Professor Greg Towers, BSc, PhD

Professor of Molecular Virology
Centre: Centre for Immunobiology and Infection
Email: g.towers@qmul.ac.ukWebsite: https://www.towerslab.co.uk/
Profile
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During his PhD Greg studied HIV transcriptional regulation with Mary Collins at the Institute of Cancer Research in South Kensington, London awarded in 1995. He then carried out a post doc with Jonathan Stoye at the National Institute of Medical Research in Mill Hill London where he helped identify the antiviral restriction factor Fv1 (1995-98). He then worked at Gene Therapy Institute Genethon in Paris as a staff scientist in Paris, France, where he studied mechanisms of Fv1 restriction and how similar antiviral activities in human cells limit gene therapy efficacy (1998-99). In 1999 he moved to London to the lab of Robin Weiss at UCL and won Wellcome career development (2001-05) and then senior fellowships (2005-15) to establish his lab followed by an Investigator Award (2020-25) and most recently a Wellcome Discovery Award. He was awarded a chair in Molecular Virology from UCL in 2006. He moved his lab from UCL to QMUL in 2025 where he is now a Professor of Molecular Virology in the Blizard Institute in Whitechapel. His lab studies innate immune systems, how viruses evade or activate them, and how this links to viral tropism and pathogenesis. He also studies innate immune sensing in cancer and how this links to outcome and chemotherapeutic efficacy. |
Teaching
Greg continues to teach guest lectures at UCL and is considering teaching opportunities at QMUL.
Research
Research Interests:
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Innate immunity has evolved to protect us from infection and probably also cancer. Innate Immune sensors detect when things go wrong, cellular transformation or infection, and their activation leads to gene expression change. For example, chemokines and cytokines regulate adaptive immune responses and interferons induce expression of genes with antiviral and antibacterial activity. However, pathogens have evolved to infect us despite our immune defences. In this case, the responses that have evolved to protect us are dysregulated and over activated leading to disease. We would like to understand in molecular detail how all this works. We use viruses including HIV, SARS-CoV-2, Zika Virus, Middle Eastern Respiratory Syndrome Coronavirus (MERS-CoV) to ask questions such as, how do viruses escape innate immunity to promote infection but then activate it to promote disease? How does innate immunity get activated and what is the nature of the response that is unleashed? How do antiviral factors work and how do viruses evolve to escape them? We also consider how all this works in cancer, with our work in cancer informing our work in infection and vice versa. We would like to understand what is special about pandemic viruses, can we predict which viruses are most dangerous by working out which ones are the best at innate immune evasion and antagonism? Can we use the information we glean from studying how viruses work to make broad-specificity host-targeting antivirals (we can but can we make them effective enough for the clinic). Do anti-cancer chemotherapy drugs work by activating innate and adaptive immunity against cancer and can innate immune activation explain cancer outcome? Can we make gene therapy work better by making inhibitors of innate immunity that enhance gene delivery? We are molecular biologists but collaborate to access advanced structural biology, AI, microscope and computational approaches. We are funded by the Wellcome Trust, UKRI, the Rosetrees Foundation and the Evolution Education Trust. We are always looking for smart people to join us. |
Publications
Reuschl et al. (2024) Evolution of enhanced innate immune suppression by SARS-CoV-2 Omicron subvariants. Nat Microbiol 9:451-463.
Dickson et al. (2024) The HIV capsid mimics karyopherin engagement of FG-nucleoporins. Nature 626:836-42
Bouhaddou et al. (2023) SARS-CoV-2 variants evolve convergent strategies to remodel the host response. Cell 186:4597-4614.e26.
Zuliani-Alvarez et al. (2022) Evasion of cGAS and TRIM5 defines pandemic HIV. Nat Microbiol 7:1762-1776
Thorne et al. (2022) Evolution of enhanced innate immune evasion by SARS-CoV-2. Nature 602:487-495
https://scholar.google.co.uk/citations?user=m2mpiBUAAAAJ&hl=en