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4 results on '"Fisher-Pearson N"'

1. Global burden of bacterial antimicrobial resistance in 2019: a systematic analysis

Author

Murray, CJL, Ikuta, KS, Sharara, F, Swetschinski, L, Aguilar, GR, Gray, A, Han, C, Bisignano, C, Rao, P, Wool, E, Johnson, SC, Browne, AJ, Chipeta, MG, Fell, F, Hackett, S, Haines-Woodhouse, G, Hamadani, BHK, Kumaran, EAP, McManigal, B, Agarwal, R, Akech, S, Albertson, S, Amuasi, J, Andrews, J, Aravkin, A, Ashley, E, Bailey, F, Baker, S, Basnyat, B, Bekker, A, Bender, R, Bethou, A, Bielicki, J, Boonkasidecha, S, Bukosia, J, Carvalheiro, C, Castaneda-Orjuela, C, Chansamouth, V, Chaurasia, S, Chiurchiu, S, Chowdhury, F, Cook, AJ, Cooper, B, Cressey, TR, Criollo-Mora, E, Cunningham, M, Darboe, S, Day, NPJ, De Luca, M, Dokova, K, Dramowski, A, Dunachie, SJ, Eckmanns, T, Eibach, D, Emami, A, Feasey, N, Fisher-Pearson, N, Forrest, K, Garrett, D, Gastmeier, P, Giref, AZ, Greer, RC, Gupta, V, Haller, S, Haselbeck, A, Hay, S, Holm, M, Hopkins, S, Iregbu, KC, Jacobs, J, Jarovsky, D, Javanmardi, F, Khorana, M, Kissoon, N, Kobeissi, E, Kostyanev, T, Krapp, F, Krumkamp, R, Kumar, A, Kyu, HH, Lim, C, Limmathurotsakul, D, Loftus, MJ, Lunn, M, Ma, J, Mturi, N, Munera-Huertas, T, Musicha, P, Mussi-Pinhata, MM, Nakamura, T, Nanavati, R, Nangia, S, Newton, P, Ngoun, C, Novotney, A, Nwakanma, D, Obiero, CW, Olivas-Martinez, A, Olliaro, P, Ooko, E, Ortiz-Brizuela, E, Peleg, AY, Perrone, C, Plakkal, N, Ponce-de-Leon, A, Raad, M, Ramdin, T, Riddell, A, Roberts, T, VictoriaRobotham, J, Roca, A, Rudd, KE, Russell, N, Schnall, J, Scott, JAG, Shivamallappa, M, Sifuentes-Osornio, J, Steenkeste, N, Stewardson, AJ, Stoeva, T, Tasak, N, Thaiprakong, A, Thwaites, G, Turner, C, Turner, P, van Doorn, HR, Velaphi, S, Vongpradith, A, Huong, V, Walsh, T, Waner, S, Wangrangsimakul, T, Wozniak, T, Zheng, P, Sartorius, B, Lopez, AD, Stergachis, A, Moore, C, Dolecek, C, Naghavi, M, Murray, CJL, Ikuta, KS, Sharara, F, Swetschinski, L, Aguilar, GR, Gray, A, Han, C, Bisignano, C, Rao, P, Wool, E, Johnson, SC, Browne, AJ, Chipeta, MG, Fell, F, Hackett, S, Haines-Woodhouse, G, Hamadani, BHK, Kumaran, EAP, McManigal, B, Agarwal, R, Akech, S, Albertson, S, Amuasi, J, Andrews, J, Aravkin, A, Ashley, E, Bailey, F, Baker, S, Basnyat, B, Bekker, A, Bender, R, Bethou, A, Bielicki, J, Boonkasidecha, S, Bukosia, J, Carvalheiro, C, Castaneda-Orjuela, C, Chansamouth, V, Chaurasia, S, Chiurchiu, S, Chowdhury, F, Cook, AJ, Cooper, B, Cressey, TR, Criollo-Mora, E, Cunningham, M, Darboe, S, Day, NPJ, De Luca, M, Dokova, K, Dramowski, A, Dunachie, SJ, Eckmanns, T, Eibach, D, Emami, A, Feasey, N, Fisher-Pearson, N, Forrest, K, Garrett, D, Gastmeier, P, Giref, AZ, Greer, RC, Gupta, V, Haller, S, Haselbeck, A, Hay, S, Holm, M, Hopkins, S, Iregbu, KC, Jacobs, J, Jarovsky, D, Javanmardi, F, Khorana, M, Kissoon, N, Kobeissi, E, Kostyanev, T, Krapp, F, Krumkamp, R, Kumar, A, Kyu, HH, Lim, C, Limmathurotsakul, D, Loftus, MJ, Lunn, M, Ma, J, Mturi, N, Munera-Huertas, T, Musicha, P, Mussi-Pinhata, MM, Nakamura, T, Nanavati, R, Nangia, S, Newton, P, Ngoun, C, Novotney, A, Nwakanma, D, Obiero, CW, Olivas-Martinez, A, Olliaro, P, Ooko, E, Ortiz-Brizuela, E, Peleg, AY, Perrone, C, Plakkal, N, Ponce-de-Leon, A, Raad, M, Ramdin, T, Riddell, A, Roberts, T, VictoriaRobotham, J, Roca, A, Rudd, KE, Russell, N, Schnall, J, Scott, JAG, Shivamallappa, M, Sifuentes-Osornio, J, Steenkeste, N, Stewardson, AJ, Stoeva, T, Tasak, N, Thaiprakong, A, Thwaites, G, Turner, C, Turner, P, van Doorn, HR, Velaphi, S, Vongpradith, A, Huong, V, Walsh, T, Waner, S, Wangrangsimakul, T, Wozniak, T, Zheng, P, Sartorius, B, Lopez, AD, Stergachis, A, Moore, C, Dolecek, C, and Naghavi, M

Abstract

BACKGROUND: Antimicrobial resistance (AMR) poses a major threat to human health around the world. Previous publications have estimated the effect of AMR on incidence, deaths, hospital length of stay, and health-care costs for specific pathogen-drug combinations in select locations. To our knowledge, this study presents the most comprehensive estimates of AMR burden to date. METHODS: We estimated deaths and disability-adjusted life-years (DALYs) attributable to and associated with bacterial AMR for 23 pathogens and 88 pathogen-drug combinations in 204 countries and territories in 2019. We obtained data from systematic literature reviews, hospital systems, surveillance systems, and other sources, covering 471 million individual records or isolates and 7585 study-location-years. We used predictive statistical modelling to produce estimates of AMR burden for all locations, including for locations with no data. Our approach can be divided into five broad components: number of deaths where infection played a role, proportion of infectious deaths attributable to a given infectious syndrome, proportion of infectious syndrome deaths attributable to a given pathogen, the percentage of a given pathogen resistant to an antibiotic of interest, and the excess risk of death or duration of an infection associated with this resistance. Using these components, we estimated disease burden based on two counterfactuals: deaths attributable to AMR (based on an alternative scenario in which all drug-resistant infections were replaced by drug-susceptible infections), and deaths associated with AMR (based on an alternative scenario in which all drug-resistant infections were replaced by no infection). We generated 95% uncertainty intervals (UIs) for final estimates as the 25th and 975th ordered values across 1000 posterior draws, and models were cross-validated for out-of-sample predictive validity. We present final estimates aggregated to the global and regional level. FINDINGS: On the bas

Published
2022

2. HIV/HBV coinfection remodels the immune landscape and natural killer cell ADCC functional responses.

Author

Sun B, da Costa KAS, Alrubayyi A, Kokici J, Fisher-Pearson N, Hussain N, D'Anna S, Piermatteo L, Salpini R, Svicher V, Kucykowicz S, Ghosh I, Burns F, Kinloch S, Simoes P, Bhagani S, Kennedy PTF, Maini MK, Bashford-Rogers R, Gill US, and Peppa D

Subjects
Humans, Male, Female, Adult, Hepatitis B immunology, Hepatitis B complications, Middle Aged, Hepatitis B, Chronic immunology, Hepatitis B, Chronic complications, Hepatitis B, Chronic virology, HIV Infections immunology, HIV Infections complications, Killer Cells, Natural immunology, Coinfection immunology, Antibody-Dependent Cell Cytotoxicity
Abstract

Background and Aims: HBV and HIV coinfection is a common occurrence globally, with significant morbidity and mortality. Both viruses lead to immune dysregulation including changes in natural killer (NK) cells, a key component of antiviral defense and a promising target for HBV cure strategies. Here we used high-throughput single-cell analysis to explore the immune cell landscape in people with HBV mono-infection and HIV/HBV coinfection, on antiviral therapy, with emphasis on identifying the distinctive characteristics of NK cell subsets that can be therapeutically harnessed., Approach and Results: Our data show striking differences in the transcriptional programs of NK cells. HIV/HBV coinfection was characterized by an over-representation of adaptive, KLRC2 -expressing NK cells, including a higher abundance of a chemokine-enriched ( CCL3/CCL4 ) adaptive cluster. The NK cell remodeling in HIV/HBV coinfection was reflected in enriched activation pathways, including CD3ζ phosphorylation and ZAP-70 translocation that can mediate stronger antibody-dependent cellular cytotoxicity responses and a bias toward chemokine/cytokine signaling. By contrast, HBV mono-infection imposed a stronger cytotoxic profile on NK cells and a more prominent signature of "exhaustion" with higher circulating levels of HBsAg. Phenotypic alterations in the NK cell pool in coinfection were consistent with increased "adaptiveness" and better capacity for antibody-dependent cellular cytotoxicity compared to HBV mono-infection. Overall, an adaptive NK cell signature correlated inversely with circulating levels of HBsAg and HBV-RNA in our cohort., Conclusions: This study provides new insights into the differential signature and functional profile of NK cells in HBV and HIV/HBV coinfection, highlighting pathways that can be manipulated to tailor NK cell-focused approaches to advance HBV cure strategies in different patient groups., (Copyright © 2024 American Association for the Study of Liver Diseases.)

Published
2024
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3. Characterization of humoral and SARS-CoV-2 specific T cell responses in people living with HIV.

Author

Alrubayyi A, Gea-Mallorquí E, Touizer E, Hameiri-Bowen D, Kopycinski J, Charlton B, Fisher-Pearson N, Muir L, Rosa A, Roustan C, Earl C, Cherepanov P, Pellegrino P, Waters L, Burns F, Kinloch S, Dong T, Dorrell L, Rowland-Jones S, McCoy LE, and Peppa D

Subjects
Adult, Aged, Antibodies, Viral blood, Antibodies, Viral immunology, Antibody Formation immunology, Antigens, Viral immunology, CD4-Positive T-Lymphocytes immunology, CD8-Positive T-Lymphocytes immunology, COVID-19 blood, COVID-19 immunology, COVID-19 virology, Cohort Studies, Female, Genome, Human, HIV Infections blood, Humans, Interferon-gamma metabolism, Male, Middle Aged, Phenotype, Species Specificity, Tissue Donors, HIV Infections immunology, HIV Infections virology, Immunity, Humoral, SARS-CoV-2 physiology, T-Lymphocytes immunology
Abstract

There is an urgent need to understand the nature of immune responses against SARS-CoV-2, to inform risk-mitigation strategies for people living with HIV (PLWH). Here we show that the majority of PLWH with ART suppressed HIV viral load, mount a detectable adaptive immune response to SARS-CoV-2. Humoral and SARS-CoV-2-specific T cell responses are comparable between HIV-positive and negative subjects and persist 5-7 months following predominately mild COVID-19 disease. T cell responses against Spike, Membrane and Nucleoprotein are the most prominent, with SARS-CoV-2-specific CD4 T cells outnumbering CD8 T cells. We further show that the overall magnitude of SARS-CoV-2-specific T cell responses relates to the size of the naive CD4 T cell pool and the CD4:CD8 ratio in PLWH. These findings suggest that inadequate immune reconstitution on ART, could hinder immune responses to SARS-CoV-2 with implications for the individual management and vaccine effectiveness in PLWH., (© 2021. The Author(s).)

Published
2021
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4. Failure to seroconvert after two doses of BNT162b2 SARS-CoV-2 vaccine in a patient with uncontrolled HIV.

Author

Touizer E, Alrubayyi A, Rees-Spear C, Fisher-Pearson N, Griffith SA, Muir L, Pellegrino P, Waters L, Burns F, Kinloch S, Rowland-Jones S, Gupta RK, Gilson R, Peppa D, and McCoy LE

Subjects
Adenine analogs & derivatives, Adenine therapeutic use, Adult, Alanine, Amides, Antiretroviral Therapy, Highly Active methods, BNT162 Vaccine, CD4 Lymphocyte Count, CD4-CD8 Ratio, CD4-Positive T-Lymphocytes immunology, CD4-Positive T-Lymphocytes virology, CD8-Positive T-Lymphocytes immunology, CD8-Positive T-Lymphocytes virology, COVID-19 immunology, COVID-19 prevention & control, COVID-19 virology, Emtricitabine therapeutic use, HIV Infections drug therapy, HIV Infections immunology, HIV Infections virology, HIV-1 growth & development, HIV-1 immunology, Heterocyclic Compounds, 3-Ring, Heterocyclic Compounds, 4 or More Rings therapeutic use, Humans, Neutralization Tests, Piperazines, Pyridones, RNA, Viral blood, RNA, Viral immunology, SARS-CoV-2 immunology, Tenofovir analogs & derivatives, Treatment Failure, CD4-Positive T-Lymphocytes pathology, CD8-Positive T-Lymphocytes pathology, COVID-19 Vaccines administration & dosage, HIV Infections pathology, HIV-1 pathogenicity
Abstract

Competing Interests: LEM has received honorarium for lectures from the London School of Hygiene and Tropical Medicine. SR-J has received honorarium for lectures from the London School of Hygiene and Tropical Medicine, declares additional grant support from UK Research and Innovation, EDCTP, Kumamoto University, the Rosetrees Trust, and the Global Challenges Research Fund, and is a trustee and past president of the Royal Society of Tropical Medicine and Hygiene. RKG has received consulting fees from UMOVIS Lab and Janssen. FB has received payment for teaching research methods from Gilead Sciences. LW has received honorarium for participation in advisory boards, speaker fees, or both from Gilead Sciences, ViiV, Janssen, MSD, Theratechnologies, Mylan, and Cipla, and has also received conference attendance support from ViiV. All other authors declare no competing interests. ET and AA contributed equally to this Correspondence. This Correspondence was supported by a Medical Research Council (MRC) grant to LEM (MR/R008698/1), a MRC studentship (MR/N013867/1), and a MRC grant (MR/M008614) and a National Institutes of Health grant (R01AI55182) to DP. We thank Peter Cherepanov of the Francis Crick Institute (London, UK) for supplying recombinant S1 antigen. We are grateful to Rebecca Matthews, Paulina Prymas, Marzia Fiorino, Thomas Fernandez, Nnenna Ngwu, the clinical research teams at the Mortimer Market Centre (London, UK) and the Ian Charleson Day Centre (London, UK), and all the clinic staff and participants.

Published
2021
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