The Journal of Infectious Diseases

Publisher: Memorial Institute for Infectious Diseases (Chicago, Ill.); John McCormick Institute for Infectious Diseases; John Rockefeller McCormick Memorial Fund; Infectious Diseases Society of America

Description

Impact factor 5.85

  • 5-year impact
    5.91
  • Cited half-life
    8.00
  • Immediacy index
    1.56
  • Eigenfactor
    0.10
  • Article influence
    2.15
  • Other titles
    Journal of infectious diseases (Online), The journal of infectious diseases (Online. University of Chicago Press), JID
  • ISSN
    1537-6613
  • OCLC
    41275996
  • Material type
    Document, Periodical, Internet resource
  • Document type
    Internet Resource, Computer File, Journal / Magazine / Newspaper

Publications in this journal

  • The Journal of Infectious Diseases 01/2015;
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    ABSTRACT: Background. Influenza vaccine immunogenicity is suboptimal in immunocompromised patients. However, there are limited data on the interplay of T- and B- cell responses to vaccination with simultaneous immunosuppression. Methods. We collected peripheral blood mononuclear cells from transplant recipients pre and one-month post seasonal influenza vaccination. Pre- and post-vaccination, H1N1-specific T- and B-cell activation were quantified using flow cytometry. We further developed a mathematical model using T- and B-cell markers, and mycophenolate mofetil (MMF) dosage. Results. In the 47 patients analyzed, seroconversion to H1N1-antigen was 34%. H1N1-specific IL-4-producing CD4+ T-cell frequencies significantly increased after vaccination in 53% of the patients. Pre-vaccination expression of H1N1-induced HLA-DR and CD86 on B-cells was high in patients that seroconverted. Seroconversion against H1N1 was strongly associated with HLA-DR-expression on B-cells, which was dependent on the increase of H1N1-specific IL-4+CD4+ T-cells pre-to-post vaccine (R2=0.35). High doses of MMF ≥2g/d led to lower seroconversion rates, lower increase of H1N1-specific IL-4+CD4+ T-cells and reduced HLA-DR-expression on B-cells. The mathematical model incorporating a MMF-inhibited positive feedback loop between H1N1-specific IL-4+CD4+ T-cells and HLA-DR-expression on B-cells captured seroconversion with high specificity. Conclusions. Seroconversion is associated with influenza-specific Th2 and B-cell activation and appears to be modulated by MMF.
    The Journal of Infectious Diseases 01/2015;
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    ABSTRACT: in press
    The Journal of Infectious Diseases 12/2014; in press(MS #56202R1).
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    ABSTRACT: Daptomycin is a lipopeptide antibiotic that is used clinically against many Gram-positive bacterial pathogens, and is considered a key front-line bactericidal antibiotic to treat multidrug-resistant enterococci. Emergence of daptomycin resistance during therapy of serious enterococcal infections is a major clinical issue. In this work, we show that deletion of the gene encoding the response regulator, LiaR (a member of the LiaFSR system that controls cell envelope homeostasis), from daptomycin-resistant E. faecalis, not only reversed resistance to two clinically available cell membrane-targeting antimicrobials (daptomycin and telavancin), but also resulted in hypersusceptibility to these antibiotics, as well as to a variety of antimicrobial peptides of diverse origin and with different mechanisms of action. The changes in susceptibility to these antibiotics and antimicrobial peptides correlated with in vivo attenuation in a Caenorhabditis elegans model. Mechanistically, deletion of liaR altered the localization of cardiolipin microdomains in the cell membrane. Our findings suggest that LiaR is a master regulator of the enterococcal cell membrane response to diverse antimicrobial agents and peptides; as such, LiaR represents a novel target to restore the activity of clinically available antimicrobials against these organisms and, potentially, increase susceptibility to endogenous antimicrobial peptides.
    The Journal of Infectious Diseases 10/2014;
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    ABSTRACT: Identifying the source of resurgent parasites is paramount to strategic and successful intervention for malaria elimination. Although malaria incidence in Panama is low, a recent outbreak resulted in a six-fold increase in reported cases. We hypothesized parasites sampled from this epidemic might be related and exhibit clonal population structure. We tested the genetic relatedness using informative single nucleotide polymorphisms and drug resistance loci. We found the parasites to be clustered into three clonal subpopulations and shared relatedness with parasites from Colombia. Two clusters of Panamanian parasites shared identical drug resistance haplotypes, and all clusters shared a chloroquine-resistance genotype matching the pfcrt haplotype of Colombian origin. Our findings suggest these resurgent parasite populations are highly clonal and likely resulted from epidemic expansion of imported or vestigial cases. Outbreak investigation using genetic tools can illuminate potential sources of epidemic malaria and guide strategies to prevent further resurgence in areas of malaria elimination.
    The Journal of Infectious Diseases 10/2014;
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    ABSTRACT: The discovery of obligatory intracellular bacteria of the genus Wolbachia in filariae infecting humans led to the use of antibiotics as a potent treatment option. Mansonella perstans is the cause of the second most prevalent filariasis in Gabon, but so far reports on the presence of Wolbachia in this nematode have been inconsistent. We report on the presence of Wolbachia in M. perstans in patients from Gabon, which we identified using PCR with primer sets specific for 16S rDNA and ftsZ. Sequence analysis revealed a single consensus sequence, which could be phylogenetically assigned to Wolbachia of the supergroup F. Wolbachia could only be identified in 5 out of 14 and 7 out of 14 cases, depending on the investigated gene; detection of Wolbachia was associated with higher filaremia. Before generalizing the use of antibiotics for mansonellosis, further clarification of the obligatory nature of the endosymbiosis in this nematode is needed.
    The Journal of Infectious Diseases 06/2014;
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    ABSTRACT: BACKGROUND: ZNRD1 was identified as a host protein required for the completion of the human immunodeficiency virus (HIV) lifecycle in a genome-wide screen using small interfering RNA gene silencing. Subsequently, a genome-wide association study (GWAS) of host determinants for HIV-1 disease identified an association of single nucleotide polymorphisms (SNPs) in the ZNRD1 region with CD4(+) T-cell depletion. METHODS: We investigated the effects of SNPs in the ZNRD1 region on human immunodeficiency virus type 1 (HIV-1) infection and progression to clinical outcomes in 5 US-based HIV-1 longitudinal cohorts consisting of men who have sex with men, males with hemophilia, and injection drug users (IDUs) (n = 1865). SNP function was evaluated by electrophoretic mobility shift assay and promoter luciferase assay. RESULTS: A haplotype in the ZNRD1 gene showed significant association with a 35% decreased risk of HIV-1 acquisition (OR = 0.65, 95% CI, .47-.89), independent of HLA-C rs9264942, in European Americans. The SNP rs3132130 tagging this haplotype, located in the ZNRD1 5' upstream region, caused a loss of nuclear factor binding and decrease in ZNRD1 promoter activity. ZNRD1 variants also affected HIV-1 disease progression in European- and African-American cohorts. CONCLUSIONS: This study provides novel evidence that ZNRD1 polymorphism may confer host resistance to HIV-1 acquisition. Published by Oxford University Press on behalf of the Infectious Diseases Society of America 2014. This work is written by (a) US Government employee(s) and is in the public domain in the US.
    The Journal of Infectious Diseases 05/2014; 210(10):1539-48.
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    ABSTRACT: Ingestion of B. anthracis spores causes gastrointestinal (GI) anthrax. Humoral immune responses, in particular, IgA secreting B-1 cells, play a critical role in the clearance of GI pathogens. Here, we investigated whether B. anthracis impacts the function of colonic B-1 cells to establish active infection. GI anthrax infection led to significant inhibition of immunoglobulins (e.g., IgA) and increased program death-1 (PD-1) on B-1 cells. Furthermore, infection also diminished type 2 innate lymphoid cells (ILC2) and their ability to enhance differentiation and immunoglobulin production by secreting IL-5. Such B-1 cell and ILC2 dysfunction is potentially due to cleavage of p38 and Erk1/2 MAPK in these cells. Conversely, mice that survived infection generated neutralizing antibodies via the formation of robust germinal center B cells in Peyer's patches and had restored B-1 and ILC2 function. These data may provide additional insight for designing efficacious vaccines and therapeutics against such a deadly pathogen.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: The development of drugs and vaccines to reduce malaria transmission is an important part of eradication plans. The transmission reducing activity (TRA) of these agents is currently determined in the standard membrane feeding assay (SMFA) based on subjective microscopical read-outs and with limitations in up-scaling and throughput. Utilising a Plasmodium falciparum strain expressing the firefly luciferase protein, we present a luminescence based approach to SMFA evaluation that eliminates the requirement for mosquito dissections in favour of a simple approach where whole mosquitoes are homogenised and examined directly for luciferase activity. Analysis of 6860 Anopheles stephensi mosquitoes across 68 experimental feeds shows that the luminescence assay was as sensitive as microscopy for infection detection. The mean luminescence intensity of individual and pooled mosquitoes accurately quantifies mean oocyst intensity and generates comparable TRA estimates. The luminescence assay presented here could increase SMFA throughput so that 10-30 experimental feeds could be evaluated in a single 96-well plate. This new method of assessing Plasmodium infection and transmission intensity could expedite the screening of novel drug compounds, vaccine candidates and sera from malaria exposed individuals for TRA. Luminescence-based estimates of oocyst intensity in individual mosquitoes should be interpreted with caution.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: Streptococcus (S.) pneumoniae is the most common causative pathogen in community-acquired pneumonia. Mast cells are mainly located at the host-environment interface where they function as sentinels. To study the role of mast cells during pneumonia caused by S.pneumoniae. Lung tissue of patients who had died from pneumococcal pneumonia or a non-pulmonary cause was stained for mast cells and tryptase. Wild type (WT) and mast cell deficient (Kit(W-sh/W-sh)) mice were observed or sacrificed after induction of pneumonia by intranasal inoculation of S.pneumoniae. In separate experiments WT mice were treated with mast cell stabilizing agents doxantrazole or cromoglycate. The constitutive presence of tryptase positive mast cells was reduced in affected lungs from pneumonia patients. Kit(W-sh/W-sh) mice showed a prolonged survival during the first days after LD100 and LD50 infection, while overall mortality did not differ from that in WT mice. Relative to WT mice, Kit(W-sh/W-sh) mice showed reduced bacterial counts with less bacterial dissemination to distant organs and less inflammation. Neither doxantrazole nor cromoglycate influenced antibacterial defense or inflammatory responses after airway infection with S.pneumoniae. Mast cells exhibit an unfavorable role in host defense during pneumococcal pneumonia by a mechanism independent of degranulation.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: The Phase III Zostavax Efficacy and Safety Trial of 1 dose of licensed zoster vaccine (ZV) (Zostavax; Merck) in 50-59 year-olds showed approximately 70% vaccine efficacy (VE) to reduce the incidence of herpes zoster (HZ). An objective of the trial was to assess immune response biomarkers measuring antibodies to varicella zoster virus (VZV) [by glycoprotein enzyme-linked immunosorbent assay] as correlates of protection (CoPs) against HZ. The principal stratification 'vaccine efficacy curve' framework for statistically evaluating immune response biomarkers as CoPs was applied. The VE curve describes how VE against the clinical endpoint (HZ) varies across participant subgroups defined by biomarker readout measuring vaccine-induced immune response. The VE curve was estimated using several subgroup definitions. The fold rise in VZV antibody titers from pre-immunization to 6 weeks was an excellent CoP, with VE increasing sharply with fold rise [VE estimated at 0% for the subgroup with no rise and at 90% for the subgroup with 5.26-fold rise]. In contrast, VZV antibody titers measured 6 weeks after immunization did not predict VE, with similar estimated VE across titer subgroups. The analysis illustrates the value of the VE curve framework for assessing immune response biomarkers as CoPs in vaccine efficacy trials.
    The Journal of Infectious Diseases 05/2014;
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    ABSTRACT: It is well established that immunization with attenuated malaria sporozoites induces CD8+ T cells that eliminate parasite-infected hepatocytes. Liver memory CD8+ T cells induced by immunization with parasites undergo a unique differentiation program and have enhanced expression of CXCR6. Following immunization with malaria parasites, CXCR6-deficient memory CD8+ T cells recovered from the liver display altered cell-surface expression markers compared to their wild type counterparts but they exhibit normal cytokine secretion and expression of cytotoxic mediators on a per-cell basis. Most importantly, CXCR6-deficient CD8+ T cells migrate to the liver normally after immunization with malaria sporozoites or vaccinia virus, but few weeks later their numbers severely decrease in this organ, losing their capacity to inhibit malaria parasite development in the liver. These studies show for the first time that CXCR6 is critical for the development and maintenance of protective memory CD8+ T cells in the liver.
    The Journal of Infectious Diseases 05/2014;
  • The Journal of Infectious Diseases 05/2014;