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  • Journal article
    Petrarca L, Midulla F, Openshaw PJ, 2018,

    Vaccination policies in Europe: Common goals, diverse approaches and public doubts.

    , European Journal of Immunology, Vol: 48, Pages: 10-12, ISSN: 0014-2980
  • Journal article
    Li H, Bradley KC, Long JS, Frise R, Ashcroft JW, Hartgroves LC, Shelton H, Makris S, Johansson C, Cao B, Barclay WSet al., 2018,

    Internal genes of a highly pathogenic H5N1 influenza virus determine high viral replication in myeloid cells and severe outcome of infection in mice.

    , PLoS Pathogens, Vol: 14, ISSN: 1553-7366

    The highly pathogenic avian influenza (HPAI) H5N1 influenza virus has been a public health concern for more than a decade because of its frequent zoonoses and the high case fatality rate associated with human infections. Severe disease following H5N1 influenza infection is often associated with dysregulated host innate immune response also known as cytokine storm but the virological and cellular basis of these responses has not been clearly described. We rescued a series of 6:2 reassortant viruses that combined a PR8 HA/NA pairing with the internal gene segments from human adapted H1N1, H3N2, or avian H5N1 viruses and found that mice infected with the virus with H5N1 internal genes suffered severe weight loss associated with increased lung cytokines but not high viral load. This phenotype did not map to the NS gene segment, and NS1 protein of H5N1 virus functioned as a type I IFN antagonist as efficient as NS1 of H1N1 or H3N2 viruses. Instead we discovered that the internal genes of H5N1 virus supported a much higher level of replication of viral RNAs in myeloid cells in vitro but not in epithelial cells and that this was associated with high induction of type I IFN in myeloid cells. We also found that in vivo during H5N1 recombinant virus infection cells of haematopoetic origin were infected and produced type I IFN and proinflammatory cytokines. Taken together our data infer that human and avian influenza viruses are differently controlled by host factors in alternative cell types; internal gene segments of avian H5N1 virus uniquely drove high viral replication in myeloid cells, which triggered an excessive cytokine production, resulting in severe immunopathology.

  • Conference paper
    Griesenbach U, 2018,

    THE UPS AND DOWNS OF CF GENE THERAPY

    , Joint 10th Annual Scientific Meeting of the Australian-Gene-and-Cell-Therapy-Society (AGCTS) and Australasian-Society-for-Stem-Cell-Research (ASSCR), Publisher: WILEY, ISSN: 1099-498X
  • Conference paper
    Jha A, Thwaites RS, Tunstall T, Kon OM, Shattock RJ, Openshaw PJ, Hansel TTet al., 2018,

    Human Nasal Challenge with TLR7/8 Agonist Resiquimod (R848) Induces Mucosal Interferon-alpha, with Increased Responsiveness in Asthmatic Volunteers

    , International Conference of the American-Thoracic-Society, Publisher: AMER THORACIC SOC, ISSN: 1073-449X
  • Conference paper
    Hippolyte SS, Simmonds NJ, Bilton D, Griesenbach U, Keogh Ret al., 2017,

    DIABETES AND PSEUDOMONAS, A TERRIBLE COMBINATION? EXAMINING THE UK CYSTIC FIBROSIS REGISTRY FOR A SEX DIFFERENCE IN OUTCOMES (2008-2013)

    , Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A2-A3, ISSN: 0040-6376
  • Conference paper
    Hippolyte SS, Simmonds NJ, Bilton D, Griesenbach U, Keogh Ret al., 2017,

    ARE GIRLS ALWAYS THINNER THAN BOYS? USING UK CYSTIC FIBROSIS (CF) REGISTRY DATA (2008-2013) TO EXAMINE WEIGHT CHANGES BETWEEN THE SEXES FROM CHILDHOOD AND BEYOND

    , Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A76-A77, ISSN: 0040-6376
  • Conference paper
    Vlachantoni I, Ascough S, Grimaldi R, Leenhouts K, Chiu C, Openshaw Pet al., 2017,

    PHASE 1 TRIAL OF AN INTRANASAL RESPIRATORY SYNCYTIAL VIRUS (RSV) SUBUNIT CANDIDATE VACCINE: SAFETY RESULTS FROM THE MUC-SYNGEM STUDY

    , Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A43-A44, ISSN: 0040-6376
  • Conference paper
    Atsumi N, Pilou A, Pringle I, Ashworth RC, Meng C, Chan M, Gill DR, Hyde S, Morgan C, Alton EWFW, Griesenbach Uet al., 2017,

    GENE THERAPY FOR PULMONARY ALVEOLAR PROTEINOSIS

    , Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A72-A73, ISSN: 0040-6376
  • Conference paper
    Saleh AD, Clarke NK, Meng C, Jacobson MR, Davies JC, Durham SR, Alton EWFW, Griesenbach Uet al., 2017,

    DEVELOPMENT OF ASSAYS TO ASSESS SAFETY AND EFFICACY OF LENTIVIRAL GENE THERAPY FOR CYSTIC FIBROSIS

    , Winter Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A57-A57, ISSN: 0040-6376
  • Journal article
    Rowe SM, Daines C, Ringshausen FC, Kerem E, Wilson J, Tullis E, Nair N, Simard C, Han L, Ingenito EP, Mckee C, Lekstrom-Himes J, Davies JCet al., 2017,

    Tezacaftor-Ivacaftor in Residual-Function Heterozygotes with Cystic Fibrosis

    , New England Journal of Medicine, Vol: 377, Pages: 2024-2035, ISSN: 0028-4793

    BACKGROUNDCystic fibrosis is an autosomal recessive disease caused by mutations in the CFTR gene that lead to progressive respiratory decline. Some mutant CFTR proteins show residual function and respond to the CFTR potentiator ivacaftor in vitro, whereas ivacaftor alone does not restore activity to Phe508del mutant CFTR.METHODSWe conducted a randomized, double-blind, placebo-controlled, phase 3, crossover trial to evaluate the efficacy and safety of ivacaftor alone or in combination with tezacaftor, a CFTR corrector, in 248 patients 12 years of age or older who had cystic fibrosis and were heterozygous for the Phe508del mutation and a CFTR mutation associated with residual CFTR function. Patients were randomly assigned to one of six sequences, each involving two 8-week intervention periods separated by an 8-week washout period. They received tezacaftor–ivacaftor, ivacaftor monotherapy, or placebo. The primary end point was the absolute change in the percentage of predicted forced expiratory volume in 1 second (FEV1) from the baseline value to the average of the week 4 and week 8 measurements in each intervention period.RESULTSThe number of analyzed intervention periods was 162 for tezacaftor–ivacaftor, 157 for ivacaftor alone, and 162 for placebo. The least-squares mean difference versus placebo with respect to the absolute change in the percentage of predicted FEV1 was 6.8 percentage points for tezacaftor–ivacaftor and 4.7 percentage points for ivacaftor alone (P<0.001 for both comparisons). Scores on the respiratory domain of the Cystic Fibrosis Questionnaire–Revised, a quality-of-life measure, also significantly favored the active-treatment groups. The incidence of adverse events was similar across intervention groups; most events were mild or moderate in severity, with no discontinuations of the trial regimen due to adverse events for tezacaftor–ivacaftor and few for ivacaftor alone (1% of patients) and placebo (<1%).CONCLUSI

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