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  • Journal article
    Pollock KM, Montamat-Sicotte DJ, Cooke GS, Kapembwa MS, Kon OM, Grass L, Sampson RD, Taylor GP, Lalvani Aet al., 2015,

    Differences in antigen-specific CD4+ responses to opportunistic infections in HIV infection

    , Immunity, Inflammation and Disease, Vol: 3, Pages: 141-153, ISSN: 2050-4527

    HIV-infected individuals with severe immunodeficiency are at risk of opportunistic infection (OI). Tuberculosis (TB) may occur without substantial immune suppression suggesting an early and sustained adverse impact of HIV on Mycobacterium tuberculosis (MTB)-specific cell mediated immunity (CMI). This prospective observational cohort study aimed to observe differences in OI-specific and MTB-specific CMI that might underlie this. Using polychromatic flow cytometry, we compared CD4+ responses to MTB, cytomegalovirus (CMV), Epstein-Barr virus (EBV) and Candida albicans in individuals with and without HIV infection. MTB-specific CD4+ T-cells were more polyfunctional than virus specific (CMV/EBV) CD4+ T-cells which predominantly secreted IFN-gamma (IFN-γ) only. There was a reduced frequency of IFN-γ and IL-2 (IL-2)-dual-MTB-specific cells in HIV-infected individuals, which was not apparent for the other pathogens. MTB-specific cells were less differentiated especially compared with CMV-specific cells. CD127 expression was relatively less frequent on MTB-specific cells in HIV co-infection. MTB-specific CD4+ T-cells PD-1 expression was infrequent in contrast to EBV-specific CD4+ T-cells. The variation in the inherent quality of these CD4+ T-cell responses and impact of HIV co-infection may contribute to the timing of co-infectious diseases in HIV infection.
  • Journal article
    Lalvani A, Pareek M, Almanza LCB, 2015,

    Pre-entry screening for tuberculosis: the need for better evidence

    , PATHOGENS AND GLOBAL HEALTH, Vol: 109, Pages: 44-45, ISSN: 2047-7724
  • Journal article
    Sridhar S, Begom S, Hoschler K, Bermingham A, Adamson W, Carman W, Riley S, Lalvani Aet al., 2015,

    Longevity and Determinants of Protective Humoral Immunity after Pandemic Influenza Infection

    , AMERICAN JOURNAL OF RESPIRATORY AND CRITICAL CARE MEDICINE, Vol: 191, Pages: 325-332, ISSN: 1073-449X
  • Journal article
    Lalvani A, 2014,

    Preventing infectious disease pandemics with T cells

    , IMMUNOLOGY, Vol: 143, Pages: 23-23, ISSN: 0019-2805
  • Journal article
    Sridhar S, Karnani N, Connell DW, Millington KA, Dosanjh D, Bakir M, Soysal A, Deeks J, Lalvani Aet al., 2014,

    INCREASED RISK OF MYCOBACTERIUM TUBERCULOSIS INFECTION IN HOUSEHOLD CHILD CONTACTS EXPOSED TO PASSIVE TOBACCO SMOKE

    , PEDIATRIC INFECTIOUS DISEASE JOURNAL, Vol: 33, Pages: 1303-1306, ISSN: 0891-3668
  • Conference paper
    Kow KJH, Connell DW, Singanayagam A, Ap Dafydd D, Jarvis H, O'Donoghue M, Wickremasinghe MI, Lalvani A, Kon OMet al., 2014,

    INTRATHORACIC LYMPH NODE TUBERCULOSIS - A COMPREHENSIVE CLINICAL DESCRIPTION

    , Meeting of the British-Thoracic-Society, Publisher: BMJ PUBLISHING GROUP, Pages: A157-A158, ISSN: 0040-6376
  • Journal article
    Elderfield RA, Watson SJ, Godlee A, Adamson WE, Thompson CI, Dunning J, Fernandez-Alonso M, Blumenkrantz D, Hussell T, MOSAIC Investigators, Zambon M, Openshaw P, Kellam P, Barclay WSet al., 2014,

    Accumulation of human-adapting mutations during circulation of A(H1N1)pdm09 influenza virus in humans in the United Kingdom.

    , Journal of virology, Vol: 88, Pages: 13269-13283, ISSN: 0022-538X

    <h4>Unlabelled</h4>The influenza pandemic that emerged in 2009 provided an unprecedented opportunity to study adaptation of a virus recently acquired from an animal source during human transmission. In the United Kingdom, the novel virus spread in three temporally distinct waves between 2009 and 2011. Phylogenetic analysis of complete viral genomes showed that mutations accumulated over time. Second- and third-wave viruses replicated more rapidly in human airway epithelial (HAE) cells than did the first-wave virus. In infected mice, weight loss varied between viral isolates from the same wave but showed no distinct pattern with wave and did not correlate with viral load in the mouse lungs or severity of disease in the human donor. However, second- and third-wave viruses induced less alpha interferon in the infected mouse lungs. NS1 protein, an interferon antagonist, had accumulated several mutations in second- and third-wave viruses. Recombinant viruses with the third-wave NS gene induced less interferon in human cells, but this alone did not account for increased virus fitness in HAE cells. Mutations in HA and NA genes in third-wave viruses caused increased binding to α-2,6-sialic acid and enhanced infectivity in human mucus. A recombinant virus with these two segments replicated more efficiently in HAE cells. A mutation in PA (N321K) enhanced polymerase activity of third-wave viruses and also provided a replicative advantage in HAE cells. Therefore, multiple mutations allowed incremental changes in viral fitness, which together may have contributed to the apparent increase in severity of A(H1N1)pdm09 influenza virus during successive waves.<h4>Importance</h4>Although most people infected with the 2009 pandemic influenza virus had mild or unapparent symptoms, some suffered severe and devastating disease. The reasons for this variability were unknown, but the numbers of severe cases increased during successive waves of human infection i
  • Journal article
    Kwok KO, Cowling BJ, Wei VWI, Wu KM, Read JM, Lessler J, Cummings DA, Peiris JSM, Riley Set al., 2014,

    Social contacts and the locations in which they occur as risk factors for influenza infection

    , PROCEEDINGS OF THE ROYAL SOCIETY B-BIOLOGICAL SCIENCES, Vol: 281, ISSN: 0962-8452
  • Journal article
    Roy A, Eisenhut M, Harris RJ, Rodrigues LC, Sridhar S, Habermann S, Snell L, Mangtani P, Adetifa I, Lalvani A, Abubakar Iet al., 2014,

    Effect of BCG vaccination against Mycobacterium tuberculosis infection in children: systematic review and meta-analysis

    , BMJ: British Medical Journal, Vol: 349, ISSN: 0959-535X

    Objectives To determine whether BCG vaccination protects against Mycobacterium tuberculosis infection as assessed by interferon γ release assays (IGRA) in children.Design Systematic review and meta-analysis. Searches of electronic databases 1950 to November 2013, checking of reference lists, hand searching of journals, and contact with experts.Setting Community congregate settings and households.Inclusion criteria Vaccinated and unvaccinated children aged under 16 with known recent exposure to patients with pulmonary tuberculosis. Children were screened for infection with M tuberculosis with interferon γ release assays.Data extraction Study results relating to diagnostic accuracy were extracted and risk estimates were combined with random effects meta-analysis.Results The primary analysis included 14 studies and 3855 participants. The estimated overall risk ratio was 0.81 (95% confidence interval 0.71 to 0.92), indicating a protective efficacy of 19% against infection among vaccinated children after exposure compared with unvaccinated children. The observed protection was similar when estimated with the two types of interferon γ release assays (ELISpot or QuantiFERON). Restriction of the analysis to the six studies (n=1745) with information on progression to active tuberculosis at the time of screening showed protection against infection of 27% (risk ratio 0.73, 0.61 to 0.87) compared with 71% (0.29, 0.15 to 0.58) against active tuberculosis. Among those infected, protection against progression to disease was 58% (0.42, 0.23 to 0.77).Conclusions BCG protects against M tuberculosis infection as well as progression from infection to disease.
  • Journal article
    Goujon C, Moncorge O, Bauby H, Doyle T, Barclay WS, Malim MHet al., 2014,

    Transfer of the Amino-Terminal Nuclear Envelope Targeting Domain of Human MX2 Converts MX1 into an HIV-1 Resistance Factor

    , JOURNAL OF VIROLOGY, Vol: 88, Pages: 9017-9026, ISSN: 0022-538X

This data is extracted from the Web of Science and reproduced under a licence from Thomson Reuters. You may not copy or re-distribute this data in whole or in part without the written consent of the Science business of Thomson Reuters.

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