Professor Clare Jolly, BSc. (Hons.); PhD
Professor of Virus Cell Biology
Centre: Centre for Immunobiology and Infection
Email: clare.jolly@qmul.ac.ukWebsite: https://www.linkedin.com/in/clare-jolly-6a9533371/Twitter: @@Jolly_lab
Profile
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Clare completed her undergraduate degree followed by a PhD on rotavirus under the supervision of Dr Ian Holmes at the University of Melbourne, Australia. In 2001 she was awarded a Wellcome Travelling Fellowship and moved to the UK for postdoc with Professor Quentin Sattentau on mechanisms of HIV-1 replication and spread in T cells, initially at Imperial College London and then the University of Oxford. During her postdoc she discovered that HIV-1 disseminates between T cells by highly-efficient cell-to-cell spread at immune cell contacts called the virological synapse. In 2008, supported by a MRC Career Development Award, Clare established her independent research group at University College London, focussing on the cell biology of HIV-1 infection in T cells. In 2021 she was appointed Professor of Virus Cell Biology at UCL. In September 2025, Clare and her research group moved to QMUL and joined the Centre for Immunobiology and Infection at the Blizard Institute. Her research is funded by the Wellcome and UKRI. |
Research
Research Interests:
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Our research seeks to understand the cell biology of HIV-1 infection in CD4+ T cells, specifically how HIV-1 hijacks the host cell machinery to most efficiently replicate and disseminate between T cells, with a particular focus on the process of cell-to-cell spread. We ask the fundamental questions of “what makes a cell permissive to virus infection” and “what are the biological consequences for both the virus and the host”? Dissecting the molecular details of key virus-host interactions not only provides new insights into HIV-1 biology, but may also ultimately inform novel antiviral strategies. More broadly, viruses are fantastic tools to understand how cells work and our research also seeks to provide new mechanistic insight into T cell biology in health and disease. Since 2020, we have also been working on SARS-CoV-2 with emphasis on innate immunity and virus-host interactions to understand what made SARS-CoV-2 a successful human pandemic virus. We take a multidisciplinary approach employing molecular virology, cell biology and immunology, alongside advanced imaging and ‘omics technologies to address our research questions. Lab members:
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Publications
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Mesner et al. (2023) SARS-CoV-2 evolution influences GBP and IFITM sensitivity. PNAS 120(5). e2212577120 doi:10.1073/pnas.2212577120 Thorne et al. (2022) Evolution of enhanced innate immune evasion by SARS-CoV-2. Nature 604 pE14 doi:10.1038/s41586-021-04352-y Reuschl et al. (2022) HIV-1 Vpr drives a tissue residency-like phenotype during selective infection of resting memory T cells. Cell Reports 39(2). doi:10.1016/j.celrep.2022.110650 |
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Mesner et al. (2020) Loss of Nef-mediated CD3 down-regulation in the HIV-1 lineage increases viral infectivity and spread. PNAS doi:10.1073/pnas.1921135117 Len et al. (2017). HIV-1 Activates T Cell Signaling Independently of Antigen to Drive Viral Spread. Cell Reports doi:10.1016/j.celrep.2016.12.057 Jolly C., et al., (2004) HIV-1 cell to cell transfer across an Env-induced, actin-dependent synapse. J Exp Med 199: 283-93. doi: 10.1084/jem.20030648 |
Supervision
Taylor Bronzovich