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• Journal article
  Mall MA, Wainwright CE, Legg J, Chilvers M, Gartner S, Dittrich A-M, Stehling F, Conner S, Grant S, Suresh N, Weinstock TG, Davies JCet al., 2025,

  Elexacaftor/tezacaftor/ivacaftor in children aged ≥6 years with cystic fibrosis heterozygous for<i> F508del</i> and a minimal function mutation: results from a 96-week open-label extension study

  , EUROPEAN RESPIRATORY JOURNAL, Vol: 66, ISSN: 0903-1936
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  • Citations: 1
• Journal article
  Hawkins A, Pantazi P, Yang L, Coyne CB, Bokun V, Lemme-Dumit JM, Pasetti MF, Barnett S, Culley FJ, Holder Bet al., 2025,

  Long-term culture and passaging of term trophoblast for the investigation of syncytiotrophoblast function

  , PLACENTA, Vol: 166, Pages: 25-32, ISSN: 0143-4004
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  • Citations: 1
• Journal article
  Sayec ML, Davies G, Waller MD, Davies JC, Simmonds NJ, Jones A, Brugha R, Dawson C, Macedo P, Ruiz G, Hughes D, Shah V, Pao C, Shafi N, Brown S, Watson D, Baker L, Lillis A, Ruffles T, Needham Y, Safavi S, Bokobza I, Holt L, Longmate J, Sketchley S, Cameron L, Bossley CJet al., 2025,

  A standard operating procedure for reducing risk from medications prohibited during clinical trials in cystic fibrosis

  , Journal of Cystic Fibrosis, ISSN: 1569-1993
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• Journal article
  Chen J-L, Wang B, Lu Y, Antoun E, Bird O, Drennan PG, Yin Z, Liu G, Yao X, Pidoux M, Bates A, Jayathilaka D, Wang J, Angus B, Beer S, Espinosa A, Baillie JK, Semple MG, Openshaw PJM, Alex B, Andrikopoulos P, Bach B, Barclay WS, Bogaert D, Chand M, Chechi K, Cooke GS, da Silva Filipe A, de Silva T, Docherty AB, dos Santos Correia G, Dumas M-E, Dunning J, Fletcher T, Green CA, Greenhalf W, Griffin JL, Gupta RK, Harrison EM, Ho AYW, Holden K, Horby PW, Ijaz S, Khoo S, Klenerman P, Law A, Lewis MR, Liggi S, Lim WS, Maslen L, Merson L, Meynert AM, Moore SC, Noursadeghi M, Olanipekun M, Osagie A, Palmarini M, Palmieri C, Paxton WA, Pollakis G, Price N, Rambaut A, Robertson DL, Russell CD, Sancho-Shimizu V, Sands CJ, Scott JT, Sigfrid L, Solomon T, Sriskandan S, Stuart D, Summers C, Swann OV, Takats Z, Takis P, Tedder RS, Thompson AAR, Thomson EC, Thwaites RS, Turtle LCW, Zambon M, Drake TM, Fairfield CJ, Knight SR, Mclean KA, Murphy D, Norman L, Pius R, Shaw CA, Connor M, Dalton J, Gamble C, Girvan M, Halpin S, Harrison J, Jackson C, Lee J, Marsh L, Plotkin D, Roberts S, Saviciute E, Clohisey S, Hendry R, Knight S, Leeming G, Norris L, Scott-Brown J, Tait S, Wham M, Carson G, Grammatikopoulos T, McDonald SE, Shaw V, Keating S, Donegan C, Spencer RG, Donohue C, Griffiths F, Hardwick H, Oosthuyzen W, Rostron T, Waugh C, Sopp P, Knight JC, Fullerton JN, Coles M, Smith GL, Mentzer AJ, Peng Y, Dong Tet al., 2025,

  T cell memory response to MPXV infection exhibits greater effector function and migratory potential compared to MVA-BN vaccination

  , Nature Communications, Vol: 16, ISSN: 2041-1723

  In 2022, a global mpox outbreak occurred, and remains a concern today. The T cell memory response to MPXV (monkeypox virus) infection has not been fully investigated. In this study, we evaluate this response in convalescent and MVA-BN (Modified Vaccinia Ankara - Bavarian Nordic) vaccinated individuals using VACV-infected cells. Strong CD8+ and CD4+ T cell responses are observed, and T cell responses are biased towards viral early expressed proteins. We identify seven immunodominant HLA-A*02:01 restricted MPXV-specific epitopes and focus our detailed phenotypic and scRNAseq analysis on the immunodominant HLA-A*02:01-G5R18-26-specific CD8+ T cell response. While tetramer+CD8+ T cells share similar differentiation and activation phenotypes, T cells from convalescent individuals show greater cytotoxicity, migratory potential to site of infection and TCR clonal expansion. Our data suggest that effective functional profiles of MPXV-specific memory T cells induced by Mpox infection may have an implication on the long-term protective responses to future infection.

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• Conference paper
  Tiddens H, Makani P, Bonte M, Cregan R, Rea D, Persaud T, Twomey E, McGrane S, Caudri D, Dodd JD, McKone EF, Semple T, Davies JC, McNally Pet al., 2025,

  Changes in Low Attenuation Regions and Arterial and Venous Blood Volume Distribution in Response to CFTR Modulator Therapy in People With Cystic Fibrosis

  , International Conference of the American-Thoracic-Society (ATS), Publisher: AMER THORACIC SOC, ISSN: 1073-449X
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• Journal article
  Harker JA, Thwaites RS, 2025,

  Unravelling the interplay between respiratory disease and the immune landscape in long COVID

  , NATURE IMMUNOLOGY, Vol: 26, Pages: 640-641, ISSN: 1529-2908
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• Journal article
  Siegal EZ, Schoevers JMH, Terstappen J, Delemarre EM, Johnston SL, van Beek LF, Bogaert D, Chiu C, Diavatopoulos DA, Ferreira DM, Gordon SB, Hayden FG, de Jonge MI, Mccall MBB, Mcshane HI, Minassian AM, Openshaw PJM, Pollard AJ, Sattabongkot J, Read RC, Troelstra A, Viveen MC, Wilder-Smith A, van Wijk M, Bont LJ, Mazur NIet al., 2025,

  Risk analysis for outpatient experimental infection as a pathway for affordable RSV vaccine development

  , NPJ VACCINES, Vol: 10
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• Journal article
  Talwar S, Harker J, Openshaw P, Thwaites Ret al., 2025,

  Autoimmunity in long COVID

  , Journal of Allergy and Clinical Immunology, Vol: 155, Pages: 1082-1094, ISSN: 0091-6749

  Long COVID (also termed postacute sequelae of SARS-CoV-2, or PASC) affects up to 10% of people recovering from infection with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Diagnosis is hampered by diffuse symptomatology, lack of biomarkers, incomplete understanding of pathogenesis, and lack of validated treatments. In terms of pathogenesis, hypothesized causes include virus persistence, the legacy of endotheliitis and thrombosis, low-grade tissue-based inflammation and/or scarring, perturbation of the host virome/microbiome, or triggering of autoimmunity. Several studies show preexisting and/or de novo production of autoantibodies after infection with SARS-CoV-2, but the persistence of these antibodies and their role in causing long COVID is debated. Here, we review the mechanisms through which autoimmune responses can arise during and after viral infection, focusing on the evidence for B-cell dysregulation and autoantibody production in acute and long COVID.

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• Journal article
  Sagawe JS, Loake V, Openshaw P, Kemp P, Culley Fet al., 2025,

  Aging enhances pro-atrogenic gene expression and skeletal muscle loss following respiratory syncytial virus infection

  , GeroScience, Vol: 47, Pages: 1485-1500, ISSN: 2509-2723

  Aging and many age-related health conditions are associated with skeletal muscle loss. Furthermore, older adults are more susceptible to severe respiratory infections, which can in turn lead to muscle wasting. The mechanisms by which respiratory viral infection can impact skeletal muscle in older adults are not well understood. We determined the effects of acute infection with respiratory syncytial virus (RSV) on the lung and skeletal muscle of aged mice. RSV infection caused more severe disease in aged mice with enhanced weight loss, reduced feeding, higher viral load, and greater airway inflammation. Aged but not young mice showed decreased leg muscle weight at the peak of illness and decreased size of leg muscle fibers. Aged mice increased muscle-specific expression of atrophy-promoting enzymes (Atrogin-1 and MuRF-1) and failed to increase the rate of muscle protein synthesis during RSV infection. In aged mice, the changes in Atrogin-1 and MuRF-1 gene expression in skeletal muscle correlated with IL-6 levels in the lungs. These findings indicate that RSV infection of aged mice provides a model for studying the diverse adverse systemic consequences of respiratory viral infections on health and wellbeing in older adults.

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• Journal article
  Frost FJ, Peckham DG, Felton IC, Snowball JE, Gray RD, Jones AM, Simmonds NJ, Lord RW, Lip GYH, Chandler H, Murphy K, Downey DG, Sheppard DN, Davies JC, Bull J, Sommer P, Cupid B, Allen L, Duckers Jet al., 2025,

  Managing an ageing cystic fibrosis population: challenges and priorities

  , European Respiratory Review, Vol: 34, ISSN: 0905-9180

  The increasing life expectancy of people with cystic fibrosis (pwCF), largely driven by advancements in early diagnosis, multidisciplinary care and the recent introduction of cystic fibrosis transmembrane conductance regulator (CFTR) modulator therapies, is likely to herald a shift in the focus of care toward managing the complexities of ageing. This review highlights key challenges and research priorities for addressing the health needs of an ageing CF population. A growing body of evidence underscores the heightened risks of cancers, cardiovascular diseases and changing nutritional and metabolic profiles as pwCF age. CFTR modulators have improved clinical outcomes, but their effects on inflammation, immunity and long-term disease trajectories remain incompletely understood. Nutritional management, particularly the implications of obesity and body composition, poses new challenges, as does the potential accelerated ageing of immune and pulmonary systems in CF. Emerging issues such as menopause in females with CF, lifetime antimicrobial resistance and the interplay between chronic inflammation and ageing further complicate the care landscape. The review emphasises the urgent need for multidisciplinary research programmes that integrate clinical, patient and community perspectives. Leveraging established CF registries, clinical trial networks and collaborations with ageing research frameworks is critical to addressing these challenges. Ultimately, the goal is to ensure that pwCF not only live longer but also experience improved quality of life and holistic wellbeing as they realise the full benefits of therapeutic advances.

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