman@nbt.nhs.uk

Project Summary

Dermatophytosis (known as tinea or ringworm) is one of the most common fungal infections affecting 20-25% of the global population and also affect pet and farm animals. The rising incidence of treatment-resistant dermatophytosis, e.g. terbinafine-resistant Trichophyton indotinea, represent an increasing clinical challenge and urges a more comprehensive understanding of the disease and the antifungal host mechanisms in the skin.

A large genetic epidemiological study recently conducted by our collaborators at McGill University has revealed several new genetic risk factors for dermatophytosis. Increased expression of SLURP1 showed to be associated with a lower risk of dermatophytosis.

The physiological function of SLURP1 in the skin is to regulate keratinocytes proliferation and apoptosis through the cholinergic pathways. The role of SLURP1 in keratinocyte biology is supported by a rare, autosomal recessive skin disorder that is caused by mutations in SLURP1, named Mal de Meleda, also known as keratosis palmoplantaris. The disease is characterised by hyperkeratosis of the hands and feet. Importantly, Mal de Meleda patients suffer from recurrent fungal skin infections, suggesting a role of SLURP1 in dermatophytosis.

Immune mechanisms against dermatophytes remain incompletely understood. However, there is evidence suggesting that mast cells are involved in antifungal immune defences. SLURP1 contributes to mast cell activation under skin stress conditions. We therefore hypothesise that the association of SLURP1 expression with protection from dermatophytosis may be explained by a mast cell-dependent mechanism.

This project will (1) determine the role of SLURP1 in the keratinocyte response to dermatophytes; (2) examine how SLURP1 modulates the mast cell response to dermatophytes; and (3) investigate the impact of SLURP1 on the susceptibility to dermatophytosis in intact skin.

We will use a bespoke set of cell culture approaches to study the interaction between keratinocytes, mast cells, human skin explants and dermatophytes and employing CRISPR-Cas9 to create SLURP1 knock-out cells. 

Apply now

Please apply by submitting an application form and completing our EDI survey. 

Application form   EDI survey 

Theme(s): Microbial Evolution and Drug Resistance

Lead partner: University of Exeter 
Supervisor: Jane Usher, j.usher@exeter.ac.uk 

Joint partner: UKHSA 
Joint partner supervisor: Andy Borman, andy.borman@nbt.nhs.uk 

Project Summary

Antimicrobial resistance (AMR) is a growing global health challenge, yet the role of environmental reservoirs in sustaining and spreading resistance remains underexplored. Microplastics, now ubiquitous across terrestrial and marine ecosystems, represent a unique potential vector: they provide surfaces for microbial colonisation, facilitate gene exchange, and travel across ecological boundaries. Early evidence, including our preliminary data, suggests that microplastics may act as reservoirs and drivers of AMR.

This project will investigate the potential of microplastics to harbour and promote AMR, with a particular focus on extreme environments. Notably, we have obtained two Antarctic isolates attached to microplastic particles, already adapted to the ocean’s cold, pH, and salinity. These samples offer a rare opportunity to study microbial adaptation under harsh conditions, while providing insights into how resistant organisms may persist and spread even in remote ecosystems.

Our approach will combine environmental microbiology, genomics, and comparative analyses. Using isolates from both environmental samples and the extensive collections held by our partners (including rare and historical strains within the National Collection of Pathogenic Fungi), we will characterise microbial communities, identify resistance determinants, and examine conditions that favour the persistence and transfer of AMR on microplastic surfaces.

By partnering with public health agencies (UKHSA) and leveraging their expertise in pathogen surveillance and AMR research, we will ensure that findings are relevant to both environmental and clinical contexts.

The outcomes of this project could transform our understanding of microplastics not only as pollutants, but also as hidden reservoirs of AMR with implications for ecosystems, food chains, and human health. This work will inform risk assessments, support policy development on plastic waste and AMR, and help safeguard both environmental and public health.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

Application form   EDI survey 

Lead partner: University of Exeter 
Supervisor: William Horsnell, w.horsnell@exeter.ac.uk

Joint partner: UKHSA 
Joint partner supervisor: Javier Salguero, Javier.salguero@ukhsa.gov.uk

Project Summary

Fibrotic hypersensitivity pneumonitis (FHP) is a devastating and debilitating lung disease. Median survival from diagnosis is only 5 years, like many deadly cancers. FHP causes significant morbidity and mortality, with inexorable deterioration in breathlessness, cough and quality of life, with patients becoming housebound and dependent on oxygen. FHP is the most common subtype within the group of lung conditions termed “progressive pulmonary fibrosis” (PPF), accounting for a third of PPF cases in the UK. Fungal pathogens have been associated with causing FHP. We hypothesise that exposure to common fungal pathogens such Aspergillus fumigatus (Af) influence the severity and progression of FHP. 

In this project samples collected as part of the trial to assess the effectiveness and cost-effectiveness of oral Corticosteroids in patients with fibrotic hypersensitivity pneumonitis (CHORUS) will be used. The study is aiming to recruit >200 participants. Samples collected will include blood and bronchial lavage (BAL) with associated clinical readouts of lung function.

Using these samples the project student will assess how FHP alters the cellular immunity in the BAL of FHP patients. This will be achieved through restimulation of live cells from BAL with mitogens and relevant antigens. The phenotypes of these cells will then be established using flow cytometry. From this the student will aim to identify immune signatures associated with FHP. This will be informative for understanding how manipulation of FHP immunity may help to treat this disease. The student will then establish the extent that FHP patients demonstrate antigen specific immunity to Af and how this associates with risk of disease severity.

The project will address in detail for the first time how a common environmental cause of chronic lung disease influences risk FHP and what the associated immune signatures of this disease are.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

Application form   EDI survey 

Theme(s): Detection, Prevention and Intervention; Infection and Cellular Biology

Lead partner: University of Exeter 
Supervisor: Neil Gow, n.gow@exeter.ac.uk

Joint partner: UKHSA 
Supervisor: Andrew Borman, andy.borman@nbt.nhs.uk

Project Summary:

Trichophyton mentagrophytes ITS type VIIIe (called T. indotinea) is an emerging fungal pathogen that is rapidly spreading across the world. First reported in 2018 in the UK, it now accounts for nearly 40% of dermatophyte isolates sent to the UKHSA Mycology Reference Laboratory. This epidemic is especially concerning because all strains are resistant to terbinafine, the first-choice antifungal to treat dermatophytosis. Dermatophytes, including Trichophyton species, cause infections of keratinized tissues, including the skin, hair or nails, but we know very little about what makes T. indotineae such a successful pathogen.

This project will therefore characterize the immune response to, and fungal virulence of, T. indotineae, in comparison to other prevalent pathogenic Trichophyton spp. 

The student will use Trichophyton type strains and recent clinical isolates from the UKHSA Mycology Reference Laboratory, to characterise the host immune response, including assays to determine cytokine production, phagocytosis and killing, neutrophil ROS production and NETosis, T-cell differentiation, epithelial invasion & cell viability and immune-profiling using soluble immune receptor probes (PRR-Fc). 

On the pathogen side, we will generate a spatial model of the Trichophyton cell wall using a combination of cryo-TEM, solid-state NMR, immunofluorescence antibody and PRR-Fc mapping and cell wall composition analysis. In addition, we will assess morphological and growth characteristics of Trichophyton spp. using growth assays including a range of simulating media, stress inducing conditions and antifungal drugs. 

The student will also use an ex-vivo human skin model to look at fungal growth and morphology, tissue invasion, immune markers and omics approaches to study host-pathogen interactions. Reverse genetics approaches will be developed to test emerging hypotheses and the origin of clinical resistance to terbinafine. Together, the student will gain experience in a range of immunological, microbiological and microscopical techniques and contribute significantly to our much-needed understanding of the pathobiology of T. indotineae.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

Application form   EDI survey 

Theme(s): Infection and Cellular biology.

Lead partner: University of Surrey 
Supervisor: Rachel Simmonds, rachel.simmonds@surrey.ac.uk

Joint partner: APHA 
Supervisor: Javier Salguero-Bodes, javier.salguero@ukhsa.gov.uk

Project Summary

Skin is a high complex organ, which is an essential and effective barrier to infection. Yet some pathogens are able to overcome these protections and infect skin. Spatial relationships can be visualised experimentally using tissue sections and specific stains. In the past, our understanding of the interaction between pathogens and different cells within skin was undertaken on a case-by-case basis. However, recent advances in technology mean that it is now possible to observe the behaviour of many markers at once. These exciting approaches are extremely powerful tools to understand host-pathogen interactions. 

Prof Simmonds’ group (University of Surrey) works on Buruli ulcer, a chronic skin infection caused by a bacteria in the same family as TB and Leprosy. The disease is important in West Africa and Australia, and is of great interest because of the lack of typical signs of infection such as pain and inflammation and is hard to treat even in high-resource settings. Our research has shown that the interaction between the bacteria and macrophages may be important in controlling changes in the skin that determine whether an infection results in clinical disease. 

In this project, and in collaboration with Prof Javier Salguero-Bodes (UKHSA) you will use cutting edge multi-analyte phenotyping to investigate the interaction between Mycobacterium ulcerans and different cells in the skin experimentally infected animals. To investigate the mechanisms involved, you will use genetically engineered animals, and/or animals treated with drugs that change immune cell function and analyse changes in these spatial relationships. 

You will receive excellent training in cellular and molecular biology, as well as experimental models of infection, including work in high containment. You will be part of a worldwide effort to understand this neglected disease, and the research is expected to help us design better treatments to shorten healing times in Buruli ulcer patients. 

Apply now

Please apply by submitting an application form and completing our EDI survey. 

Application form   EDI survey 

Theme(s): Detection, Prevention and Intervention

Lead partner: University of Surrey 
Supervisor: Dr Jorge Gutierrez-Merino, j.gutierrez@surrey.ac.uk

Joint partner: APHA 
Supervisor: 

Project Summary

Honeybee hives may hold the key to tracking infectious diseases in our environment. This project investigates how the unique microbial communities within honey and beebread can act as early warning indicators for pathogens affecting plants, animals, and humans across the UK. 

As honeybees forage for nectar and pollen, they also collect microbes from plants, soil, water, and waste. Our recent research, published in Environmental Microbiome (2023) (https://doi.org/10.1186/s40793-023-00460-6), showed that each hive possesses a distinctive microbial fingerprint, containing genetic traces of bacteria linked to both plant and zoonotic diseases.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

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Theme(s): Detection, Prevention and Intervention; Infection and Cellular Biology

Lead partner: University of Surrey 
Supervisor: Dr Matthew Siggins, m.siggins@surrey.ac.uk 

Joint partner: APHA 
Supervisor: Dr Amin Asfor, amin.asfor@apha.gov.uk

Project Summary

Antimicrobial resistance is a major One Health and global challenge. As antibiotics lose effectiveness, bacterial infections in humans and animals are becoming harder to treat. Vaccines are a critical tool to reduce antibiotic use and control AMR, but for many priority pathogens they remain unavailable or inadequate. Building on our Nature Communications discovery that hyaluronan promotes bacterial transit to lymph nodes via the lymphatic system, this project advances VAXHA, a versatile live bacterial vaccine vector designed for low-cost manufacture and global use. By directing antigens to lymph nodes—where durable immune responses are generated—VAXHA is designed to produce stronger and longer-lasting antibody and T-cell protection than conventional approaches.

Working within advanced, specialist facilities across the University of Surrey and APHA, the student will progress through three phases: first, molecular engineering of the live bacterial vaccine platform to enhance performance and safety; second, immune profiling to determine how lymph-node targeting shapes the quality and durability of B- and T-cell responses, integrating quantitative ex vivo and in vivo readouts; and third, protection studies in vivo to test whether improved delivery translates into stronger, longer-lasting immunity. Methods will include fluorescence microscopy, flow cytometry, cell culture, and AI-driven analysis.

Full interdisciplinary training will be provided across microbiology, molecular biology, immunology, and data science. Students will have opportunities to present their work, collaborate across partners, and undertake diverse professional skills training. Ultimately, this project will uncover how lymph-node targeting orchestrates improved protective B- and T-cell immunity, and it will advance the VAXHA vaccine platform towards practical use across a range of One Health pathogens.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

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Theme(s): Detection, Prevention and Intervention, Understanding Disease Spread, Infection and Cellular Biology

Lead partner: University of Surrey 
Supervisor: Graham Stewart, g.stewart@surrey.ac.uk

Joint partner: APHA 
Supervisor: Daryan Kaveh, daryan.kaveh@apha.gov.uk

Project Summary

Mycobacterium bovis is the causative agent of bovine tuberculosis (bTB) and the predominant cause of zoonotic tuberculosis worldwide. In the UK and Ireland, control of bTB is complicated by a reservoir of infection in badgers. Transmission between badgers and cattle (and vice versa) is not well understood but may involve an environmental step between hosts. We hypothesise that interaction with environmental amoebae increases infectivity of M. bovis. In preliminary experiments to support this PhD project we showed that M. bovis actively escapes predation by the soil and dung-dwelling amoeba, Dictyostelium discoideum. It does this using the ESX-1 and ESX-5b type VII secretion systems as part of an extensive programme of mechanisms involving hundreds of genes.

In this project, the student will characterise how M. bovis changes its physiology during infection of Dictyostelium and establish if these changes pre-adapt the bacterium for mammalian infection, as is the case for other bacterial pathogens such as Legionella pneumophila, Vibrio cholerae and Salmonella enterica. Indeed, for Legionella the demonstration that passage through amoebae increased infectivity was critical to understanding the paradox that concentrations of Legionella below the experimentally determined infective dose were able to cause human infection. Thus, it is important that we understand the effect of amoeba passage on M. bovis physiology and how this affects infectivity. This fundamental biology could transform our understanding of bTB transmission and will help design measures to control environmental transmission of M. bovis in badgers and cattle. Specifically, the findings will guide validation of disinfection strategies for bTB breakdown farms with the potential to significantly impact persistence rates and infection of reintroduced cattle.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

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Theme(s): Understanding Disease Spread

Lead partner: University of Surrey 
Supervisor: Klara Wanelik, k.wanelik@surrey.ac.uk

Joint partner: DSTL 
Supervisor: Thomas Laws, trlaws@mail.dstl.gov.uk

Project Summary

Superspreaders are the minority of individuals responsible for the majority of disease spread and come in two forms. Supershedders spread more disease because they shed more pathogen. Supercontacters spread more disease because they have more social contacts. The presence of supershedders and/or supercontacters in a population is likely to be associated with distinctive patterns of disease spread which, if detected early, could be used to better design disease control strategies.

In this project, you will use a novel epidemiological modelling approach to simulate disease outbreaks in closed populations (representative of e.g. a military base or naval vessel) and to better understand the role of supershedders and/or supercontacters in driving patterns of disease spread. Your model will incorporate both within-host and between-host dynamics.

Project objectives: 

1. In a scenario where there are only supershedders, identify which physiological features of supershedders (e.g. infectious period, pathogen load) impact on patterns of disease spread and how.
2. In a scenario where there are only supercontacters, identify which behavioural features of supercontacters (e.g. contact frequency, contact duration, contact heterogeneity) impact on patterns of disease spread and how.
3. In a more realistic scenario where there are supershedders and supercontacters, identify which features of supershedders and supercontacters impact on patterns of disease spread and how.

You will use openly available datasets for a representative range of viral pathogens to parameterise and test your model. This will include Ebola and Lassa virus – two major pathogens of strategic importance that exhibit contrasting dynamics. 

This project is an exciting opportunity to contribute to preparedness for pathogen X, a pandemic pathogen that has not yet been characterised. It would suit those with an interest in infectious diseases, public health and/or epidemiological modelling. Experience in epidemiological modelling is desirable but not essential. The individual will work closely with Dstl.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

Application form   EDI survey 

Theme(s): Microbial Evolution and Drug Resistance; Understanding Disease Spread

Lead partner: University of Surrey 
Supervisor: Bingxin Lu, b.lu@surrey.ac.uk

Joint partner: Pirbright Institute 
Supervisor: Tim Downing, Tim.Downing@pirbright.ac.uk

Project Summary

Poxviruses pose a major threat to human and livestock health, such as mpox, which remains a continuing threat. Poxviruses evolve through a combination of mutation, recombination, and gene transfer. These processes permit the exchange of new DNA segments, which may encode proteins with novel functions in new viral hosts, resulting in new outbreaks and epidemic threats. Moreover, high rates of rearrangements and repetitiveness in poxvirus genomes obscure the adaptation and origins of different lineages. Existing tools to study these processes were developed for prokaryotic or eukaryotic organisms and certain virus types, but none have been optimised for poxviruses. Additionally, we are now in a much better position to understand poxvirus adaptation, thanks to recent advances in extensive short- and long-read genome sequencing of human and livestock poxviruses. This means new inferences are possible, if appropriate scientific methods are used.

This project will explore published diverse poxvirus genomes using better gene transfer and recombination analysis. It will leverage two novel approaches: pangenome graphs and artificial intelligence-informed phylogenetics. We will use unsupervised machine learning methods based on DNA similarity and related pangenome graph information to identify regions of interest in individual virus genomes. This will be designed to identify gene transfer and recombination in new, unknown samples. Identified gene transfer and recombination events will be verified using phylogenetic methods and compared to the results of existing tools to validate and improve the new approaches.

This project will train you in cutting-edge methods (machine learning, genomics/pangenomics, and viral genetics) that will shed new light on gene transfer, recombination, and genomic diversity in poxviruses. It will create improved genome analysis methods for poxviruses to pin-point genes driving outbreaks with pandemic potential. This project will lay a foundation on which to explore virus evolution, and to apply these machine-learning and pangenomic tools to other viruses.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

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Theme(s): Infection and Cellular Biology; Understanding Disease Spread

Lead partner: University of Surrey 
Supervisor: Paola Campagnolo, p.campagnolo@surrey.ac.uk

Joint partner: The Pirbright Institute 
Supervisor: Kevin Maringer, Kevin.Maringer@pirbright.ac.uk

Project Summary

Dengue is the most significant mosquito-borne viral disease globally, affecting over half the world’s population across tropical and subtropical countries while also emerging in Europe, due to climate change. Over 80% of people living with diabetes reside in dengue-endemic countries. In coming decades, we expect a significant increase in the burden of both diseases. People living with diabetes are more likely to develop severe (haemorrhagic) dengue symptoms, yet our understanding of the role of diabetes in dengue virus transmission and disease severity is limited.

Our preliminary data suggest that dengue haemorrhage is exacerbated by dysfunctional interactions between microvascular cells (endothelial cells and pericytes) in people living with diabetes. The first aim of this project is to use RNA-Seq, proteomics, functional assays (angiogenesis and permeability assays) and novel 3D in vitro co-culture models (organoids, microfluidics) developed at Surrey to characterise the mechanisms underlying worsened vascular outcomes in diabetic dengue patients.

Our data also suggest that dengue virus readily infects vascular pericytes and (rarely) endothelial cells in vitro. The second aim will explore the impact of diabetic conditions on dengue virus replication and functional microvascular outcomes during infection in vitro in The Pirbright Institute’s high-containment facilities.

Finally, previous reports suggest that mosquitoes fed with high-glucose blood more readily transmit dengue virus. The third aim will explore potential roles for enhanced virus replication and diabetic blood-induced hyperpermeability in the mosquito midgut in enhancing dengue virus transmission.

Technical training: cell culture, in vitro 3D multicellular cardiovascular models, vascular function assays, omics analyses, high containment virus work (CL3), mosquito husbandry and transmission assays.

Impact: The studentship will explore an urgent understudied area in a world of increasing dengue and diabetes rates, both in the Global North and South, helping to elucidate cellular mechanisms leading to enhanced dengue virus transmission and disease severity.

Apply now

Please apply by submitting an application form and completing our EDI survey. 

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Theme(s): Dr Matteo Barberis, m.barberis@surrey.ac.uk  

Lead partner: University of Surrey 
Supervisor: Patrizia Camelliti, p.camelliti@surrey.ac.uk

Joint partner: Pirbright Institute  
Supervisor: Dr Matteo Barberis, m.barberis@surrey.ac.uk  

Project Summary

This project aims at gaining systematic and mechanistic insights into viral infections. Specifically, it is designed to understand the metabolic and proteomic response of persistent infections in mosquitoes through a systems Biology strategy that integrates multiple levels of –omics data with experimentation. Viruses that use invertebrates as part of their lifecycle include well-known viruses such as Dengue virus, Chikungunya virus, and yellow fever virus. Persistent viral infections do not result in pathological injury to their hosts, but the presence of the infection causes a metabolic burden, which can impact the host. This interaction is not well understood. However, we know that successful infection of mosquitoes is multi-factorial and the mosquito metabolism is an understudied aspect of this interaction. Our hypothesis is that mosquito metabolism, and its regulation from the proteome, is critical to sustaining persistent infections and that specific metabolites can be identified that provide an environment allowing for viral persistence. 

The student will utilise a series of mutant viruses from highly attenuated to wild type that will enable us to interrogate the role of metabolism in determining whether the virus is able to establish a persistent infection. They will use a combination of in vitro and in silico approaches to generate and prepare samples for metabolomic and proteomic analyses, using the wild-type and mutant strains of Venezuelan equine encephalitis virus (VEEV). The metabolomic and proteomic data will be integrated and annotated onto biochemical maps, which will be analysed to identify metabolic/proteomic targets in different states of viral infection. The results will be verified by targeting some of these key targets as indicators during viral infections and testing the outcomes for various viruses. Outcomes from this project will help us understand the relationship between mosquitoes and persistent viruses and will inform novel targeting strategies for the control of important mosquito-borne viruses.

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Please apply by submitting an application form and completing our EDI survey. 

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Theme(s): Infection and Cellular Biology

Lead partner: University of Surrey 
Supervisor: Dr Patrizia Cameliliti, p.camelliti@surrey.ac.uk

Joint partner: Pirbright Institute 
Supervisor: Dr Natacha Ogando, Natacha.ogando@pirbright.ac.uk

Project Summary

Global pork supplies are threatened by African swine fever (ASF), a devastating disease affecting pigs and wild boar. The causative agent, ASF virus (ASFV) targets macrophages and replicates in lymphoid organs such as spleen. Understanding host-ASFV interactions is critical for the development of ASF vaccines and ASF resilient animals. Still, most studies have predominantly focused on 2D macrophage cultures, which inadequately capture the complexity of immune processes during infection. In contrast, cutting-edge 3D culture systems better mimic in vivo conditions, enabling the investigation of dynamic cell-cell and cell-pathogen interactions within host tissues. Moreover, 3D cultures provide a sustainable platform that reduces the use of animals in research.

This interdisciplinary project, in collaboration with Dr Priscilla Tng (ASF Vaccinology), aims to develop a porcine spleen-derived 3D model to study complex host immune responses during ASFV infection. Two complementary approaches will be explored to study the interface between innate and adaptive immunity: organotypic slices prepared from freshly isolated spleen, and 3D spheroids generated using spleen isolated cells. Then, established 3D models will be used to study host immune processes and immune cell dynamics modulated by multiple ASFV strains of varying virulence. The project will involve working in high containment facility, and cross-disciplinary training in tissue bioengineering-, virology, immunology and computational data analysis, which will be provided on site.

Importantly, this work will develop a sustainable and ethically responsible 3D spleen model platform applicable to different areas of host-pathogen research, disease modelling and pharmacology, spanning both veterinary and biomedical research fields. Furthermore, this project will provide a novel perspective on host immune responses to ASFV infection and potentially identify mechanisms that can lead to the development of ASF control strategies to improve livestock health and global food security.

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Please apply by submitting an application form and completing our EDI survey. 

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Theme(s): Understanding Disease Spread; Detection, Prevention and Intervention

Lead partner: University of Surrey 
Supervisor: Gianni Lo Iacono, g.loiacono@surrey.ac.uk

Joint partner: Pirbright Institute  
Supervisor: Marion England, marion.england@pirbright.ac.uk

Project Summary

Mosquitoes are among the deadliest animals on Earth, transmitting diseases that affect people, animals, and ecosystems. This challenge is intensifying with climate and land-use change. For example, the spread of tiger mosquitoes across Europe, introduced through the trade of used tyres and plants, has brought dengue and chikungunya to new regions. Rift Valley fever and West Nile virus are two major mosquito-borne diseases that cause periodic outbreaks with serious health and economic impacts. Although most common in sub-Saharan Africa, both are expanding their range as environmental conditions shift.

These diseases are tightly linked to environmental factors. Rainfall creates breeding sites, while temperature affects mosquito survival and development. Understanding these relationships can help predict when and where outbreaks might occur. Our team has successfully used environmental data to model gastrointestinal diseases, and we now aim to extend these methods to mosquito-borne infections, which are more complex, and more exciting, because transmission involves both mosquitoes and humans.

In this project, you will apply a novel epidemiological modelling approach to simulate disease outbreaks based on environmental data.

Objectives:

1. Develop an agent-based model of a vector-borne disease influenced by environmental factors.
2. Using the technique developed for gastrointestinal diseases, estimate the crude probability of detecting a case based on weather and land-use conditions.
3. Improve the technique by explicitly incorporating mosquito-borne transmission. You will achieve this by allowing the probability model to retain a “memory” of past events and validating it with the agent-based model.
4. Apply the validated model to real-world data.

You will use open datasets on Rift Valley fever and West Nile virus from endemic regions and explore potential disease risks under UK climate change scenarios. This exciting project suits students interested in infectious diseases, public health, data science, or modelling; prior experience in modelling is helpful but not essential.

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Theme(s): Infection and Cellular Biology.

Lead partner: University of Surrey 
Supervisor: Marine Petit, m.petit@surrey.ac.uk

Joint partner: The Pirbright Institute 
Supervisor: Nicolas Locker, nicolas.locker@pirbright.ac.uk

Project Summary

Ticks are blood-feeding arthropods that serve as highly efficient vectors for viral pathogens. Global surveillance reveals troubling trends: increasing tick populations, expansion into new geographical regions, and rising prevalence of tick-borne viruses. Yet the biological mechanisms that make ticks such effective viral vectors remain poorly understood. For example, we still don't understand how viruses activate innate immunity and cellular stress responses when they infect tick cells. This PhD project interrogates the intricate interplay between cellular stress networks and tick-borne bunyavirus infection dynamics, trying to decipher determinants of successful tick cell infection.

Our preliminary data reveal viral modulation of host stress responses during tick-borne Bunyavirus infection. For example, we observe the upregulation of mitochondrial proteomes associated with apoptotic signalling, and we establish direct protein-protein interactions between viral nucleoprotein and cellular stress response components, including mitochondrial stress mediators and stress granules. These observations position mitochondria as central nodes in the virus-host interface, yet current experimental pipelines lack depth to comprehensively delineate how mitochondria sense viruses, orchestrate stress signalling cascades, and ultimately govern viral replication kinetics in tick cells.

Leveraging our combined expertise in tick-arbovirology, tick cell biology, and viral stress biology, this project pursues three integrated objectives:

1. Engineering a toolkit for dissecting mitochondrial dynamics in tick cells,
2. Defining the functional roles of infection-induced DEAD-box RNA helicases in modulating mitochondrial homeostasis,
3. Establishing causal relationships between stress granule formation and bunyavirus replication efficiency.

The candidate will acquire proficiency in advanced methodologies including high-containment laboratory work, tick cell culture, quantitative molecular virology (RT-qPCR, immunoblotting, confocal microscopy), mitochondrial functional assays and tick cell gene editing techniques.

This project will elucidate fundamental principles governing cellular stress responses during tick-virus interactions, uncover mechanisms exploited by tick-borne viruses to infect and persist in tick cells, and generate testable hypotheses for rational vector-targeted intervention strategies.

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Theme(s): Microbial Evolution and Drug Resistance; Infection and Cellular Biology.

Lead partner: University of Surrey 
Supervisor: Jai Mehat, jw.mehat@surrey.ac.uk 

Joint partner: The Pirbright Institute 
Supervisor: Dr Erica Bickerton, erica.bickerton@pirbright.ac.uk

Project Summary

The University of Surrey, in collaboration with The Pirbright Institute, are offering an exciting PhD opportunity to investigate the complex interplay between avian coronavirus infectious bronchitis virus (IBV) and Avian Pathogenic Escherichia coli (APEC) in poultry.

Project Background

The poultry industry is vital for feeding a growing global population but faces significant challenges from infectious diseases. Co-infections with IBV and APEC represent a major threat, causing immune suppression and secondary infections that lead to systemic colibacillosis and economic losses. Available vaccines offer limited protection, reflecting both narrow strain coverage and limited insight into how IBV increases susceptibility to APEC infection. This project aims to close this knowledge gap by exploring the cooperative dynamics by which IBV enhances APEC colonisation and bacterial opportunism, and identify viral-bacterial strain combinations that lead to the most severe disease outcomes.

Approaches

We will employ cutting-edge in vitro and ex vivo models to investigate the synergistic dynamics of IBV and APEC co-infection across key mucosal sites. 

Using three-dimensional “inside-out” chicken enteroids incorporating a leukocyte component, we will explore how enterotropic IBV infection alters intestinal barrier integrity and promotes bacterial infiltration, using advanced microscopy approaches to visualise interactions in detail. Complementary high-resolution metagenomic analyses of IBV-infected chickens will identify virus-induced shifts in the gut microbiota that may enhance APEC colonisation and shedding. In parallel, studies of IBV-APEC interactions in the avian respiratory tract will determine how IBV infection facilitates extra-intestinal dissemination and increases susceptibility to APEC.

Impact and Career Opportunities

This PhD opportunity offers the unique benefit of collaboration between the University of Surrey and The Pirbright Institute, creating a dynamic environment that bridges academic and applied science. This research will provide critical insights into viral-bacterial co-infections- a key challenge in One-Health contexts, paving the way for improved disease control strategies and reducing reliance on antimicrobials.

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Theme(s): Infection and Cellular Biology

Lead partner: University of Surrey 
Supervisor: Samaneh Kouchaki, samaneh.kouchaki@surrey.ac.uk 

Joint partner: The Pirbright Institute 
Supervisor: James Kelly, james.kelly@pirbright.ac.uk 

Project Summary

Post-translational modifications (PTMs), including phosphorylation, ubiquitination, and glycosylation, are crucial for viral functions like replication, capsid maturation, and evading the host immune system. PTMs can also be a key factor in cross-species transmission.

Host range of retroviruses like HIV is notably limited by species-specific variations of the antiviral protein TRIM5. TRIM5 acts by ubiquitinating the viral capsid, tagging it for destruction by the proteasome. However, retroviruses evolve to evade their native host's TRIM5, while remaining susceptible to that of other species. For example, the cross-species jump of HIV from monkeys to humans, required HIV to adapt and bypass inactivation by human-specific TRIM5. This illustrates how PTMs can play a key role in cross-species transmission.

This interdisciplinary project will investigate the role of PTMs in the cross-species jump of swine vesicular disease virus (SVDV). An enterovirus that emerged from the human virus Coxsackievirus B5 (CVB5) through a human to pig species-jump in the 1960s. By leveraging cutting-edge AI and advanced molecular virology we will pinpoint the PTMs crucial for viral adaptation to new species.

Phase1: Identification of PTMs using cutting-edge AI models

At the Surrey Institute for People-Centred AI, CVSSP, and School of Health Sciences (supervised by Samaneh Kouchaki and Ayse Demirkan), the student will develop AI-driven PTM prediction models using mass-spectrometry proteomics, and structural modelling to identify key PTMs. This will reveal how the PTM landscape of CVB5/SVDV was reshaped by its 60-year evolution in pigs. 

Phase 2: Characterisation of PTMs through in vitro and live virus studies

Working in high-containment labs at the world-leading Pirbright Institute, the student will investigate how PTMs shape the enterovirus life cycle and control host-specificity of CVB5/SVDV.

This research will reveal mechanisms underlying cross-species adaptation in enteroviruses and provide new insights for rational antiviral design and zoonotic risk assessment across human and animal health.

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Theme(s): Infection and Cellular Biology

Lead partner: University of Surrey 
Supervisor: Gill Elliott, g.elliott@surrey.ac.uk

Joint partner: The Pirbright Institute 
Supervisor: Nicolas Locker, nicolas.locker@pirbright.ac.uk

Project Summary

Many viruses induce the formation of novel membraneless biocondensates which are involved in a range of processes including genome replication, virus assembly and inhibition of immune responses. We have discovered a novel biocondensate that is induced in the cytoplasm of herpes simplex virus infected cells which we have termed virus-induced cytoplasmic complexes (VICCs). These structures are induced later in infection and contain at least one virus protein specifically targeted there (VICC-protein). Nonetheless, their role in virus infection remains unknown. In this exciting project, you will train across an interdisciplinary team of three research-active groups where you will learn a wide range of skills and cutting-edge technology to address the purpose and nature of these novel VICC biocondensates. 

In the Elliott group (University of Surrey), you will utilise HSV1 expressing a GFP-tagged VICC-protein in a range of virological and bioimaging experiments (eg confocal, live-cell, and super-resolution microscopy) to investigate the cell biology, kinetics and dynamics of VICC assembly and determine their contribution to efficient virus production and/or regulation of innate immune responses. Methodology to purify VICCs will be developed in the Locker group (Pirbright Institute) in collaboration with the SEISMIC facility (Kings College London), leveraging biochemical and in situ dissection processes to isolate and determine the viral and cellular proteome of VICCs. Compositional analysis of these structures will subsequently inform parallel virological studies. To assess if VICCs are a panviral feature of alphaherpesviruses, animal herpesviruses that express homologues of the VICC-protein will be engineered to express GFP-tagged protein, and VICC formation examined by microscopy. 

By defining these new virus-induced structures across the alphaherpesvirus family, you will make a vital contribution to current understanding of the herpesvirus-host cell relationship and establish the potential for VICCs to be exploited as a new panviral target for herpesvirus infection in humans and animals. 

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Theme(s): Detection, Prevention and Intervention

Lead partner: University of Surrey 
Supervisor: Suzie Hingley-Wilson, s.hingley-wilson@surrey.ac.uk

Joint partner: UKHSA 
Supervisor: Ginny Moore, ginny.moore@ukhsa.gov.uk

Project Summary

Tuberculosis (TB) is often called the forgotten pandemic, causing over 1.3 million deaths every year. Much of this burden is in West Africa, where many of the TB-causing strains are not the usual suspect Mycobacterium tuberculosis (Mtb). Up to 50% of TB cases may be misdiagnosed, with many caused by other lineages of the Mycobacterium tuberculosis complex (MTBC) or by non-tuberculous mycobacteria (NTM), such as Mycobacterium abscessus (MABC). Research from our lab also revealed a high proportion of mixed MTBC infections and potential non-tuberculous mycobacteria (NTM) causing TB (Owusu et al., 2022). Treatment for Mtb, MTBCs and NTMs differs significantly, and misapplication of these treatments can lead to exacerbation of existing infections or complete treatment failure. 

This PhD project will help with misdiagnosis and improve treatment prescribing, by developing and validating a cutting-edge diagnostic test to differentiate NTMs and MTBC strains using our industrial partner VIDIIA’s rapid AI-assisted diagnostics. The test will focus on MTBC’s and clinically relevant NTMs, such as M. abscessus. Many NTMs are ubiquitous in the environment and their presence in hospital water systems can be associated with calamitous outbreaks. Therefore, this diagnostic test will be adapted to be of use in patient and environmental samples. Initially, cutting edge bioinformatics will be used to further develop the differentiative test to define the loop mediated isothermal amplification (LAMP) or Clustered regularly interspaced short palindromic repeats (CRISPR) primers. Environmental diagnostics will be tested at UKHSA using their “model” hospital ward, before testing on real-life samples in the UK and in Ghana.

This project could help save lives by enabling accurate and rapid diagnosis in high-burden areas, breaking the cycle of treatment failure, AMR, and disease transmission. Students will gain valuable experience in bioinformatics, molecular diagnostics and translational science, while contributing to a project with real-world impact on global health.

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Theme(s): Detection, Prevention and Intervention; Infection and Cellular Biology

Lead partner: University of Surrey 
Supervisor: Salvatore Santamaria, s.santamaria@surrey.ac.uk

Joint partner: UKHSA 
Supervisor: Anika Singanayagam, Anika.Singanayagam@ukhsa.gov.uk

Project Summary

Upper respiratory tract infections are the leading cause of acute disease worldwide causing over 12 billion episodes each year. Seasonal respiratory viruses, including influenza and respiratory syncytial virus (RSV), drive major morbidity and mortality despite the use of current vaccines and antivirals that target the pathogen. There is an unmet need for treatments that, in contrast to currently available prophylactics/interventions, do not require annual reformulation or close monitoring of mutations. Therapeutics targeting the host response, a conserved mechanism of defence during viral infections, may provide an universal weapon in the arms race against respiratory viruses. Extracellular matrix (ECM)-associated metalloproteinases called ADAMTSs are emerging as regulators of antiviral immunity: genetic manipulation of ADAMTS4 or ADAMTS5 improves survival following influenza infection of mice, yet the mechanistic basis of this immune regulation is unresolved. 

We hypothesise that pharmacologic inhibition of ADAMTS paralogues may improve survival after lung viral infection by reprograming host responses and limiting damaging inflammation.

By leveraging selective anti-ADAMTS4 and ADAMTS5 monoclonal antibodies (mAbs), we will dissect protease-dependent control of virus-host interactions in advanced cellular models and translational assays to accelerate preclinical development.

We have already generated 1) a mAb blocking ADAMTS4 activity; 2) a mAb that increases extracellular ADAMTS5 levels by blocking ADAMTS5 internalisation into the cells and subsequent degradation. Both antibodies demonstrated efficacy in ex-vivo models of osteoarthritis. In this project, we aim to repurpose anti-ADAMTS mAbs and assess their feasibility as treatments for viral lung infections by achieving three specific aims:

1. Reformatting, expression and purification of humanised anti-ADAMTS and anti-ADAMTS5 mAbs.
2. Assessing the effect of anti-ADAMTS mAbs on cell lines and primary cells infected with RSV and influenza virus.
3. Understanding the impact of ADAMTS mAbs on the innate immune responses to respiratory viral infection and subsequent disease.

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Theme(s): Infection and Cellular Biology

Lead partner: University of Surrey 
Supervisor: Dr David J Allen, d.j.allen@surrey.ac.uk

Joint partner: UKHSA 
Supervisor: Dr Alex Stewart, alex.stewart@apha.gov.uk 

Project Summary

Virus infections of pigs have a global economic impact of billions of dollars annually. Alongside affecting animal health directly, they cause secondary bacterial coinfections driving antibiotic use, contributing to AMR, and indirectly affect human health through impacting food security and livelihoods through losses. Endemic and emerging viruses in pig populations include flaviviruses, picornaviruses, nidoviruses and parvoviruses.

Understanding virus-host interactions such as immune responses mediated by type-I interferons (IFN-I) that initiate antiviral responses are underexplored as pathways to developing countermeasures. 

Early virus-host interactions do not occur in isolation: sites targeted by viruses have populations of resident commensal bacteria (‘microbiota’) which can modulate immune responses. Lactic acid bacteria (LAB) – common beneficial commensals – activate IFN-I responses via intracellular sensors STING and MAVS which are important components of signalling systems that initiate IFN-I antiviral responses to DNA and RNA viruses, respectively.

Therefore: can LAB trigger an antiviral response for therapeutic use?

The project will answer this question through three objectives:

1. Build cell-based laboratory models for measuring IFN-I responses following infection with RNA/DNA viruses, in the presence/absence of LAB, and with/without STING or MAVS.
2. Determine components of LAB critical for the activation of STING or MAVS, and characterise IFN-antagonistic viral proteins in these systems.
3. Test LAB – or LAB components – against a panel of viruses to demonstrate their potential as a therapeutic.

The project provides training in laboratory techniques, including CRISPR, RNA knockdown/out, stable cell line production, molecular biology, quantitative RT-PCR, sequencing, protein-protein interaction assays, bacterial culture, recombinant protein expression, cell transfection, and virus/cell culture, and working with APHA who have collections of porcine viruses for study in laboratory and in vivo challenge systems.

This one-health research will establish potential for use of LAB as a probiotic, and/or identify components of LAB for development as therapeutics, to control viral infections in pig herds.

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Theme(s): Infection and Cellular biology; Detection, Prevention and Intervention.

Lead partner: University of Surrey 
Supervisor: Dr Qibo Zhang, quibo.zang@surrey.ac.uk

Joint partner: UKHSA 
Supervisor: Dr Julie Tree, julia.tree@ukhsa.gov.uk 

Project Summary

Rationale

Immunity against virus infection critically depend on T cell and antibody responses produced in the immune system. Development of immunomodulatory agents/drugs to enhance these immune responses is an important strategy for better efficacy of treatment such as antibody-based or anti-viral therapy. Testing of new drugs typically involves the use of animal models to generate pre-clinical data. There is a growing momentum to replace/reduce animal experimentation. The availability of complex in vitro models such as human organoid system may provide experimental data that better predict clinical outcomes in humans. This PhD project aims to evaluate the effectiveness of new immunomodulatory agents and antivirals in anti-viral immunity using human tissue-derived immune organoids. 

Approaches

Using an in vitro immune organoid culture system established in Dr Zhang’s lab, which is based on immune tissue/cells from children & adults and able to study immune responses to microbial infection and vaccines, this project will characterise/evaluate the effectiveness of immunomodulatory agents and antivirals on enhancement of anti-viral response. Both T cell- and antibody-mediated immunity to influenza A(H1N1) (a prototype of highly pathogenic avian influenza virus), SARS-CoV-2 and Herpes simplex virus(HSV) will be analysed. CD4/CD8 T cell responses, cytokine profiles, and antibody responses induced by the virus antigens, with/without immunomodulatory agents (e.g. TLR4, TLR7/8 agonists, IFNβ) will be evaluated, using state-of-the-art techniques including confocal microscopy, flowcytometry, immunoassays and virus neutralisation analysis (within Biosafety Level 3 facilities). 

The PhD student will be jointly supervised by multidisciplinary teams at UoS (Dr Zhang and Prof Elliot) and UKHSA (Drs Tree and Horton), with expertise/experience in immunology, anti-viral drug testing and viral infection biology. 

Impact

An in vitro immune organoid system with capacities for testing immunotherapeutic anti-viral agents and better predicting clinical outcomes will speed up development of effective anti-viral drugs for humans and improve pandemic preparedness against new virus infection.

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Theme(s): Infection and Cellular Biology

Lead partner: University of Surrey 
Supervisor: Lisa Holbrook, l.holbrook@surrey.ac.uk

Joint partner: UKHSA 
Supervisor: Stuart Dowall, stuart.dowall@ukhsa.gov.uk 

Collaborative partner: The Pirbright Institute

Project summary

Rift Valley fever virus (RVFV) is a mosquito-transmitted, zoonotic, emerging bunyavirus categorised by WHO as a high-consequence, priority pathogen due to its emergence and lack of effective and safe antiviral treatments. It causes viral haemorrhagic fever in humans and livestock characterised by necrotic lesions in major organs, thrombocytopenia (low platelet numbers), coagulation defects as well as increased vascular permeability resulting in oedema, hypotension, shock, and death. How RVFV induces pathology remains largely unknown and understanding the molecular and immune mechanisms underlying RVFV pathology will identify new avenues for therapeutics development.

Viruses associated with haemorrhagic fever cause destruction or dysfunction of platelets, leading to thrombocytopenia. Platelets are essential in haemostasis, for integrity of the vascular system and immunity. They can be activated aberrantly by interaction with viruses or virus-infected cells. Activated platelets adhere to endothelial cells, thereby reducing the number of circulating platelets, altering endothelial cell function, and increasing vascular permeability. In this project we hypothesise that RVFV activates platelets which induces thrombocytopenia. Treatments that prevent or correct platelet loss and dysfunction in RVFV infection have the potential to ameliorate platelet-mediated pathology and to significantly improve clinical outcome. Additionally, platelets secrete redox proteins (thiol isomerases) which conversely enable virus entry and fusion, therefore thiol isomerases may also contribute to RVFV pathogenesis.

This project will examine the molecular and immune interactions between RVFV and platelets leading to pathology by characterising the mode of RVFV-induced platelet activation and thrombocytopenia using a combination of in vitro and in vivo methods. Confirmation of in vitro mechanisms will be evaluated using material from RVFV challenge animal models allowing comparison with disease severity. Platelet redox changes as both a marker of platelet function and, additionally as a potential facilitator of RVFV infection will also be explored in both the vitro and in vivo models of RVFV infection.

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Theme(s): Detection, Prevention and Intervention; Understanding Disease Spread

Lead partner: University of Surrey 
Supervisor: Joaquin Prada, j.prada@surrey.ac.uk

Joint partner: UKHSA 
Supervisor: Victor del Rio Vilas, victor.delriovilas@ukhsa.gov.uk

Project Summary

Infectious disease outbreaks such as Ebola virus disease, Marburg virus disease, and Mpox, and other emerging diseases, pose significant global health threats due to their high case fatality rates and transmissibility. Globalization and more frequent human-wildlife contact have increased the risk of disease emergence, necessitating a One Health approach for effective detection and prevention. High community engagement and public trust are critical components for controlling outbreaks, including the use of tools such as community-based surveillance, community-led strategies, and social mobilisation alongside traditional health and water and sanitation interventions. However, rigorous, context-sensitive evaluations of these approaches are lacking, particularly in terms of equity, sustainability, and cultural relevance. This project aims to uncover these gaps through the following objectives:

1. Evaluate the effectiveness of community engagement as a key strategy to outbreak control through a mixed-methods approach, combining applied epidemiology with qualitative, community-based participatory research.
2. Investigate how government actions and community trust influence compliance and outbreak trajectories through mathematical modelling to simulate and project different epidemiological scenarios.
3. Quantify sustainability of community-based interventions by integrating acceptability with economic evaluations of their costs. 

The student will acquire a broad and valuable expertise in mathematical modelling, operational research, health economics and stakeholder elicitation methods through this unique collaboration between the University of Surrey and the UK Health Security Agency. The findings will inform ministries of health and public health agencies by providing evidence-based policy recommendations to enhance community engagement in outbreak preparedness and response. The project aims to contribute to the development of more equitable, culturally grounded, and effective public health strategies for managing infectious disease threats with pandemic potential.

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Theme(s): Microbial Evolution and Drug Resistance; Understanding disease spread

Lead partner: University of Sussex 
Supervisor: William Hughes, william.hughes@sussex.ac.uk

Joint partner: APHA 
Supervisor: Nigel Semmence, nigel.semmence@apha.gov.uk

Collaborative partner: The Pirbright Institute

Project Summary

Honeybees are of tremendous economic importance, providing essential pollination services for many crops in addition to honey and other apicultural products. However, the productivity of apiculture, and the agriculture that relies upon it, is increasingly threatened by a diversity of pathogens, ectoparasite vectors and other stressors. There is growing recognition of the importance of the complex interactions between the host, pathogens and stressors, including those that may individually have only sublethal effects. Chronic Bee Paralysis Virus (CBPV) is a relatively neglected disease that is both an important problem for UK apiculture and an intriguing pathogen from a virology perspective. It is a single-strand, positive-sense RNA virus that has multiple modes of transmission, can replicate in multiple host species, causes multiple syndromes of symptoms, and often occurs at low prevalence but can cause rapid collapse of colonies and even whole apiaries. However, the virology and dynamics of CBPV are still poorly understood, which hinders the development of appropriate management strategies.

This exciting, cross-agency project will address this knowledge gap by investigating CBPV epidemiology and evolutionary dynamics at within-host, colony and population levels. Virus replication and mutation rates in different tissues and hosts will be examined to establish the significance of virus structure and how the virus persists within hosts. Laboratory experiments with controlled virus inoculations and qPCR will be used to examine the physiological basis for the different syndromes of symptoms and the dynamics of transmission between hosts. Field samples and syndromic surveillance will be incorporated into spatial and phylogenetic analyses to investigate virus patterns across the UK. The significance of interactions with other pathogens and stressors will be incorporated at all three levels. The results will both advance our fundamental understanding of host-virus dynamics and be of applied impact in informing the management of an important, neglected disease.

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Theme(s): Investigating the antigenicity and cross-reactivity of lyssaviruses and coronaviruses to inform intervention strategies

Lead partner: University of Sussex 
Supervisor: Edward Wright, ew323@susex.ac.uk 

Joint partner: APHA 
Supervisor: Dr Arran Folly, arran.folly@apha.gov.uk

Project Summary

Honeybees and other pollinators are of tremendous economic importance, providing essential pollination services to agriculture, but they are increasingly threatened by a diversity of pathogens and other stressors. There is growing recognition of the need for a better understanding of the complex interactions between the host, pathogens and stressors for the sustainable provision of pollination services. Chronic Bee Paralysis Virus (CBPV) is a relatively neglected disease that is both an important problem for UK bees and an intriguing pathogen from a virology perspective, but it is still poorly understood, which greatly hinders the development of appropriate management strategies. 

This exciting project will address this knowledge gap by investigating the host-pathogen dynamics of CBPV in honeybees at within-host, colony and population levels in a cross-agency collaboration between the University of Sussex (Prof William Hughes), APHA (Dr Arran Folly), National Bee Unit (Nigel Semmence) and Pirbright Institute (Dr Naomi Forrester-Soto). The work will involve quantifying virus replication and mutation rates, controlled virus inoculation experiments to examine host-pathogen transmission dynamics and integrating field sampling and syndromic surveillance into spatial and phylogenetic analyses to investigate virus patterns across the UK.

The results will both advance our fundamental understanding of host-virus dynamics and be of applied impact in informing the management of an important, neglected disease. The student will receive an exciting diversity of interdisciplinary training, including two professional internships at APHA and the Pirbright Institute, encompassing cutting-edge virology, laboratory experiments, and advanced statistical analyses, as well as first-hand experience of applied stakeholder knowledge exchange with the National Bee Unit. The project will provide the student with an outstanding range of skills and experience to support a subsequent career across a broad diversity of fields in academia and industry, health and veterinary sciences, agriculture and conservation.

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Theme(s): Microbial Evolution and Drug Resistance; Understanding Disease Spread

Lead partner: University of Sussex 
Supervisor: Dr Mark Paget, m.paget@sussex.ac.uk

Joint partner: UKHSA
Supervisor: Daniel Horton, Dan.horton@apha.gov.uk

Project Summary

Non-tuberculous mycobacteria (NTM), such as the Mycobacterium avium complex and Mycobacterium abscessus, are opportunistic pathogens that pose significant health risks, particularly to individuals with weakened immune systems, causing pulmonary and disseminated infections. As oligotrophs, they can grow in low-nutrient environments such as water systems where they often form biofilms - complex and structured bacterial communities that are tolerant to antimicrobial agents including disinfectants and other biocides. Biofilm-like structures can also form in chronic pulmonary infections and are extremely difficult to eradicate due to high levels of antibiotic tolerance. 

This research project aims to elucidate the regulatory mechanisms by which NTMs respond to nitrogen starvation, which is especially experienced by cells in deeper layers of biofilms. Like all bacteria, NTMs respond to nitrogen limitation by switching on genes involved in scavenging and nutrient uptake. An additional and critical response is to down-regulate hundreds of genes involved in growth, in order to preserve resources. While this global response can be observed using next-generation sequencing experiments, the actual mechanisms involved are very poorly understood and are distinct from those in well-studied organisms such as E. coli. Addressing this fundamental question has direct clinical and public health implications: understanding how biofilm-associated NTM persist in nutrient-poor environments could unlock new strategies to combat their presence in water systems and infections, ultimately helping to reduce the rising incidence of NTM disease. 

The project will involve a wide variety of molecular biology and microbiological techniques, including the use of biofilm model environments for NTMs, for which the student will receive training in a supportive and friendly environment.

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Theme(s): Microbial Evolution and Drug Resistance

Lead partner: University of Sussex 
Supervisor: Adam Eyre-Walker, a.c.eyre-walker@sussex.ac.uk 

Joint partner: APHA 
Supervisor: Hassan Hartman, Hassan.Hartman@ukhsa.gov.uk 

Project Summary

Like all organisms, bacteria must adapt to their ever-changing environment. However, unlike eukaryotes they can achieve this in two very different ways; by undergoing adaptive evolution in the genes that they already have, as eukaryotes do, and by acquiring new genes from other sources. The aim of the project is to study both aspects of adaptation in bacteria, considering both pathogenic and non-pathogenic species. During the project we will construct pangenomes from species which have tens of thousands of sequenced strains and apply newly developed tests to investigate whether the accessory genes, genes that are present in only some strains, are adaptive. At the same time, we will apply a range of other population genetic tests to investigate adaptation in both the core and accessory genes. The project will analyse pre-existing data using a variety of population genetic tests. The project will offer the student training in Big Data, bioinformatics, computer programming, statistical analysis, population genomics and evolutionary biology.

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Theme(s): Microbial Evolution and Drug Resistance

Lead partner: University of Sussex 
Supervisor: Maria Krutikov, m.krutikov@bsms.ac.uk 

Joint partner: UKHSA
Supervisor: Natalie Adams, natalie.adams@ukhsa.gov.uk

Project Summary

Norovirus is a highly contagious gastro-intestinal virus which is responsible for a large number of outbreaks in health and care settings. This leads to hospitalisations and operational challenges like bed closures, with significant financial and social ramifications. Surveillance is limited, given challenges with sampling and data collection which include an overstretched workforce and difficulties consenting older people with dementia. Given the extreme vulnerability of care-home residents to severe infection, accurate data on norovirus transmission between health and care settings is crucial to inform preventive measures. 

Wastewater sampling (WWS) is a population-level, anonymous, low-cost, inclusive tool to measure infectious pathogens, yet little is known about its practical applications for infection prevention and its correlation with clinical infection in care-homes. Understanding the reliability of WWS for norovirus surveillance could inform local and national policy. 

This project aims to apply inclusive approaches to norovirus detection to describe transmission between health and care settings to enhance surveillance and preparedness in care-homes. Specifically, an established WWS study from two care-homes in Sussex (WATCH study), within the Vivaldi-Social Care infection dataset will provide access to longitudinal clinical, environmental, and wastewater samples from these sites over three-months. Additionally, clinical specimens from symptomatic patients tested at the regional laboratory at University Hospitals Sussex will be integrated into the study. These unique samples will facilitate analyses to address questions around transmission.

The project will address these main objectives:

• Measuring norovirus levels in environmental, stool and wastewater samples.
• Comparing temporal variations in norovirus within care-home environmental and clinical samples with contemporaneously collected wastewater samples and clinical symptoms data, to explore representativeness of wastewater for clinical infection.
• Comparing care-home and local clinical norovirus isolates to identify transmission between settings.
• Describing associations of norovirus detections with infection outcomes through data linkage to routine health data from Vivaldi-Social Care.

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Theme(s): Detection, Prevention and Intervention; Understanding Disease Spread

Lead partner: University of Sussex 
Supervisor: James Price, j.price@bsms.ac.uk 

Joint partner: UKHSA
Supervisor: Jasmin Islam, jasmin.islam@ukhsa.gov.uk 

Project Summary

Antimicrobial resistance (AMR) is one of the most urgent global health threats, and healthcare plays a critical role in its emergence and spread. Hospital wastewater often contains high levels of resistant bacteria, resistance genes, and antimicrobial drug residues. Yet, we still know surprisingly little about biological mechanisms linking how we manage the AMR burden in wastewater to how resistance spreads in the wider environment.

Working in partnership between Brighton and Sussex Medical School and the UK Health Security Agency, the student will describe the burden of AMR in hospital wastewater, investigate the mechanistic and ecological effects of intervention strategies, and identify how antibiotic residues influence microbial selection and gene transfer. Experimental and computational models will be used to understand how these biological changes could alter infection risks and AMR transmission within and beyond hospitals.

This PhD will apply Targeted Waste Stewardship, a novel bioscience-led intervention that separates and safely contains waste from two key patient groups:

1. Those colonised or infected with multidrug-resistant organisms, to prevent excretion of resistant bacteria into wastewater
2. Those receiving last-line antimicrobial drugs, to limit release of active drug residues into wastewater that create selective pressures driving AMR.

Both groups are likely major contributors to persistence and spread of AMR within hospitals and in connected wastewater environments. By interrupting these pathways, we aim to reduce environmental AMR contamination and downstream transmission risks.

This interdisciplinary PhD offers a unique opportunity to combine environmental microbiology and OneHealth approaches to tackle the real-world AMR problem. The results will advance our understanding of microbial ecology and AMR transmission in hospital systems and the wider environment, while informing more sustainable healthcare infection prevention practices. The student will develop a broad skillset including infection biology, genomics, bioinformatics and systems modelling, which will prepare them for a future career.

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Theme(s): Infection and Cellular Biology; Detection, Prevention and Intervention

Lead partner: University of Sussex 
Supervisor: Antony Oliver, antony.oliver@sussex.ac.uk

Joint partner: Dstl
Supervisor: Bethany Auld, bauld@mail.dstl.gov.uk

Project Summary

Several filoviruses, including Ebola and Marburg viruses, cause severe haemorrhagic fevers in humans and non-human primates, with case fatality rates of up to 90%. Transmitted zoonotically from animal reservoirs, these viruses remain a persistent threat to global health security, particularly in regions with limited access to diagnostics and effective countermeasures. Their potential for rapid spread, high mortality, and societal disruption also makes them a priority for biodefence research.

Current filovirus vaccines are highly specific, providing protection only against individual species or strains rather than the entire filovirus family. This limitation leaves significant gaps in outbreak preparedness and response.

This PhD project, jointly supported by the University of Sussex and the Defence Science and Technology Laboratory, aims to develop a pan-filovirus vaccine antigen using cutting-edge artificial intelligence (AI), machine learning and bioinformatic tools. Platforms such as AlphaFold will be used for structure prediction, while BEpiPred will support B-cell epitope mapping to identify conserved antigenic regions shared across multiple filovirus species. These computational insights will inform antigen design to elicit broad, cross-reactive immune responses.

Experimental validation will employ pseudotyped viruses—non-replicative particles engineered to express viral envelope proteins—enabling safe, high-throughput assessment of antigen expression, immunogenicity, and neutralisation potency and breadth under containment level 2 conditions. Data from these assays will guide refinement and selection of the most promising vaccine candidates.

This interdisciplinary studentship offers a unique opportunity to work at the interface of AI, structural biology, and molecular virology. The ultimate goal is to produce a prototype antigen suitable for preclinical evaluation, thereby strengthening global filovirus preparedness and demonstrating the transformative potential of AI in aiding vaccine design.

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Theme(s): Detection, Prevention and Intervention; Infection and Cellular Biology.

Lead partner: University of Sussex 
Supervisor: Leandro Castellano, l.castellano@sussex.ac.uk

Joint partner: The Pirbright Institute
Supervisor: Dalan Bailey, dalan.bailey@pirbright.ac.uk 

Project Summary

The escalating frequency of outbreaks caused by emerging and zoonotic viruses that have high mortality rates underscores the urgent need for strategies to minimise their impact. One group of viruses of particular concern is the henipaviruses, particularly Nipah virus (NiV), with mortality rates of up to 100%. It is therefore important to deepen our understanding of how these viruses interact with the host to enable the development of robust interventions to safeguard both human and animal health.

To address the shortfall in our understanding of host-virus interactions regarding henipaviruses, we have developed a functional genetic screen combining CRISPR/Cas9 and pseudotyped viruses (PV) technologies that has significant advantages over similar studies based on authentic (live) virus infection assays. This innovative screening platform, Ceudovitox, allows us to enhance our understanding of the molecular mechanisms of viral entry and enables us to build a detailed interactome map of host proteins and pathways involved in this process, ultimately supporting the development of therapeutic strategies to block virus infection.

Using cutting-edge NGS technology and advanced biochemical assays, this project will explore henipaviruses' entry mechanisms using NiV and Cedar virus (CedV) – another henipavirus - as prototype examples. The ultimate goal is to develop effective treatments for this group of viruses. 

The student will be trained in different aspects of molecular biology, bioinformatics, and virology:

Molecular biology - They will learn how to perform molecular biology and biochemical techniques, such as CRISPR/Cas9 genome editing, western blotting, RT-qPCR, cloning, reporter assays, and prepare libraries for NGS-related approaches.

Tissue culture - The project will give the student a firm grounding in mammalian cell culture and in generating pseudotyped viruses for use in various entry and inhibition assays. 

Viral infection in vitro models - CL3 training to handle wildtype virus and microscopy of virus-infected cells. This will build on the cell culture training and develop it to include viral infections and plaque assays. 

Bioinformatics - They will learn how to analyse NGS data, as well as genome mapping, sequence alignment and visualisation, pathway enrichment analysis, primer design, guide RNA design, and others.tial of AI in aiding vaccine design.

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Theme(s): Microbial Evolution and Drug Resistance

Lead partner: University of Sussex 
Supervisor: Frances Pearl, f.pearl@sussex.ac.uk

Joint partner: The Pirbright Institute
Supervisor: Tim Downing, Tim.Downing@pirbright.ac.uk

Project Summary

Mutational signatures are unique patterns of DNA base substitutions that reflect the specific mutagenic processes responsible for them. In cancer research, identifying these signatures within a tumour can reveal valuable information about the biological mechanisms driving its development. In this project, you will analyse the mutational signatures found in viral and bacterial pathogens and investigate the underlying causes of these mutation patterns.

DNA molecules tend to accumulate certain types of base changes called transitions (four options: C to T, T to C, A to G, G to A) more often than transversions (eight options: C to A, A to C, C to G, G to C, T to A, A to T, T to C, C to T). Transversions occur less often and may indicate adaptive evolution or reduced sequence conservation. The surrounding nucleotide context also influences these changes. For instance, many hosts recognise CpG dinucleotides as foreign, leading some pathogens to evolve AT-rich genomes as an immune evasion strategy.

This project will explore how these mutational patterns vary across pathogens that infect different hosts. In particular, you will investigate the role of host-driven processes such as APOBEC-mediated deamination, which shaped viral genomes during events like the recent mpox outbreak. By comparing mutation profiles across RNA and DNA viruses from livestock and birds including those with zoonotic potential, you will assess how nucleotide changes are linked to host switching and pathogen adaptation. These insights can improve our understanding of pathogen evolution and help inform risk assessments for future outbreaks and pandemics.

You will receive training in bioinformatics, molecular biology, genome analysis, and phylogenetics. The project will develop your skills in data interpretation, scientific communication, and critical analysis, while contributing to a novel and growing area of pathogen genomics. This research provides a new perspective on how host and environmental factors shape mutational signatures across diverse microbial genomes.

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Theme(s): Infection and Cellular Biology

Lead partner: University of Sussex 
Supervisor: Ben Towler, b.towler@sussex.ac.uk

Joint partner: The Pirbright Institute
Supervisor: Nicolas Locker, nicolas.locker@pirbright.ac.uk

Project Summary

Viral infection and RNA biology are intimately linked with viruses exploiting post-transcriptional and translational regulatory mechanisms to create an environment that favours replication. RNA degradation is a key component of post-transcriptional control, with RNA decay processes implicated in various diseases including cancer and neurodevelopmental disorders. Previous work has highlighted a role for RNA decay during viral infection, including both stimulatory and inhibitory effects of the ribonuclease XRN1 on viral biology. Another key player in RNA degradation is DIS3L2, which degrades RNA marked for destruction with a non-templated 3’ uridylated tail. Interestingly, 3’ uridylation has been implicated in viral RNA decay, however, how DIS3L2 activity impacts viral infection remains unexplored. 

We uncovered that cellular stress impacts DIS3L2 activity and that DIS3L2-deficient cells have defects in mitochondrial biology including differential decay of metabolic transcripts, increased oxygen consumption rate and an altered unfolded protein response. Mitochondria have been demonstrated to play both anti- and pro-viral roles with many, including the Locker laboratory, revealing viral rewiring of mitochondrial systems. Therefore, given the importance of mitochondrial function during viral infection and metabolic sensitivity to DIS3L2 activity, we hypothesise that DIS3L2 may play a direct and/or indirect role during viral infection through degrading both viral and metabolic RNAs, contributing to mitochondrial adaptation during infection. To address this, this project aims to:

1. Investigate the impact of flaviviruses on DIS3L2 activity
2. Establish the influence of DIS3L2 deficiency and altered mitochondrial function on viral replication
3. Characterise the mechanisms promoting increased oxygen consumption in DIS3L2-deficient cells

This is an exciting collaborative project at the interface of RNA and viral biology. Using advanced transcriptomic, molecular and bioinformatic approaches together with viral and metabolic assays we aim to improve understanding of RNA decay and mitochondrial function during viral infection which may uncover novel therapeutic avenues. 

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Theme(s): Detection, Prevention and Intervention; Microbial Evolution and Drug Resistance; Understanding Disease Spread; Infection and Cellular Biology

Lead partner: APHA 
Supervisor: Guanghui Wu, Guanghui.wu@apha.gov.uk

Joint partner: University of Exeter  
Supervisor: Orly Razgour, O.Razgour@exeter.ac.uk

Project Summary

Bats are essential for ecosystems but also host viruses with zoonotic potential, including lyssaviruses and coronaviruses. Despite their importance, the viral diversity of British bats remains poorly characterized. Understanding this diversity is critical for anticipating emerging threats, not by predicting spillover with certainty, but by identifying viruses and ecological contexts that may increase risk. Advances in metagenomics and artificial intelligence (AI) now allow rapid detection of novel viruses and inference of host–virus associations, providing a powerful foundation for proactive surveillance.

Approach

This PhD project will create the first atlas of the British bat virome by combining high-throughput metagenomic sequencing with AI-driven analytics. The student will:

• Perform shotgun metagenomics on bat tissues, gut contents, and guano collected via APHA’s annual intake (>1,000 carcasses) and field collaborations.
• Develop machine-learning pipelines to detect unknown viral sequences and predict host–virus associations.
• Integrate ecological and spatiotemporal data to identify patterns linked to zoonotic potential.
• Experimental validation of priority viruses (PCR, serology) will complement computational predictions.

Potential Impact

The project will deliver:

• A validated AI-assisted pipeline for virus discovery.
• The first public dataset of British bat viral diversity.
• A prototype dashboard highlighting ecological and viral factors associated with zoonotic potential.

This studentship offers a unique opportunity for multidisciplinary training in virology (Drs. Guanghui Wu and Lorraine McElhinney, APHA), bat ecology (Dr. Orly Razgour, University of Exeter), artificial intelligence (Professor Miroslaw Bober and Dr. Syed Sameed Husain, University of Surrey), and metagenomic sequencing (Dr. Yogesh Gupta, APHA), equipping the candidate with cutting-edge skills at the interface of wildlife disease surveillance and computational biology. 

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Theme(s): Detection, Prevention and Intervention; Microbial Evolution and Drug Resistance

Lead partner: APHA 
Supervisor: Muna Anjum, muna.anjum@apha.gov.uk 

Joint partner: University of Surrey 
Supervisor: Jennifer Ritchie, j.ritchie@surrey.ac.uk

Project Summary

This 4-year PhD studentship offers an exciting opportunity to contribute to One Health research on antimicrobial resistance (AMR)

AMR is predicted to be the main cause of human death by 2050. It represents one of the greatest challenges to human, animal, and environmental health, limiting therapeutic options following infection, and forming an increasing part of environmental contamination from wastewater. 

Standardised methods for AMR surveillance are needed to accurately detect and compare AMR in different environments. While these methods exist for the use of whole genome sequences derived from single organisms, validation and standardization for detecting AMR in bacterial communities using metagenomics, is still in its infancy. 

You will join a dynamic team of academic and industry partners working on building a One Health metrology infrastructure aimed at standardising the identification, quantification and surveillance of AMR across medical, agricultural and environmental sectors. This project has the potential for significant impact and enable a more comprehensive understanding of AMR transmission and proliferation. 

Project structure:

Objective 1: Identification and quantification of bacterial AMR in metagenomic samples, at the One Health level, to enable a better understanding of the prevalence of AMR across environmental, agricultural (e.g. animal) and clinical (e.g. human) settings.

Objective 2: Evaluation of source of errors, uncertainty calculation, comparability, reproducibility and validation of metagenomic approaches within a One Health perspective.

Objective 3: Development of guidelines for determination of measurement units in Bioinformatics/Machine Learning/Artificial Intelligence-based metagenomics. This will include assessment of random and systematic errors influencing measurements, such as lengths, depth and read quality of short- and long-read metagenomic data, and mutation detections (for ARGs, MGEs data),

This project is best suited to those with a strong interest and experience in Molecular Microbiology and Bioinformatics or closely related disciplines. Experience in the application of bioinformatic tools would be desirable. The individual will work closely with teams in the University of Surrey and NML.

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Apply now

Please apply by submitting an application form and completing our EDI survey. 

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Theme(s): Infection and Cellular Biology

Lead partner: APHA 
Supervisor: Karen Mansfield, karen.mansfield@apha.gov.uk

Joint partner: University of Surrey 
Supervisor: Marine Petit, m.petit@surrey.ac.uk

Project Summary

Tick-borne viruses represent an emerging threat to global health, with climate change and ecological disruption expanding their geographic range and host diversity. Among these, Tick-Borne Encephalitis Virus (TBEV), Louping ill virus (LIV) and the recently discovered Alongshan virus (ALSV) pose significant but poorly understood zoonotic risks in the UK. Critical gaps remain in understanding their host range, tissue tropism, and transmission dynamics.

Interestingly, these viruses demonstrate remarkable adaptability, efficiently replicating in both tick vectors and vertebrate hosts, suggesting sophisticated virus-host interaction strategies. Understanding the molecular determinants of viral permissively across diverse cellular environments is pivotal for predicting spillover risk and designing control strategies. 

Through collaboration between the University of Surrey and the Animal and Plant Health Agency (APHA), this project combines expertise in tick-borne virus research and vector biology to address viral threats at the human-animal health interface. Three objectives guide this work:

1. Development of advanced molecular tools: Develop reporter viruses for real-time monitoring of viral replication dynamics.
2. Systematic examination of viral permissively: Compare TBEV, LIV, and ALSV infection dynamics across tick and vertebrate cell lines using high-throughput sequencing and classical virology approaches.
3. Vector competence validation: Characterize molecular pathways differentially regulated in permissive tick cells, then validate their role in supporting viral replication through targeted gene silencing.

This project will provide comprehensive training in cutting-edge molecular virology techniques (RNA-scope, reverse-genetic), high-throughput sequencing analysis, advanced microscopy, and working with pathogenic viruses in a biosafety level 3 containment laboratory. You will gain experience working with reference laboratories for vector-borne diseases and develop skills highly valued in both academic and public health sectors.

This systematic characterization of tick-borne virus host range and tissue tropism will provide critical insights for predicting spillover events and informing surveillance priorities. By establishing comprehensive permissively profiles, this research will enable evidence-based risk assessment and early warning systems.

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Theme(s): Detection, prevention and intervention

Lead partner: DSTL 
Supervisor: Josh Prince, jprince1@dstl.gov.uk

Joint partner: University of Surrey 
Supervisor: David Allen, d.j.allen@surrey.ac.uk

Project Summary

Alphaviruses are singled-stranded positive-sense RNA viruses. They are primarily transmitted by arthropods but infect a range of vertebrates and can cause significant human disease outbreaks via zoonotic spillover. Alphaviruses can be divided into two groups: arthritogenic, including chikungunya and Ross River or encephalitic, including Venezuelan, Eastern and Western Equine Encephalitis. 

This project aims to enhance alphavirus outbreak preparedness and response, aligning with One Health principles to bridge human, animal, and environmental health. Current methods for alphavirus diagnostics include RT-PCR or serological confirmation with both reliant on laboratory equipment and the latter commonly prone to cross reactivity of closely related species. There is an urgent need to design diagnostic tests for early and rapid virus detection, that are suitable for use in field settings, and which offer multiplex testing to differentiate between alphaviruses, and alphaviruses from non-alphavirus arboviruses with overlapping distributions. Low-cost diagnostics are key to underpinning our understanding and managing alphavirus infections and diseases at the human-animal interface, where climate change, urbanisation and other factors are changing the global distribution and impact of alphaviruses. 

Building on the success of recent advancements in protein design, this PhD will aim to exploit differences in surface structure to design de novo mini-protein scaffolds that bind to various but specific locations on alphavirus structural proteins. The PhD candidate will first identify suitable target locations on a virus surface, drawing on recent literature on antibody discovery and host receptor specificity, before using the latest computational tools to specifically design mini-protein binders. The designed binders will then be tested within the laboratory to assess binding affinity and specificity. Any successful candidates could then be further optimised and tested against live virus. 

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Theme(s): Infection and Cellular Biology

Lead partner: Pirbright Institute 
Supervisor: Nicolas Locker, Nicolas.locker@pirbright.ac.uk

Joint partner: University of Exeter 
Supervisor: Michael Schrader, m.schrader@exeter.ac.uk 

Project Summary

During infection, cellular organelles can be exploited by viruses to promote replication or by the host cell to generate immune responses. Peroxisomes are organelles involved in metabolic pathways regulating lipid synthesis and signalling cascades. Peroxisomes have been proposed to contribute to cellular defences against viruses, triggering antiviral immune signalling. In response, many viruses target peroxisomes to evade cellular antiviral response or remodel peroxisome lipid metabolism to favour replication (doi:10.1016/j.tcb.2024.11.006). FMDV is a highly contagious virus infecting a range of cloven-hoofed animals and a major threat to the livestock industry. FMDV circulates in cattle, pigs, buffaloes, sheep, and goats, with varying degrees of clinical outcomes and pathogenesis, and therefore has evolved to evade host responses in a species-manner. However, the molecular basis for these restrictions is unclear. 

Approach

To dissect how peroxisomes contribute to species-specific restriction of FMDV we will combine our expertise in peroxisome biology and virology. 

Objectives

To achieve this, we will:

1. Fingerprint how stimulation with viral mimics (dsRNA) alter peroxisome dynamics applying advanced imaging techniques, and biochemical analysis, in porcine PK15 cells, bovine MDBK cells, and buffalo BKC cells, the latter are of interest because they support replication despite clinical disease being limited in buffaloes. Human A549 cells will be included as FMDV has low infectivity for these cells, and humans are not susceptible to FMD.
2. Establish how peroxisomes contribute to antiviral responses following stimulation with dsRNA, using cell lines with altered peroxisomes through knock out of their specific scaffolding proteins, and measuring the impact on antiviral signalling using reporter assays and qPCR.
3. Characterise how FMDV differentially regulates peroxisome dynamics and function by applying advanced imaging and biochemical approaches. 

Achieving this will reveal novel antiviral functions of peroxisomes, their contribution to FMDV infection and in species-specific restriction of FMDV replication, highlighting novel therapeutic targets.

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Theme(s): Infection and Cellular Biology

Lead partner: Pirbright Institute 
Supervisor: Miguel Hernandez Gonzalez, Miguel.hernandez-gonzalez@pirbright.ac.uk

Joint partner: University of Surrey 
Supervisor: Carlos Maluquer de Motes, c.maluquerdemotes@surrey.ac.uk 

Project Summary

Poxviruses (POXVs) cause major epidemics in humans and animals. Smallpox alone claimed ~300 million lives in the 20th century. After its eradication, vaccination stopped, leaving human populations vulnerable to POXV infections. The 2022 global mpox outbreak, together with the rapid spread of lumpy skin disease virus in cattle, illustrates how quickly POXVs can emerge and spread. Combined with scarce antivirals and abundant animal reservoirs, this underscores the urgent need for control and preparedness. Addressing these challenges requires a deeper understanding of POXV biology and host interactions, as control efforts are complicated by the complexity of these viruses.

When a POXV infects a new cell, the viral core –containing the DNA genome– is delivered into the cytoplasm, initiating a two-step process. First, ~60% of viral genes are expressed within the core, and their mRNAs are exported into the cytoplasm to produce a wide range of proteins that reprogram host pathways to support efficient virus replication. Second, the viral genome is released from the core (i.e. uncoating) to begin replication. How mRNAs and the viral genome are released from the cores remains largely unknown. Likewise, how the viral machinery primes the core for uncoating, and how conserved these processes are among different POXVs, is still poorly understood. Critically, these processes are requisites for establishing infection and thus represent key vulnerabilities for antiviral intervention.

Our breakthrough results identify poxviral proteins involved in mRNA export and genome uncoating, providing the opportunity to uncover their mechanisms. This project will use cell biology, molecular virology, advanced microscopy and proteomics to define the functions of these proteins, assess the conservation of these processes across POXVs, and evaluate their impact on viral infectivity and host range of several POXVs, including monkeypox virus.

This PhD offers excellent training in advanced methods and a collaborative, supportive, and inspiring research environment.

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Theme(s): Infection and Cellular Biology

Lead partner: Pirbright Institute 
Supervisor: Ana Reis, ana.reis@pirbright.ac.uk

Joint partner: University of Surrey 
Supervisor: Carlos Maluquer de Motes, c.maluquerdemotes@surrey.ac.uk

Project Summary

African swine fever (ASF) is a devastating haemorrhagic disease of both domestic pig and wild boar, causing lethality rates up to 100%. It is arguably the biggest threat to the world’s pork industry. The African swine fever virus (ASFV) encodes more than 190 proteins, and many have evolved to modulate antiviral responses. Approximately 30% of the genome is dedicated to multigene family members (MGF). Adaptation of ASFV to cell lines frequently results in spontaneous loss of multiple MGFs, indicating a role in cell tropism. Emergence of attenuated field isolates is often associated with loss of MGF members. Additionally, a growing number of publications has provided evidence that MGFs control type I interferon (IFN) responses. Collectively this suggests that they evolved to overcome critical host factors controlling viral infection. 

We recently demonstrated that a class of MGF proteins recruit the cellular ubiquitin machinery to mediate host protein degradation. The motifs used by MGF proteins were also described in poxviruses by the Maluquer Lab (https://doi.org/10.1128/jvi.01374-18), reflecting a universal strategy in nucleocytoplasmic DNA viruses. We hence hypothesise that these MGF degrade critical antiviral factors involved in immune evasion, host tropism and virulence. 

This project aims to (i) identify the host proteins targeted by MGFs; (ii) elucidate the molecular determinants that mediate targeting; and (iii) characterise their impact on host signalling pathways. Building on this exciting preliminary data and using a wide range of molecular biology techniques and computational biology approaches, the project will determine how ASFV exploits host ubiquitin pathways to destroy key antiviral factors. This will open new avenues onto the role of these factors as well as therapeutic strategies that disable viral targeting and rescue antiviral activity. In the long term, the identification of key host targets of MGFs may pave the way to the generation of ASF resistant pigs.

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Theme(s): Infection and Cellular Biology

Lead partner: Pirbright Institute 
Supervisor: Wilhelm Gerner, wilhelm.gerner@pirbright.ac.uk

Joint partners: University of Surrey  
Supervisor: Christine Rollier, c.rollier@surrey.ac.uk

Project Summary

B cells play a central role in protective immune responses but are also involved in autoimmune diseases. A growing body of work highlights the importance of CD11c⁺T-bet⁺CD21⁻/dim “atypical” B cells, first linked to chronic infection and autoimmunity but now recognised as part of the normal memory pool following vaccination or acute infection with pathogens such as influenza A virus and SARS-CoV-2. Studies in mice and humans suggest that these cells often arise from extrafollicular B cell responses. These responses generate antibodies rapidly yet may differ in durability and quality from classical germinal centre reactions. Understanding how these responses are regulated is key to designing vaccines that elicit both fast and long-lasting protection.

In pigs, CD11c⁺T-bet⁺CD21⁻/dim B cells remain largely unexplored. Preliminary work in our group has identified T-bet⁺ B cells across multiple porcine tissues and demonstrated that CD11c⁺T-bet⁺ B cells can recognise viral antigens such as influenza haemagglutinin and coronavirus spike proteins. These findings allow investigations how this subset contributes to antiviral immunity in an agriculturally and biomedically relevant species.

This PhD project will characterise CD11c⁺T-bet⁺ B cells in pigs to uncover how extrafollicular responses shape humoral immunity. Specifically, the student will:

Map the development and distribution of these B cells across tissues and age groups.

Use in vitro systems to define stimuli and signalling pathways driving their differentiation.

Analyse their role during infection and immunisation with key viral pathogens (influenza A virus, PRRSV, ASFV) using biobanked and new samples.

Working closely with immunology teams at The Pirbright Institute and University of Surrey, this project offers training in advanced flow cytometry, tissue analysis, and molecular profiling, thereby providing the opportunity to contribute to next-generation vaccine research in a cutting-edge translational setting.

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Theme(s): Detection, Prevention and Intervention; Microbial Evolution and Drug Resistance; Infection and Cellular Biology; Understanding Disease Spread

Lead partner: Pirbright Institute 
Supervisor: Steve Fiddaman, steve.fiddaman@pirbright.ac.uk

Joint partner: University of Surrey 
Supervisor: Oluwole Oni, o.oni@surrey.ac.uk

Project Summary

Rationale

Marek’s Disease Virus (MDV) is a tumour-causing herpesvirus of chickens which is estimated to cost the poultry industry $1-2 billion per year. Over the last century, MDV has undergone a considerable increase in virulence, reaching a mortality rate of >90% in unvaccinated birds. Although MDV vaccines do exist, the virus typically evolves to break through vaccine protection every 15-20 years and poses a serious threat to the poultry industry. Despite its importance, very little is known about the circulating diversity of MDV or the genetic basis of virulence evolution. With advances in metagenomic sequencing, we are now in a position to generate a large dataset of MDV genomes and analyse the diversity and evolution of this economically important pathogen. 

Approaches

Working closely with the WOAH-accredited MDV Reference Lab at Pirbright and collaborators in other countries, you will generate a large dataset of MDV genomes using state-of-the-art sequencing methodologies (RNA baiting and Nanopore long-read sequencing).You will then use computational techniques to analyse how different strains are related to each other (e.g. do we see different strains in different geographic regions, or between commercial chicken populations vs. backyard chickens?). You will also identify rapidly evolving genes which are likely to be virulence factors. If you enjoy lab work, there will also be plenty of opportunity to functionally assess virulence factor function, e.g. through genetic modification of MDV using CRISPR, laboratory assays, and (ultimately) in vivo experiments. 

Impact

This project will allow us to understand MDV diversity and evolution in much greater depth, enabling us to establish genomic surveillance of MDV in the UK and abroad and identify lineages of concern as they arise and spread. Furthermore, characterising novel MDV virulence factors will have significant impacts in designing next-generation vaccines. 

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Theme(s): Understanding Disease Spread; Infection and Cellular Biology

Lead partner: Pirbright Institute 
Supervisor: Ahmed Samy Ibrahim, ahmed.ibrahim@pirbright.ac.uk

Joint partner: University of Surrey 
Supervisor: Fernando Martinez Estrada, f.martinezestrada@surrey.ac.uk

Project Summary

Infectious Bursal Disease Virus (IBDV) destroys developing B cells in the bursa of Fabricius (a unique lymphoid organ in birds essential for B cell development), leading to immunosuppression in poultry. However, the severity of disease varies dramatically between strains, from very virulent (vvIBDV), which causes acute systemic infection with high mortality, to variant and some reassortant strains, which cause localised and subclinical infections.

While B cells are the primary target, macrophages are increasingly recognized as key intermediaries in determining disease outcome. They can be infected by IBDV, release inflammatory mediators, and influence how B cells promoting apoptosis, viral replication, and systemic infection. The central hypothesis is that macrophage–B-cell crosstalk in response to different IBDV pathotypes plays a key role in determining IBDV pathogenicity.

Most IBDV research focuses directly on B cells; understanding macrophage–B-cell crosstalk in vitro and in vivo could reveal previously unappreciated immune regulatory mechanisms that define virulence.

By integrating bulk RNA-Seq, reverse genetics, and ex vivo single and co-culture systems, the project can identify specific B cells and macrophage pathways associated with clinical and subclinical IBDV infection. Further, including vvIBDV, subclinical, and engineered chimeric strains enables causal linkage between viral genetics, immune signalling, and pathogenic outcome.

Identifying macrophage and B cells derived mediators associated with clinical and subclinical infection can guide vaccine adjuvant design, improve control strategies, and breeding programs for resistance outcomes with direct industry and food security implications. Moreover, using chickens as a phylogenetically distinct vertebrate model, and IBDV as a virus that specifically targets B cells and can infect macrophages, will help uncover fundamental principles of innate–adaptive immune crosstalk that shape viral immunopathogenesis, providing valuable comparisons to well-characterized systems such as mammals and humans.

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Theme(s): Microbial Evolution and Drug Resistance; Infection and Cellular Biology;

Lead partner: Pirbright Institute 
Supervisor: Dr Lidia Dykes, lidia.dykes@pirbright.ac.uk

Joint partner: University of Sussex
Supervisor: Dr David J Allen, d.j.allen@surrey.ac.uk

Project Summary

Many pathogenic viruses have single-stranded RNA genomes (ssRNA) which can self-anneal forming RNA secondary and more complex structures. These RNA structures regulate molecular processes during viral replication [1]. Some of these RNA structures are conserved among different, and even unrelated, viruses [2-3]. However, due to computational constraints, RNA structure conservation in the absence of sequence similarity is poorly studied. To address this gap, we will utilise recent advances in computational RNA structure prediction [4] to identify and characterise highly conserved secondary and tertiary structures in ssRNA viral genomes.

You will focus on a viral family that includes numerous viruses of medical and veterinary importance called Picornaviridae [5]. We anticipate that, despite genomic changes acquired during evolution, picornaviruses retain common ancestral RNA structures that regulate vital viral processes. To test this, you will receive training in latest bioinformatic methods to computationally predict highly conserved RNA secondary and tertiary structures encoded by different picornaviruses. Then, you will verify these RNA structures using mutagenesis, reverse genetics, and biochemical techniques. Initially, your experimental work will focus on two genomic regions (encoding the 2A-2B and 3Dpol proteins), which are expected to contain conserved RNA structures regulating viral translation and replication. You will also examine the three-dimensional (3D) structure of conserved RNA elements encoded at the 5’ end of picornavirus genomes and their interacting proteins using advanced computational methods. Finally, you will investigate how mutations affect RNA structure during outbreaks caused by different picornaviruses using clinical sequence data.

Conserved RNA structures may offer targets for therapeutics that can avert replication across multiple viral species, which means your results will be novel and publishable. Additionally, this study creates novel methods in virus RNA structure analysis that can be applied to wider taxonomic groups of viruses. 

References

1. RNA Structure—A Neglected Puppet Master for the Evolution of Virus and Host Immunity
2. Comprehensive survey of conserved RNA secondary structures in full-genome alignment of Hepatitis C virus
3. Conserved RNA secondary structures in Picornaviridae genomes
4. Advances and opportunities in RNA structure experimental determination and computational modeling
5. Family: Picornaviridae

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Theme(s): Microbial Evolution and Drug Resistance; Infection and Cellular Biology

Lead partner: Pirbright Institute 
Supervisor: James Kelly, james.kelly@pirbright.ac.uk 

Joint partner: University of Sussex
Supervisor: Andre Gerber, a.gerber@surrey.ac.uk

Project Summary

Viruses, despite encoding much of their own replication machinery, remain entirely reliant on host translation machinery to produce viral proteins. This dependency fuels an evolutionary arms race, with viruses hijacking translation pathways and hosts developing countermeasures. Consequently, interplay between viral infection and host translation is a key determinant of host specificity and virus–host co-evolution.

This project investigates how host translation machinery shaped the evolution of swine vesicular disease virus (SVDV); a porcine picornavirus descended from human picornavirus Coxsackievirus B5 (CVB5). By dissecting cross-species adaptations, we aim to uncover molecular principles governing viral host-shifts and host-range expansion.

Objective 1: Determine how species-specific interactions with key translation factor eIF4G shapes viral host-range 

Picornaviruses hijack host translation by cleaving eIF4G, effectively shutting down host protein production while allowing continued viral translation. Preliminary findings show CVB5 preferentially cleaves human eIF4G, while SVDV favours pig eIF4G - suggesting adaptation to cleave pig eIF4G was pivotal in SVDV’s evolution. Using biochemical/molecular biology approaches - including CRISPR-Cas9 gene-editing - we will pinpoint host sequence determinants and viral adaptions governing eIF4G cleavage specificity. This will advance our understanding of how viruses tune translation to adapt to new species, providing insights into mechanisms underlying future species-jumps.

Objective 2: Identifying species-specific RNA-binding proteins (RBPs) that determine viral host-range

RBPs play critical roles in regulating viral translation. We will use biochemical methods combined with quantitative mass-spectrometry to identify human- and porcine-specific RBPs that interact with viral RNA. This analysis will elucidate how species-specific RNA-protein interactions influence viral host-range and whether SVDV evolved to exploit porcine RBPs for efficient translation. Identification/characterisation of critical RBPs will uncover their contribution to viral adaptation, potentially revealing new targets for antiviral therapies.

Experienced supervisors will provide guidance/mentorship in:

• Handling high-consequence viruses within high-containment facilities
• Advanced biochemical/molecular biology techniques
• Employing cutting-edge assays for identifying/studying RBPs

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Theme(s): Detection, Prevention and Intervention; Infection and Cellular Biology; Understanding Disease Spread

Lead partner: Pirbright Institute 
Supervisor: Dalan Bailey, dalan.bailey@pirbright.ac.uk

Joint partner: University of Sussex
Supervisor: Edward Wright, ew323@sussex.ac.uk

Project Summary

Exciting new evidence indicates that the two endemic, human alphacoronaviruses, 229E and NL63, emerged from bat reservoirs at some point in human history. Although this “origin-story” is like SARS-CoV-2, the missing links, i.e. 229E- and NL63-related viruses in bats, were found in Africa not Asia. 

We have recently identified that some of these viruses can use established coronavirus receptors to enter cells, however, the detailed evolutionary origin of these viruses and their ability to infect human cells remains unclear. Our overarching objective for this studentship is therefore to ‘Understand the zoonotic risk of these 229E and NL63-like bat coronaviruses’. In simpler terms, can these viruses also jump into humans? The knowledge we acquire in this studentship will be used to develop candidate immunogens and therapeutics to these viruses before extensive spillover can occur, aiding global pandemic preparedness. 

Initially, the project will focus on assay development and optimization, using existing global sequence databases to develop a library of lentiviral pseudotypes expressing 229E and NL63-related alphacoronavirus spikes, and examining their entry into cells. Subsequently, we will develop in-house monoclonal antibodies (derived from mouse immunizations), using these and polyclonal sera from human volunteers, to map the breadth of virus neutralization to 229E, NL63 and the related bat viruses. This information will be used to identify the relationship between genotype, antigenicity and immune escape, guiding vaccine development.

The PhD student, based at Pirbright – a National Virology Centre – and Sussex, will gain significant experience in molecular virology and immunology assays, cell biology and tissue culture techniques, whilst working in one of the most rapidly expanding fields in viral immunology (epitope mapping, multivalent vaccines and antigenic conservation). Supervision will be provided by an experienced team of virologists, cell biologists and immunologists and the student will be supported to publish, attend international conferences and build their network.

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Theme(s): Infection and Cellular Biology

Lead partner: UKHSA 
Supervisor: Laura Hunter, laura.hunter@ukhsa.gov.uk

Joint partner: University of Surrey 
Supervisor: Graham Stewart, g.stewart@surrey.ac.uk 

CASE partner: Certara | Accelerating Medicines with Biosimulation and Tech-enabled Services

Project Summary

Mycobacterium tuberculosis is the leading single cause of death by an infectious disease, killing 1.3 million people in 2022. New antibiotics have recently been added to the multidrug panels that constitute the backbone of tuberculosis (TB) treatment. However, M. tuberculosis still presents a frustrating recalcitrance to drug therapy, with treatment regimens typically lasting from 4-6 months even for fully drug sensitive infections. In addition, the only available TB vaccine (BCG) provides only limited protection against infection. One of the main reasons that TB is difficult to target with drugs or immunological strategies is that the bacterium induces and establishes a protected niche in pulmonary granulomas, lesions comprising focussed clusters of immune cells. The granuloma is also the mechanism which drives TB transmission. Surprisingly, we don’t currently have a good understanding of the temporal and spatial dynamics of granuloma formation.

In this project the student will characterise the cellular interactions during the development of the TB granuloma and will combine experimental laboratory-based analysis of immune cell populations and other immunological markers in TB granuloma tissues, with computational modelling of cellular interactions between the TB-bacillus and immune system. Mechanistic, dynamic models will be built in user-friendly software supporting modelling by biologists. The model will be calibrated with experimental data obtained by the student and used to facilitate understanding of complex underlying biology and generation of hypotheses for the next stage of experimental work. An understanding of the granuloma and the capability to computationally model the effects of drug/immune interventions will make a major contribution towards the development of novel TB control strategies.

The project will be based at UKHSA, but with aspects performed at the University of Surrey and with Certara, a company supporting drug development with modelling, thus providing a unique experience of research in university, government agency and industry environments.

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