Supervisors and projects

Helen is broadly interested in infectious disease dynamics and microbial ecology & evolution, especially for bacterial and viral pathogens. Her interdisciplinary research group uses both mathematical modelling and wet lab experiments to address these topics. Current research topics in her group include evolution of antibiotic resistance, stress-induced mutagenesis in bacteria, and dose-response relationships for pathogens infecting hosts.

Alexander group website

Research Explorer for Helen Alexander

Possible project: Modelling evolution of antibiotic resistance and optimal drug dosing, optionally linked to experimental quantification of bacterial population dynamics

Link to publications available

Katie's personal website

1. Evaluating the trajectory of HIV drug resistance, 
2. Using phylogenetics to understand transmission of bacterial drug resistance
3. Quantifying the impact of RSV vaccines using mathematical modelling

Our research is aimed at understanding the molecular mechanisms by which pathogens adapt to, and manipulate, their hosts. This research enhances basic understanding of small RNA regulation and trafficking and illuminates host-pathogen interactions that could play a role in persistence and tolerance. We use both viral and helminth models to examine the mechanisms by which small RNAs are regulated to control cells, and how these can traffic outside of cells.  One application of our work is the development of small RNA based diagnostics for helminth infection, building on our findings related to nematode secreted RNAs in body fluids.

Buck lab website

Research Explorer entry for Amy Buck

Possible projects:  Argonaute exchange between stromal and immune cells: tracking RNA communication in action

Developing country collaborators:  Dr Vincent Tanya, Cameroon Academy of Sciences, Yaoundé, Cameroon.

The mechanisms involved in immunity to malaria are complex and not fully understood, but it is known that antibodies play an important role. We are using and developing new next-generation sequencing and single-cell genomics techniques to characterise immunity to malaria to understand the exact nature of non-sterilising asymptomatic immunity to malaria. By understanding the timings and contributions of different immune effector mechanisms, as well as the antigen epitopes involved, we aim to contribute to the design of an effective malaria vaccine.

Cowan lab website

Research Explorer entry for Graeme Cowan

Possible project:  Characterisation of the T-cell response in malaria

Macrophages play a key role in the pathogenesis of Infectious diseases.  We are interested in understanding how key macrophage innate immune functions protect healthy individuals against infection, despite recurring challenge, and how these core responses are perturbed by human disease inducing susceptibility to infection.  We believe that by optimising innate immune responses we can limit our reliance on antimicrobial therapy and provide an alternative strategy to that focused on targeting pathogens by vaccine responses or with antimicrobials to which they can develop resistance.  In this context we study a variety of bacterial infections but focus in particular on Streptococcus pneumoniae and other respiratory pathogens.  We also examine Staphylococcus aureus and are interested in how HIV and other viral infections alter the macrophage responses to bacteria. 

Dockrell lab website

Research Explorer entry for David Dockrell

Possible project:  Genetic basis and temporal trends in AMR of ESKAPE pathogens

Toxoplasma gondii is a ubiquitous foodborne apicomplexan that infects all warm-blooded vertebrates, including more than a billion people worldwide, and can cause life-threatening illness in immunocompromised patients, the elderly, and developing foetus.

Musa's lab is interested in identifying how; (a) host cell-autonomous responses, and parasite’s virulence mechanisms, define acute and chronic infections in humans and livestock, and (b) heterogenous host cell-parasite encounters regulate overall pathogenesis. This is achieved by applying functional genomics, genome-editing, immunological, parasitology, and computational approaches that collectively enable us to comprehensively monitor host-parasite interactions within the context of in vitro and ex vivo infections.

Musa's research explorer page

Possible projects:

(1) Identifying how interferon-stimulated genes regulate Toxoplasma growth in porcine and human cells

(2) Using single-cell RNA-seq to interrogate host immunity to pathogens.

Developing country collaborators: We are also affiliated with the Centre for Tropical Livestock Health and Genetics (www.ctlgh.org) through which we have collaborative projects with scientist in several developing countries including Kenya, Ethiopia, Nigeria, Cameroon, and Tanzania.

The main interest in the Kaufman lab is the evolution of immunity, focusing on the chicken MHC.

Among his discoveries are the:

1. existence of single dominantly-expressed chicken class I and class II molecules which determine the immune response to pathogens and vaccines,

2. importance of co-evolution between polymorphic genes that lead to the expression of a single class I molecule, and

3. presence of lectin-like (NK) receptor and CD1 genes suggesting they were present in the primordial MHC.

He continues to explore the:

1. roles of chicken MHC molecules in resistance to pathogens and response to vaccines,

2. roles of polymorphism and co-evolution for MHC genes involved in antigen presentation, and

3. ramifications of our findings for the evolutionary history of the MHC.

Jim's long-term plans include whole genome studies in chickens, development of chickens as a system with a smooth transition between field and laboratory for study of natural pathogens in a natural host, and work on other vertebrates.

Kaufman lab website - please note Jim is relocating from Cambridge to Edinburgh in January 2020

Possible projects:  (1) Identifying “functional alleles” of chicken BG genes in intestinal epithelial cells; (2) Identifying proteins interacting with chicken BG molecules; (3) Expression and structure of the chicken class I molecule BF1

Our group studies how infectious diseases spread and are maintained in populations. We analyse viral sequence data, linking viral phylogenetics to epidemiological network models. Most of our work is on HIV, and we have projects based both here, using the 100,000 HIV sequences in the UK HIV Drug Resistance Database, and in Africa where we collaborate particularly closely with the MRC/UVRI Uganda Research Unit on AIDS (http://www.mrcuganda.org/) in Entebbe. The 3 postdocs in the group (2 affiliated students are based in Entebbe and Brighton) are funded by the NIH and by the Bill & Melinda Gates Foundation through consortia including colleagues in the University of California San Diego, the Wellcome Trust Sanger Institute, and UCL.

Leigh-Brown lab website

Research explorer entry for Andrew Leigh-Brown

Possible project:  Are multiple HIV strains transmitted during mother-to-child transmission?

Developing country collaborators:  Prof Pontiano Kaleebu & Dr Deo Ssemwanga, MRC/UVRI Uganda Research Unit, Entebbe, Uganda; Profs Deenan Pillay and Tulio de Oliveira, Africa Centre for Health and Population Studies, KwaZulu Natal, South Africa

Wild animals do not carry birth certificates.  How can we accurately know the age of a wild animal? If we could estimate age in the wild, we could begin to ask what causes rapid aging to accelerate? Recently, medical science has developed an epigenetic clock based on DNA methylation, and it is a highly accurate biomarker of age that can be used to predict mortality or determine if individuals have aged faster than their chronological age suggests.

This project, in collaboration with Amy Pedersen, will develop and deploy a DNA methylation clock for a wild mouse, the wood mouse Apodemus sylvaticus, to address a set of fundamental questions about the biology of ageing, such as: ‘What is the cost, in terms of age acceleration, of living in the wild?  What is the cost of nutritional deficiency?  What is the cost of infection? Of coinfection? Of treatment?  Of vaccination?’

Little lab website

Research explorer entry for Tom Little

Possible project:  What causes accelerated biological age?

The organism’s first line of defence against viruses is the innate immune system. In mammals, viral infections trigger a very potent antiviral response, known as the type-I interferon, which is essential to initiate the antiviral state in both the infected and neighbouring cells. Our group is interested in understanding how cells control the activation of the antiviral defence mechanisms, and specifically in understanding the role of miRNAs in controlling the antiviral response.

Macias lab website

Research Explorer entry for Sara Macias

Possible project:  INTERFERing with pluripotency

Immune regulation, including tolerance and repair mechanisms, are a critical aspect of the immune system to keep autoimmune, allergic and inflammatory disease at bay. In the complex and changing environment humans and animals live in, including pathogenic threats that need to be controlled, how is adequate immune regulation maintained?

Building on the vast body of knowledge which has been accrued through controlled laboratory studies mainly using the house mouse model species, our group uses an interdisciplinary, ecoimmunological approach by investigating immune regulatory phenotypes and functional markers in house mice living in their natural habitat (Isle of May, UK). Using longitudinal and interventional study designs, and cutting-edge immunological techniques, we investigate how environmental and host factors combine to shape immune regulation, with a particular focus on barrier sites such as the gut and the skin.

University profile for Iris

Contact Iris

Possible projects:  (1) The effect of seasonal weather changes on immune regulation and repair at barrier site; (2) The interplay between the gut microbiome and regulatory T cell location and phenotype in gut, and their relationship with gut and host health

African trypanosomes are protozoan parasites that cause sleeping sickness. My lab is interested in how these parasites successfully progress through their life cycle to achieve disease transmission. Particularly, we study (i) how the parasites communicate with other trypanosomes in the blood of mammalian hosts to prepare for their uptake by tsetse flies, and (ii) how they detect their transmission to the tsetse fly and undergo cellular development to assist their survival. We use a combination of molecular cell biology, parasite biology, gene expression control and parasite genetic manipulation to understand the mechanistic basis of these life cycle transitions and their implications for parasite virulence and control.

Matthews lab website

Research explorer entry for Keith Matthews

Possible project:  Cell-cell communication in African Trypanosomes

Developing country collaborators:  Vincent Delespaux, Antwerp, Burkina Faso, Ethiopia, Zambia (depending on project)

Work in my lab focuses on the ecology and evolution of these attack and defence strategies in bacteria to unravel why bacteria use particular mechanisms of attack and defence and the consequences of these strategies for their communities.  We take a multidisciplinary approach to these problems, using a combination of mathematical models, experiments, and statistical analysis of large-scale bioinformatic and epidemiological datasets.

Some current projects are:

1. How does competition shape the spatial structure of microbial communities?
2. What determines the rate of emergence of antibiotic resistance?
3. How will bacteria evolve in response to manipulation of the microbiome?

McNally lab website

Research Explorer entry for Luke McNally

Possible project:  Where should we focus efforts to tackle the antimicrobial resistance crisis?

My research interests are the infection biology of protozoan parasites of livestock and humans, with a particular focus on African trypanosomes. I am interested in how genetic variation in parasites (e.g. between different strains or species) translates to variation in phenotype – we are trying to understand this with respect to drug resistance, antigenic variation and pathogenesis for the trypanosomes of relevance to livestock, Trypanosoma congolense, T. vivax and T. brucei. Additionally, we exploit analysis of the host immune response (mainly cattle but also mouse infection models) to understand the key host-parasite interactions that determine disease outcome.

Research explorer entry for Liam Morrison

Possible project:  Exploring metabolism and drug resistance in the African trypanosomes

Developing country collaborators:  I work with GALVmed, in South Africa, Mozambique, Burkina Faso, Ethiopia and Malawi; Field scientists at the Tsetse and Trypanosomiasis Research Institute in Tanzania studying trypanosomiasis and East Coast Fever in and around the Serengeti National Park. 

Maddie’s research focuses on bacterial host pathogen- interactions, with emphasis on the molecular genetics of Mycobacterium tuberculosis dissemination and extrapulmonary spread. Tuberculosis remains one of the leading causes of death due to infectious disease worldwide, and dissemination is a critical aspect of M. tuberculosis pathogenesis because it is required both for the establishment of secondary granulomas within the lungs and extrapulmonary infections that are particularly difficult to diagnose and treat.

Her work addresses this question through the identification and characterization of bacterial virulence factors in air-liquid interface cultures and other three-dimensional models of the human lung. She has also expanded her work with these model systems to include research on the host-pathogen interactions of  Burkholderia pseudomallei and other bacterial pathogens which have re-emerged as threats to human health due to the rise of antimicrobial resistance including Pseudomonas aeruginosa and MRSA.

Find Maddie on Research Explorer

Contact Maddie

Potential rotation project: Regulation and function of miR-23/27/24 in mycobacterium infection in human and mouse lung culture models (Joint project with Amy Buck)

My group focuses on global health and tropical disease research working mainly on the neglected tropical disease schistosomiasis (bilharzia). The scientific research is focusing on developing better interventions based on enhancing the host’s immune innate and adaptive protective responses and developing improved diagnostics based on serological and molecular markers of infection/disease.  Our work integrates field studies in Africa of the host-parasite interaction focusing on parasite molecular biology and genetics, host immunity, genetics and microbiome structure and relating these to the epidemiology of the infection/disease.  Our results have been informing global schistosome and other helminth control and intervention programmes.   

Mutapi lab website

University profile for Francisca Mutapi

Possible project:  Using novel approaches to determine the efficacy of childhood vaccines

Developing country collaborators:  Prof Takafira Mduluza, Department of Biochemistry and Prof Nicholas Midzi, Medical School, University of Zimbabwe; Dr Nadine Rujeni, College of Medicine and Health Sciences, Univesity of Rwanda; Dr Pauline Mwinzi, Kenya Medical Research Institute (KEMRI)

Thumbi Mwangi is a Kenyan veterinarian using applied epidemiological modelling and data science to improve the speed and quality of policy decision making in human and animal health.  His current research includes implementation research for the elimination of dog-mediated human rabies, syndromic surveillance for early detection of zoonotic spillover, transmission and control of zoonoses, livestock interventions for improvement of human nutritional status, and more recently transmission dynamics and control of SARS-CoV2 in Kenya.

Find Thumbi on Research Explorer

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I am an evolutionary ecologist interested in understanding the causes and consequences of variation in immunity and ageing in wild and domestic ruminant populations. Most of my current work centres on the long-term study of wild Soay sheep on the remote St Kilda archipelago, but I am also closely involved in collaborations involving a range of other wild animal populations, as well as with animal health and veterinary researchers working on domestic ruminants. A focus of our recent work has been to test the power of biomarkers developed within the fields of epidemiology, biogerontology and veterinary immunology to explain variation in the ageing process in the wild, and to test their ability to predict health and productivity in ruminant livestock.

Nussey lab website

Research Explorer entry for Dan Nussey

Possible project:  Leukocyte telomere length, health and fitness in wild and domestic ruminants

Obbard lab website

Research Explorer entry for Darren Obbard

Possible project:  Phylodynamics of insect RNA viruses in the wild

Our research aims to understand how parasites impact the health and fitness of their human and animal hosts, specifically by incorporating the complexities of natural systems to better develop effective intervention strategies. We integrate an array of methodologies (lab and field experiments on a wild rodent – parasite system, modelling, statistical methods, meta-analysis, etc.) to (i) evaluate interactions that occur between co-infecting parasites and the immune response to understand rates of disease spread and impacts on host health; and (ii) strive to elucidate the factors that drive host shifts and disease emergence in multi-host parasites. 

Pedersen lab website

Research explorer for Amy Pedersen

Possible project:  The ecology of infection and immunity in wild mice

Developing country collaborators:  Prof Eric Fevre, University of Liverpool, UK - based in Nairobi, Kenya (ILRI)

My lab is intersted in two main aspects of malaria biology.

1. Organisation of signaling pathways during malaria parasite infection and transmission:  Protein phosphorylation plays a central role in numerous signalling pathways critical to cell proliferation and development.  In Plasmodium, the causal agent of malaria, protein phosphorylation is critical for its development and virulence, but the associated regulatory signalling networks are poorly understood.  Using state of the art proteomic, chemical genetic and bioinformatics tools we intend to systematically define functional signaling networks regulated by phosphorylation modulating enzymes during two key stages of the malaria parasite life cycle: host cell infection and host-to-mosquito transmission.
2. RNA binding proteins mediated regulation of Plasmodium development:  The malaria parasite has a complex life cycle requiring both a mammalian host and mosquito vector. Almost 200 RNA binding proteins (RBPs) are expressed at distinct stages of Plasmodium lifecyle where they are implicated in both parasite development, and host-to-vector and vector-to-host transitions. We recently identified a family of RBPs which play crucial roles in parasite growth in the host erythrocyte and development of the mosquito infective form. We aim to understand how these RBPs are regulated and what RNA molecules they regulate.

Philip lab website

Research explorer entry for Nisha Philip

Possible project:   Role of Ubiquitin dynamics during malaria parasite development

My research focuses on the evolution and epidemiology of emerging human and animal pathogens, in particular, fast evolving RNA viruses that have been sampled through time. I have contributed to the research on most of the major virus epidemics that have emerged in recent times including Ebola virus in West Africa, SARS-CoV, MERS-CoV, pandemic influenza in 2009, H7N9 avian influenza, hepatitis C virus and HIV. For these viruses in particular, my research has provided some of the crucial initial characterization of the epidemics, their molecular epidemiology and evolution, and the timing of their origins which, by the time the epidemic is detected, is often obscure.

Rambaut lab website

Research explorer entry for Andrew Rambaut

Our research focuses on malaria parasites, which are an excellent model system to study host-parasite-vector interactions, and because malaria parasites are important (they and their relatives cause some of the most serious infectious diseases of humans, livestock, and wildlife). We use evolutionary theories and ecological principles to help us understand what parasites do during infections, and why they do things in these ways. We are evolutionary ecologists at heart but we also dabble in parasitology, chronobiology, behavioural biology, genetic modification, mathematical modelling, immunology, various ‘omics, and biophysics.

Reece lab website

Research explorer entry for Sarah Reece

Possible projects:  Sophisticated strategies for evolutionary success in malaria parasites

Women have stronger immune responses than do men to most infections, but suffer from greater levels of autoimmunity, and this sex difference is apparent throughout the animal kingdom.

We use live imaging and the elegant genetics possible in Drosophila to understand how dynamic behaviors of immune cells differ between sexes, and how these affect the response to infection, inflammation, ageing and survival.

Jenny Regan profile

Possible project:  Can short-term rapamycin treatment in middle age maintain immune function and reduce systemic inflammation in the model organism Drosophila melanogaster?

A unique feature of human malaria caused by Plasmodium falciparum is the ability of infected erythrocytes to bind to blood vessel walls leading to blockage of micro-vascular blood flow.   This can lead to life-threatening disease due to hypoxia, acidosis, inflammatory changes, organ dysfunction and death.  The aim of our research is to characterise the parasite adhesion molecules and human cell receptors and serum proteins that interact to cause adhesion of infected erythrocytes. We focus on two adhesion types that are associated with severe malaria in young African children – rosetting with uninfected erythrocytes and binding to human brain endothelial cells. We aim to identify that receptor-ligand interactions leading to adhesion, and develop interventions to block or reverse adhesion to prevent deaths from severe malaria. 

Rowe lab website

Research explorer entry for Alex Rowe

Possible projects:  Which host receptor mediates binding of Plasmodium falciparum-infected erythrocytes to human brain endothelial cells?

Developing country collaborators:  Prof Tom Williams and Prof Kathryn Maitland, KEMRI-Welcome Research Laboratories, Kilifi, Kenya and Mbale Regional Hospital, Ugand; Dr Peter Olupot-Olupot, Mbale Regional Hospital, Uganda; Professor Ogobara Doumbo, University of Mali, Bamako, Mali

Our lab studies the mitochondrial biology of trypanosomes, single cellular organisms that are important parasites of man and livestock. Our research is driven in equal measure by two goals: to understand the fascinating biology of these parasites and to help alleviate the suffering they cause. These organisms have taken biological principles that underpin all life on earth and twisted them into something bizarre and unique. This is particularly true for their mitochondrial biogenesis and the structure and expression of their mitochondrial genome, which we study and exploit for the development of new drugs.

Schnaufer lab website

Possible project:  Mitochondrial biogenesis and function in trypanosomes

Evolution of viruses, bacteria and other parasites including malaria. My research employs computer analyses of nucleotide and protein sequence data to address a range of evolutionary questions.

Viral evolution: what are the origins of human viruses, and what factors influence their genetic diversity? A particular focus has been the origins and evolution of AIDS viruses.

Bacterial evolution: what do bacterial genome sequences tell us about evolution? Two particular areas involve the evolution of synonymous codon usage bias, and the evolution of repetitive sequence families.

Sharp lab website

Possible project:  Genome evolution of malaria parasites

The Spence lab asks how children become immune to severe malaria.  This is a key question because malaria continues to kill hundreds of thousands of children each year; parasite drug-resistance threatens malaria control worldwide; and the only licensed malaria vaccine has low and short-lived efficacy.  A better understanding of the immune response to malaria is crucial to improving disease control.

Spence Lab website

Research Explorer entry for Phil Spence

Possible project:  Mechanisms of disease tolerance in human malaria

The orchestration of a successful immune response requires a tight balance between mobilising a sufficient and correct effector response, whilst simultaneously regulating that response to prevent it becoming pathogenic. Helminth parasites excel at subverting this balance, using the host's own immune regulatory mechanisms to prevent effective immunity, resulting in immune suppression and chronic infection in the majority of individuals. 

The goals of my research are to use murine models of filariasis ( Litomosoides sigmodontis) and schistosomiasis to understand how T cell responses are positively and negatively regulated during helminth infections, and to develop therapeutic interventions allowing us to manipulate the regulatory/effector balance to restore protective immunity.

Taylor lab website

Research Explorer entry for Matt Taylor

Possible project:  Does viral infection worsen allergic inflammation by stimulating T cell plasticity

Vale lab website

Research Explorer entry for Pedro Vale

Possible project:  Mitochondrial genetic effects on antiviral innate immune responses

Prerna is a lecturer in the School of Biolgical Sciences. 

Before joining the Institute of Immunology and Infection Research she was a postdoctoral fellow at the Roslin Institute, studying the pathogenicity of Salmonella .  Since starting her own group she has continued this work, evaluating the cross-protective efficacy of a novel, live-attenuated vaccine against Salmonella infection.

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The Welburn research group focusses on human sleeping sickness and zoonotic trypanosomiasis and other neglected zoonoses in domestic wild and animal populations.  The lab's research concentrates on the design and use of molecular diagnostic tools for the study and management of the neglected zoonoses.  Research encompasses ‘grass-roots’ fieldwork in Africa to laboratory-based dissection of the problem at the gene level.  Activities include development and application of diagnostic tools and application of quantitative and qualitative methods for the estimation of disease burden of neglected zoonoses and strategies for disease control. Sue's experience ranges from the management of high-tech laboratory research to the running of applied field projects in developing countries.

Welburn lab website

Research explorer for Sue Welburn

Developing country collaborators:  Professor Charles Waiswa, COCTU (Co-ordinating Office for Control of Trypanosomiasis Uganda) and Prof John David Kabasa, Animal Resources and Biosecurity (COVAB); Makerere University, PO Box 7062 Kampala, Uganda, East Africa

My research interests concern the dynamics of infections of animals and humans at different scales, from the interaction of a parasite or virus with host cells through to global estimates of disease burden. This work involves the close integration of field studies, laboratory experiments and theoretical analyses and draws on collaborations between epidemiologists, mathematical biologists, geneticists, molecular biologists, immunologists and others. My group studies a variety of infectious disease systems ranging from prion diseases to viruses, bacteria, protozoa and helminths. The common theme is the development of a formal, quantitative understanding of the dynamics of parasites and pathogens within hosts and host populations with particular emphasis on understanding how novel pathogens, including antimicrobial resistant strains, emerge in human populations.

Woolhouse lab website

Research explorer entry for Mark Woolhouse

Possible projects:  Genomic epidemiology of antimicrobial resistance at the human and livestock interface

Developing country collaborators: Dr Steve Baker, Oxford University Clinical Research Unit, Ho Chi Minh City, Vietnam; Prof. Eric Fevre, ILRI, Nairobi, Kenya

The focus of my research is the role of the Epidermal Growth Factor (EGF-R) in the regulation of our immune system.

Zaiss lab website

Research Explorer entry for Dietmar Zaiss

Possible project:  Single cell sequencing based analysis of Listeria-specific CD4 T-cell responses

The primary interest of the Zamoyska lab is in T cell signalling (right) and how signals through the T cell receptor influence T cell homeostasis and the ability of T cells to be activated by antigens. Our research focuses on unraveling the roles and regulation of signaling molecules that are activated proximally to TCR engagement. Using genetic modification to introduce functional mutations or to manipulate expression of these molecules we aim to understand how they influence T cell activation, proliferation and differentiation into effector cells without leading to autoreactivity that can result in autoimmunity.

Zamoyska lab website

Possible project:  Regulation of T cell activation