From a background in chemistry, I completed a PhD with Dr Edgar Deu at The Francis Crick Institute, where I used chemical proteomics to investigate the malaria-causing parasite Plasmodium falciparum. As a postdoctoral researcher in the Tower’s lab I am working with clinicians at Great Ormond Street Hospital to improve the efficiency of gene therapy. Gene therapy is used to treat rare genetic disorders, for example severe combined immunodeficiency (SCID). In these cases, patient stem cells are treated in vitro with a viral vector to deliver a correct copy of the defective gene and then replaced in the patient. These treatments can provide long-term relief but are costly, as viral infection of stem cells is inefficient and requires a lot of viral vector. We have identified a protein called IFITM3 that appears to protect stem cells from viral infection. My project involves investigating molecules that cause the degradation of IFITM3 and therefore improve gene therapy efficiency.  We will also use the tools that we develop, along with proteomics techniques, to investigate the underlying mechanisms involved and how IFITM3 plays its crucial role in innate immunity.

I joined the Towers lab in 2023 as part of the Antiviral Drug Discovery (AViDD) collaboration to characterise novel drugs targeting SARS-CoV-2. My research focusses on how SARS-CoV-2 evades the innate immune response.

Viral infection stimulates a host interferon response, which triggers the addition of ADP-ribose to a range of host proteins by poly-(ADP-ribose) polymerases (PARPs). ADP-ribosylated host proteins, in turn, modulate antiviral activity and alter permissivity of the interferon-stimulated cell, thereby restricting viral infection. SARS-CoV-2 non-structural protein 3 contains a macrodomain, which the virus uses to remove ADP-ribose from host proteins, allowing it to evade the innate immune response. However, the target proteins and mechanisms of viral evasion and restriction are not well-understood. By studying how SARS-CoV-2 manipulates our immune response using its macrodomain, we can investigate the mechanism by which PARPs drive the innate immune response to viruses, and contribute to the development of antiviral therapeutics for COVID-19.

Before working at UCL, I started my career as a Scientist at GSK, developing novel Complement therapeutics for autoimmune conditions. I later completed my PhD in the GSK Immunology Network, an industry-academia collaboration, in collaboration with Trinity College Dublin and Cardiff University. My work focussed on the immunomodulatory function of atypical Complement receptor C5aR2 in myeloid cells, and its regulation of the antiviral innate immune response.

During my PhD training with Malik Peiris at the University of Hong Kong, I specialized in Virology. My PhD research focused on unravelling a fascinating mystery: Why were there no reported cases of Middle East Respiratory Syndrome (MERS) in humans in Africa? I genetically and phenotypically characterized camel MERS-CoVs obtained from African surveillance studies, in comparison with those infecting human in Middle East. Now, as a Postdoctoral Research Fellow in Towers' lab, I am excited to continue my Virology journey on coronaviruses.  I am interested to explore the evolutionary changes in the non-spike proteins of SARS-CoV-2, which are responsible for modulating the innate immune system. My objective is to identify and characterize the mechanism of new antiviral compounds that can target these proteins and how they influence the host's innate immune response to viral infections.

I am investigating how flaviviruses exploit host cyclophilins for replication and innate immune evasion. Flaviviridae include important human pathogens without effective antivirals or vaccines, for example, Dengue and Zika viruses. The cyclophilin family of proteins are reported to be co-opted by diverse viruses as cofactors. For example, in the case of Hepatitis C virus, cyclophilin A interacts with the NS5A viral protein, contributing to replication and innate immune evasion. I am taking genetic and pharmacological approaches to investigating how Dengue and Zika manipulate host cyclophilin proteins using a series of commercial inhibitors as well as novel inhibitors developed in collaboration with the medicinal chemistry group of Prof David Selwood at UCL.  This work will not only increase our understanding of cyclophilin function and and its role in innate immune defences but may also provide novel therapeutic avenues for Flaviviridae diseases. Before Joining UCL, I used state-of-the-art molecular cell biology techniques to study host-pathogen interactions at ICGEB Trieste, KCL and University of Cambridge. During my pre-doctoral and postdoctoral research I have worked on HIV-1, SARS-CoV2 and Enteric viruses characterising host virus interactions during the replication process. My long-term goal is a detailed understanding of the mechanisms that allow +ssRNA viruses to exploit host machineries to infect, replicate and transmit between diverse hosts while effectively antagonising and evading host innate immunity.

All viruses have evolved strategies to evade host innate immune sensing, and previous work in the Towers lab has linked effective immune evasion to viral pandemic potential. My current research uses HIV accessory proteins Vpr and Vpx as powerful molecular tools to dissect host innate immune and epigenetic responses to infection. Notably, pandemic HIV-1 encodes only Vpr, and evades immune sensing more effectively than non-pandemic HIV-2, which encodes both Vpr and Vpx. My work examines how Vpr/Vpx manipulate host epigenetic silencers, including HUSH and HUSH2, to regulate innate immunity. My work aims to uncover fundamental principles of antiviral defence and how viruses evolve to exploit or evade these systems.

I was awarded my PhD by the University of Sheffield in 2021, where I investigated DNA damage and senescence responses to the typhoid toxin of Salmonella Typhi. This work revealed how bacterial genotoxins drive host pathology relevant to chronic infection and cancer, and was published in Nature Communications, Cell Reports and EMBO Molecular Medicine. I remained in the same laboratory as a postdoctoral research associate for a further two years, continuing my work on bacterial-host interactions, before moving to the Towers lab at UCL and QMUL.

During my PhD, I focused my studies on innate immune sensing pathways. Specifically, I explored and characterised the MAVS-dependent antiviral response in mammalian cells. Under the guidance of Daniela Ribeiro at the University of Aveiro (Portugal) and Jonathan Kagan at Boston Children’s Hospital (USA), I delved into MAVS signalling features across different subcellular environments, as well as the impact of interorganelle contacts in the cellular defence against RNA viruses.

 As a postdoctoral researcher in the Towers’ lab, I’m excited to explore the connection between innate immunity and chemotherapy mechanisms. While cancer outcomes improve with advancing therapies, the precise mechanisms of certain standard treatments remain undetermined. Anthracyclines, powerful anticancer agents, exhibit immunomodulatory effects within the tumor microenvironment that can be crucial for combating tumor growth. My current focus is on understanding how anthracycline-mediated interferon responses are regulated. By combining these insights with other cancer therapies, I aim to get closer to efficient ways of combating drug resistance and enhance patients’ sensitivity to life-saving treatments.

During my PhD at Leipzig University (Germany), I focused on the interplay between coagulation and immune pathways, uncovering a novel regulatory link between inflammation and thrombosis, known as thromboinflammation. Specifically, I identified a molecular interaction between tissue factor, a coagulation initiator, and interferon-alpha receptor-1, a key immune regulator. This research demonstrated relevance across a range of pathological contexts, including sterile inflammation, systemic inflammation (sepsis and COVID-19), cardiovascular diseases such as myocardial infarction and atherosclerosis, and rare congenital interferonopathies.

As a postdoctoral researcher in the Towers Lab, I am investigating how coronaviruses manipulate host immune responses to evade detection. My current work focuses on SARS-CoV-2, specifically exploring how the viral proteins interacts with host transcriptional regulators to suppress interferon-stimulated genes. Using a multidisciplinary approach involving computational biology, proteomics, transcriptomics, and epigenomics, I aim to uncover the broader immune evasion mechanisms used by coronaviruses. Ultimately, I hope this research will inform new therapeutic strategies and improve global preparedness for future coronavirus outbreaks.

I undertook my PhD in the Towers lab working on lentiviral Vpr proteins. I am now working as an infection doctor at UCLH and an occasional science presenter for the BBC often with the help of the Towers lab. I maintain links with the Towers lab through my position as a Honorary Professor at UCL. I’m still on the Vpr team and help on the lab's wide ranging outreach projects.

I am a PhD student funded by the Evolution Education Trust. My project aims to understanding the relationship between transposable element expression, innate immune activation and outcome in cancer. Transposable elements (TEs) are virus-like genes that are expressed after viral infection and in cancer but whether they have a role in these processes is poorly understood. We hypothesise that TE have evolved to be expressed in these situations because they activate immune responses by mimicking viral infection. Thus, in cancer and infections, TE expression activates innate immunity and attracts immune cells, which can then resolve disease. We will test this hypothesis by exploring the relationship between transposable elements (TEs) expression and markers of innate immune activation and cancer outcome in cancer sequencing datasets. We are excited to understand how TE expression links to innate immunity because TE expression can be manipulated therapeutically thereby providing novel therapeutic opportunities to diseases where TE regulated inflammation plays a role.

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