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  • 1.
    Connolly-Andersen, Anne-Marie
    et al.
    Umeå University, Umeå, Sweden.
    Sundberg, Erik
    Umeå University, Umeå, Sweden.
    Ahlm, Clas
    Umeå University, Umeå, Sweden.
    Hultdin, Johan
    Umeå University, Umeå, Sweden.
    Baudin, Maria
    Umeå University, Umeå, Sweden.
    Larsson, Johanna
    Umeå University, Umeå, Sweden.
    Dunne, Eimear
    Royal Coll Surgeons Ireland, Dublin, Ireland.
    Kenny, Dermot
    Royal Coll Surgeons Ireland, Dublin, Ireland.
    Lindahl, Tomas L.
    Linköping University, Linköping, Sweden.
    Ramström, Sofia
    Linköping University, Linköping, Sweden.
    Nilsson, Sofie
    Umeå University, Umeå, Sweden.
    Increased Thrombopoiesis and Platelet Activation in Hantavirus-Infected Patients2015Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 212, nr 7, s. 1061-1069Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Background: Thrombocytopenia is a common finding during viral hemorrhagic fever, which includes hemorrhagic fever with renal syndrome (HFRS). The 2 main causes for thrombocytopenia are impaired thrombopoiesis and/or increased peripheral destruction of platelets. In addition, there is an increased intravascular coagulation risk during HFRS, which could be due to platelet activation.

    Methods: Thrombopoiesis was determined by quantification of platelet counts, thrombopoietin, immature platelet fraction, and mean platelet volume during HFRS. The in vivo platelet activation was determined by quantification of soluble P-selectin (sP-selectin) and glycoprotein VI (sGPVI). The function of circulating platelets was determined by ex vivo stimulation followed by flow cytometry analysis of platelet surface-bound fibrinogen and P-selectin exposure. Intravascular coagulation during disease was determined by scoring for disseminated intravascular coagulation (DIC) and recording thromboembolic complications.

    Results: The levels of thrombopoietin, immature platelet fraction, and mean platelet volume all indicate increased thrombopoiesis during HFRS. Circulating platelets had reduced ex vivo function during disease compared to follow-up. Most interestingly, we observed significantly increased in vivo platelet activation in HFRS patients with intravascular coagulation (DIC and thromboembolic complications) as shown by sP-selectin and sGPVI levels. Conclusions. HFRS patients have increased thrombopoiesis and platelet activation, which contributes to intravascular coagulation.

  • 2.
    Eklund, Daniel
    et al.
    Division of Microbiology and Molecular Medicine, Linköping University, Linköping, Sweden.
    Welin, Amanda
    Institute of Medicine, Sahlgrenska Academy, University of Gothenburg, Gothenburg, Sweden.
    Andersson, Henrik
    Division of Microbiology and Molecular Medicine, Linköping University, Linköping, Sweden.
    Verma, Deepti
    Division of Cell Biology, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Söderkvist, Peter
    Division of Cell Biology, Faculty of Health Sciences, Linköping University, Linköping, Sweden.
    Stendahl, Olle
    Division of Microbiology and Molecular Medicine, Linköping University, Linköping, Sweden.
    Särndahl, Eva
    Örebro universitet, Institutionen för läkarutbildning.
    Lerm, Maria
    Division of Microbiology and Molecular Medicine, Linköping University, Linköping, Sweden.
    Human Gene Variants Linked to Enhanced NLRP3 Activity Limit Intramacrophage Growth of Mycobacterium tuberculosis2014Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 209, nr 5, s. 749-753Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Activation of the NLRP3 inflammasome and subsequent generation of interleukin 1 beta is initiated in macrophages upon recognition of several stimuli. In the present work, we show that gain-of-function gene variants of inflammasome components known to predispose individuals to inflammatory disorders have a host-protective role during infection with Mycobacterium tuberculosis. By isolation of macrophages from patients and healthy blood donors with genetic variants in NLRP3 and CARD8 and subsequent infection of the cells with virulent M. tuberculosis, we show that these gene variants, combined, are associated with increased control of bacterial growth in human macrophages.

  • 3. Färnert, Anna
    et al.
    Williams, Thomas N.
    Mwangi, Tabitha W.
    Ehlin, Anna
    Fegan, Greg
    Macharia, Alex
    Lowe, Brett S.
    Montgomery, Scott M.
    Örebro universitet, Hälsoakademin.
    Marsh, Kevin
    Transmission-dependent tolerance to multiclonal Plasmodium falciparum infection2009Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 200, nr 7, s. 1166-1175Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Whether the number of concurrent clones in asymptomatic Plasmodium falciparum infections reflects the degree of host protection was investigated in children living in areas with different levels of transmission on the coast of Kenya. The number of concurrent clones was determined on the basis of polymorphism in msp2, which encodes the vaccine candidate antigen merozoite surface protein 2. In a low-transmission area, most children had monoclonal infections, and diversity did not predict a risk of clinical malaria. In an area of moderate transmission, asymptomatic infections with 2 clones were, compared with 1 clone, associated with an increased risk of subsequent malaria. In a comparative assessment in a high-transmission area in Tanzania, multiclonal infections conferred a reduced risk. The different nonlinear associations between the number of clones and malaria morbidity suggest that levels of tolerance to multiclonal infections are transmission dependent as a result of cumulative exposure to antigenically diverse P. falciparum infections.

  • 4.
    Jacobsen, Marc
    et al.
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
    Repsilber, Dirk
    Institute for Medical Biometry and Statistics, University of Lübeck, Lübeck, Germany.
    Gutschmidt, Andrea
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
    Neher, Albert
    Asklepios Center for Respiratory Medicine and Thoracic Surgery, Munich-Gauting, Germany .
    Feldmann, Knut
    Asklepios Center for Respiratory Medicine and Thoracic Surgery, Munich-Gauting, Germany .
    Mollenkopf, Hans J
    Microarray Core Facilities, Max Planck Institute for Infection Biology, Berlin, Germany .
    Ziegler, Andreas
    Institute for Medical Biometry and Statistics, University of Lübeck, Lübeck, Germany.
    Kaufmann, Stefan H E
    Department of Immunology, Max Planck Institute for Infection Biology, Berlin, Germany.
    Ras-associated small GTPase 33A, a novel T cell factor, is down-regulated in patients with tuberculosis2005Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 192, nr 7, s. 1211-8Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    Ras-associated small GTPases (Rabs) are specific regulators of intracellular vesicle trafficking. Interference with host cell vesicular transport is a hallmark of many intracellular pathogens, including the notable example Mycobacterium tuberculosis. We performed, by quantitative polymerase chain reaction, gene-expression analyses for selected Rab molecules in peripheral-blood mononuclear cells from patients with tuberculosis (TB) and healthy control subjects, to identify candidate genes that are critically involved in the host immune response. Comparison revealed significant differences in the expression of genes for Rab13, Rab24, and Rab33A. Rab33A gene expression was down-regulated in patients with TB and was predominantly expressed in CD8+ T cells. We excluded possible influences of differences in T cell percentages between the 2 study groups, demonstrating that Rab33A gene expression changes on the single-cell level. In vitro, Rab33A RNA expression was induced in T cells on activation and by dendritic cells infected with M. tuberculosis. Our findings identify Rab33A as a T cell regulatory molecule in TB and suggest its involvement in disease processes.

  • 5.
    Kenyon, Chris
    et al.
    HIV/STI Unit, Institute of Tropical Medicine, Antwerp, Belgium; Division of Infectious Diseases and HIV Medicine, University of Cape Town, Anzio Road, Observatory, South Africa.
    Buyze, Jozefien
    Clinical Trials Unit, Institute of Tropical Medicine, Antwerp, Belgium.
    Spiteri, G.
    European Centre for Disease Prevention and Control, Stockholm, Sweden.
    Cole, M. J.
    National Infection Service, Public Health England, London, United Kingdom.
    Unemo, Magnus
    Örebro universitet, Institutionen för medicinska vetenskaper. Region Örebro län. WHO Collaborating Centre for Gonorrhoea and other Sexually Transmitted Infections, Department of Laboratory Medicine.
    Population-level antimicrobial consumption is associated with decreased antimicrobial susceptibility in Neisseria gonorrhoeae in 24 European countries: an ecological analysis2019Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, artikkel-id jiz153Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    OBJECTIVES: There are substantial variations in Neisseria gonorrhoeae susceptibility to antimicrobials between different populations, and the reasons for this are largely unexplored. We aimed to assess if the population level consumption of antimicrobials is a contributory factor.

    METHODS: Using antimicrobial susceptibility data from 24 countries in the European Gonococcal Antimicrobial Surveillance Programme and antimicrobial consumption data from the IQVIA MIDAS database, we built mixed effects linear/logistic regression models with country-level cephalosporin, fluoroquinolone and macrolide consumption (standard doses/1000 population/year) as the explanatory variables (from 2009 to 2015) and 1-year lagged ceftriaxone, cefixime, azithromycin and ciprofloxacin geometric mean minimum inhibitory concentrations (MIC) as the outcome variables (2010 to 2016).

    RESULTS: Positive correlations were found between the consumption of cephalosporins and geometric mean MIC of ceftriaxone and cefixime (both P's <0.05). Fluoroquinolone consumption was positively associated with the prevalence of resistance to ciprofloxacin (P<0.05).

    CONCLUSIONS: Differences in population level consumption of particular antimicrobials may contribute to the variations in the level of antimicrobial resistance in N. gonorrhoeae in different settings. Further interventions to reduce misuse and overuse of antimicrobials in high-consumption populations and core-groups are required.

  • 6.
    Maravelia, Panagiota
    et al.
    Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Frelin, Lars
    Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Ni, Yi
    Department of Molecular Virology, University of Heidelberg, Heidelberg, Germany.
    Pérez, Noelia Caro
    Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Ahlén, Gustaf
    Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Jagya, Neetu
    Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Verch, Georg
    Department of Molecular Virology, University of Heidelberg, Heidelberg, Germany.
    Verhoye, Lieven
    Laboratory of Liver Infectious Diseases, Ghent University, Gent, Belgium.
    Pater, Lena
    Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Johansson, Magnus
    Örebro universitet, Institutionen för medicinska vetenskaper.
    Pasetto, Anna
    Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Meuleman, Philip
    Laboratory of Liver Infectious Diseases, Ghent University, Gent, Belgium.
    Urban, Stephan
    Department of Molecular Virology, University of Heidelberg, Heidelberg, Germany.
    Sällberg, Matti
    Division of Clinical Microbiology, Department of Laboratory Medicine, Karolinska Institutet, Stockholm, Sweden.
    Blocking entry of hepatitis B and D viruses to hepatocytes as a novel immunotherapy for treating chronic infections2020Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, artikkel-id jiaa036Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    BACKGROUND: Chronic hepatitis B and D virus (HBV/HDV) infections can cause cancer. Current HBV therapy using nucleoside analogues (NAs) is life-long and reduces but does not eliminate the risk of cancer. A hallmark of chronic hepatitis B is a dysfunctional HBV-specific T cell response. We therefore designed an immunotherapy driven by naïve healthy T cells specific for the HDV antigen (HDAg) to bypass the need for HBV-specific T cells in order to prime PreS1-specific T cells and PreS1 antibodies blocking HBV entry.

    METHODS: Ten combinations of PreS1 and/or HDAg sequences were evaluated for induction of PreS1 antibodies and HBV- and HDV- specific T cells in vitro and in vivo. Neutralization of HBV by PreS1-specific murine and rabbit antibodies was evaluated in cell culture, and rabbit anti-PreS1 were tested for neutralization of HBV in mice repopulated with human hepatocytes.

    RESULTS: The best vaccine candidate induced T cells to PreS1 and HDAg, and PreS1 antibodies blocking HBV entry in vitro. Importantly, adoptive transfer of PreS1 antibodies prevented, or modulated, HBV infection after a subsequent challenge in humanized mice.

    CONCLUSION: We here describe a novel immunotherapy for chronic HBV/HDV that targets viral entry to complement NAs and coming therapies inhibiting viral maturation.

  • 7. Mårtensson, Andreas
    et al.
    Ngasala, Billy
    Ursing, Johan
    Veiga, M. Isabel
    Wiklund, Lisa
    Membi, Christopher
    Montgomery, Scott M.
    Örebro universitet, Hälsoakademin.
    Premji, Zul
    Färnert, Anna
    Björkman, Anders
    Influence of consecutive-day blood sampling on polymerase chain reaction-adjusted parasitological cure rates in an antimalarial-drug trial conducted in Tanzania2007Inngår i: Journal of Infectious Diseases, ISSN 0022-1899, E-ISSN 1537-6613, Vol. 195, nr 4, s. 597-601Artikkel i tidsskrift (Fagfellevurdert)
    Abstract [en]

    We assessed the influence that consecutive-day blood sampling, compared with single-day blood sampling, had on polymerase chain reaction (PCR)-adjusted parasitological cure after stepwise genotyping of merozoite surface proteins 2 (msp2) and 1 (msp1) in 106 children in Tanzania who had uncomplicated falciparum malaria treated with either sulfadoxine-pyrimethamine or artemether-lumefantrine; 78 of these children developed recurrent parasitemia during the 42-day follow-up period. Initial msp2 genotyping identified 27 and 33 recrudescences by use of single- and consecutive-day sampling, respectively; in subsequent msp1 genotyping, 17 and 21 of these episodes, respectively, were still classified as recrudescences; these results indicate a similar sensitivity of the standard single-day PCR protocol--that is, 82% (27/33) and 81% (17/21), in both genotyping steps. Interpretation of PCR-adjusted results will significantly depend on methodology.

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