The Journal of Infectious Diseases (J INFECT DIS)

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

Journal description

Founded in 1904, The Journal of Infectious Diseases is the premier publication in the Western Hemisphere for original research on the pathogenesis, diagnosis, and treatment of infectious diseases; on the microbes that cause them; and on disorders of host immune mechanisms. Articles in JID include research results from microbiology, immunology, epidemiology, and related disciplines.

Current impact factor: 5.78

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 5.778
2012 Impact Factor 5.848
2011 Impact Factor 6.41
2010 Impact Factor 6.288
2009 Impact Factor 5.865
2008 Impact Factor 5.682
2007 Impact Factor 6.035
2006 Impact Factor 5.363
2005 Impact Factor 4.953
2004 Impact Factor 4.943
2003 Impact Factor 4.481
2002 Impact Factor 4.857
2001 Impact Factor 4.91
2000 Impact Factor 4.988
1999 Impact Factor 4.842
1998 Impact Factor 4.966
1997 Impact Factor 5.099
1996 Impact Factor 5.418
1995 Impact Factor 4.945
1994 Impact Factor 4.781
1993 Impact Factor 4.808
1992 Impact Factor 5.499

Impact factor over time

Impact factor

Additional details

5-year impact 5.91
Cited half-life 8.00
Immediacy index 1.56
Eigenfactor 0.10
Article influence 2.15
Website Journal of Infectious Diseases, The website
Other titles The Journal of infectious diseases, JID
ISSN 0022-1899
OCLC 1754628
Material type Periodical, Internet resource
Document type Journal / Magazine / Newspaper, Internet Resource

Publisher details

Oxford University Press (OUP)

  • Pre-print
    • Archiving status unclear
  • Post-print
    • Author cannot archive a post-print version
  • Restrictions
    • 12 months embargo
  • Conditions
    • Author's post-print in Institutional repository and Central repositories
    • Publisher's version/PDF cannot be used
    • Published source must be acknowledged
    • Must link to publisher version
    • Set phrase to accompany archived copy (see policy)
    • Eligible authors may deposit in OpenDepot
    • The publisher will deposit in PubMed Central on behalf of NIH authors
    • This policy is an exception to the default policies of 'Oxford University Press (OUP)'
  • Classification
    ​ white

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: In 2015, tuberculosis remains a major global health problem, and drug-resistant tuberculosis is a growing threat. Although tuberculosis diagnosis in many countries is still reliant on older tools, new diagnostics are changing the landscape. Stimulated, in part, by the success and roll out of Xpert MTB/RIF, there is now considerable interest in new technologies. The landscape looks promising, with a robust pipeline of new tools, particularly molecular diagnostics, and well over 50 companies actively engaged in product development. However, new diagnostics are yet to reach scale, and there needs to be greater convergence between diagnostics development and development of shorter-duration tuberculosis drug regimens. Another concern is the relative absence of non-sputum-based diagnostics in the pipeline for children and of biomarker tests for triage, cure, and progression of latent Mycobacterium tuberculosis infection. Several initiatives, described in this supplement, have been launched to further stimulate product development and policy, including assessment of needs and priorities, development of target product profiles, compilation of data on resistance-associated mutations, and assessment of market size and potential for new diagnostics. Advocacy is needed to increase funding for tuberculosis research and development, and governments in high-burden countries must invest more in tuberculosis control to meet post-2015 targets for care, control, and prevention. © The Author 2014. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail:
    The Journal of Infectious Diseases 04/2015; 211(suppl 2):S21-S28. DOI:10.1093/infdis/jiu803
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background. Four priority target product profiles for the development of diagnostic tests for tuberculosis were identified: 1) Rapid sputum-based (RSP), 2) non-sputum Biomarker-based (BMT), 3) triage test followed by confirmatory test (TT), and 4) drug-susceptibility testing (DST). Methods. We assessed the cost of the new tests in suitable strategies and of the conventional diagnosis of tuberculosis as per World Health Organization guidelines, in 36 high tuberculosis and MDR burden countries. Costs were then compared to the available funding for tuberculosis at country level. Results. Costs of diagnosing tuberculosis using RSP ranged US$93-187 million/year; if RSP unit cost is of US$2-4 it would be lower/similar cost than conventional strategy with sputum smear microscopy (US$ 119 million/year). Using BMT (with unit cost of US$2-4) would cost US$70-121 million/year and be lower/comparable cost than conventional diagnostics. Using TT with TPP characteristics (unit cost of US$1-2) followed by Xpert would reduce diagnostic costs up to US$36 million/year. Costs of using different novel DST strategies for the diagnosis of drug resistance would be higher compared with conventional diagnosis. Conclusions. Introducing a TT or a biomarker test with optimal characteristics would be affordable from a cost and affordability perspective at the current available funding for tuberculosis. Additional domestic or donor funding would be needed in most countries to achieve affordability for other new diagnostic tests.
    The Journal of Infectious Diseases 04/2015; 211(suppl 2):S67-S77. DOI:10.1093/infdis/jiu820
  • The Journal of Infectious Diseases 04/2015; 211(suppl 2):S78-S80. DOI:10.1093/infdis/jiu822
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    ABSTRACT: Background. Streptococcus pneumoniae (pneumococcus) colonizes mucosal surfaces of the upper respiratory tract (URT), resulting in invasive disease. Macrolides are known for their immunomodulatory effects. We investigated the potency of macrolides to reduce pneumococcal colonization by activating host innate immunity. Methods. The kinetics of colonization, cellular response, and inflammatory cytokine levels in the URT were assessed after nasal inoculation of pneumococci. EM900 (a novel 12-membered non-antibiotic macrolide having an immunomodulatory effect) was orally administered throughout the experiment. Survival was evaluated for 10 days. Macrolide-mediated CCL2 production from peritoneal macrophages was determined by ELISA. The cell-signaling pathway was analyzed by western blotting and gene silencing assays. Results. S. pneumoniae was significantly reduced from EM900-treated mice 14 days after pneumococcal inoculation. Macrophage recruitment and Ccl2 mRNA expression were promoted. CCL2 production from peritoneal macrophages was significantly induced by macrolides and was dependent on NF-κB phosphorylation through the MyD88- or TRIF-mediated pathway. Mortality of mice with invasive pneumococcal disease was improved by pre-treatment with EM900. Conclusions. Macrolides may inhibit invasive pneumococcal infections by accelerating the clearance of pneumococcal nasopharyngeal colonization via promotion of macrophage-mediated innate immunity.
    The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv157
  • The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv041
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    ABSTRACT: Background. Thrombocytopenia is a common finding during viral hemorrhagic fever, which includes hemorrhagic fever with renal syndrome (HFRS). The two 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. Conclusion. HFRS patients have increased thrombopoiesis and platelet activation, which contributes to intravascular coagulation.
    The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv161
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    ABSTRACT: Background. Treatment initiation rapidly kills most drug-susceptible Mycobacterium tuberculosis, but a bacterial sub-population tolerates prolonged drug exposure. We evaluated drug-tolerant bacilli in human sputum by comparing mRNA expression of drug-tolerant bacilli that survive the early bactericidal phase with treatment-naïve bacilli. Methods. M. tuberculosis gene expression was quantified via RT-PCR in serial sputa from 17 Ugandans treated for drug-susceptible pulmonary tuberculosis. Results. Within four days, bacterial mRNA abundance declined >98%, indicating rapid killing. Thereafter, the rate of decline slowed >94%, indicating drug tolerance. After 14 days, 16S rRNA transcripts/genome declined 96%, indicating slow growth. Drug-tolerant bacilli displayed marked down-regulation of genes associated with growth, metabolism and lipid synthesis and up-regulation in stress responses and key regulatory categories - including stress-associated sigma factors, transcription factors, and toxin-antitoxin genes. Drug efflux pumps were up-regulated. The isoniazid stress signature was induced by initial drug exposure then disappeared after four days. Conclusions. Transcriptional patterns suggest that drug-tolerant bacilli in sputum are in a slow-growing, metabolically and synthetically down-regulated state. Absence of the isoniazid stress signature in drug-tolerant bacilli indicates that physiological state influences drug responsiveness in vivo. These results identify novel drug targets that should aid in development of novel shorter TB treatment regimens.
    The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv149
  • [Show abstract] [Hide abstract]
    ABSTRACT: Background. HIV-infected individuals are at higher risk for chronic kidney disease compared to -uninfected individuals. We investigated whether the inflammation present in treated HIV infection contributes to kidney dysfunction among HIV-infected men receiving HAART. Methods. Glomerular filtration rate (GFR) was directly measured (using iohexol) along with 12 markers of inflammation in Multicenter AIDS Cohort Study participants. Exploratory Factor Analysis was used to identify inflammatory processes related to kidney dysfunction. The estimated levels of these inflammatory processes were used in adjusted logistic regression analyses evaluating cross-sectional associations with kidney function outcomes. Results. There were 434 HIV-infected men on HAART and 200 HIV-uninfected men. HIV-infected men were younger (median: 51 versus 53 years), had higher urine protein-to-creatinine ratios (median: 98 versus 66 mg/g) but comparable GFRs (median: 109 versus 106 ml/min|1.73m2). We found an inflammatory process dominated by markers: soluble TNF receptor 2, soluble interleukin 2 receptor α, sgp130, sCD27, and sCD14. A one standard deviation increase in that inflammatory process was associated with significantly greater odds of GFR≤90 ml/min/1.73m2 (OR=2.0) and urine protein >200 mg/g (OR=2.3). Conclusion. Higher circulating levels of immune activation markers among treated HIV-infected men may partially explain their higher burden of kidney dysfunction compared to uninfected men.
    The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv159
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    ABSTRACT: Studies in animals and human volunteers demonstrate that antibodies against the repeat- region of the Plasmodium Circumsporozoite Protein (CSP) abrogate sporozoite infection. However, the realization that the N- and C- terminal regions flanking the repeats play essential roles in parasite infectivity raised the possibility that they could be targeted by protective antibodies. We characterized a monoclonal antibody (mAb5D5) specific for the N-terminus of the P. falciparum CSP which inhibits the proteolytic cleavage of the CSP, a key requirement for parasite infection of hepatocytes. Adoptive transfer of mAb5D5 strongly inhibits the in vivo infection of sporozoites expressing the N-terminus of P. falciparum CSP, and this protection is greatly enhanced when combined with anti-repeat antibodies. Our results show that antibodies interfering with molecular processes required for parasite infectivity can exert a strong in vivo protective activity and indicate that pre-erythrocytic vaccines against Plasmodium should include the CSP N-terminal region. © The Author 2015. Published by Oxford University Press on behalf of the Infectious Diseases Society of America. All rights reserved. For Permissions, please e-mail:
    The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv154
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    ABSTRACT: Background. Human immunodeficiency virus (HIV) -infected individuals are at increased risk of invasive pneumococcal disease (IPD). In order to assess the immunogenicity of pneumococcal proteins and polysaccharide, we investigated protein and serotype-specific antibody responses after HIV-associated IPD. Methods. Specific anti-pneumococcal immunoglobulin G (IgG) to 27 pneumococcal protein antigens and 30 serotype polysaccharides was measured in plasma before and after IPD in HIV-infected individuals and compared to HIV-infected individuals without IPD. Results. Over time, 81% of IPD cases responded to at least one protein compared to 51% of non-IPD controls. HIV IPD cases responded to more proteins than non-IPD controls (8.6 ±8.4 vs. 4.2 ±7.6 proteins, p=0.01), and had a significantly higher probability of yielding an antibody response to the proteins PiaA, PsaA and PcpA. Twenty-two percent of HIV-infected individuals with IPD had a serotype specific antibody response. Younger age at the time of IPD was the only predictor of a serotype specific pneumococcal antibody response, whereas we did not identify predictors of a protein specific antibody response. Conclusion. Antibody responses occurred more frequently to pneumococcal proteins than to polysaccharide and protein antibodies persisted for longer than polysaccharide specific antibodies. PcpA, PiaA and PsaA were the most immunogenic proteins.
    The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv158
  • The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv131
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    ABSTRACT: Background. HIV infection leads to lower rates of HCV clearance after acute infection, higher HCV viremia, and accelerated progression of HCV-related fibrosis. The mechanisms underlying this acceleration of HCV progression by HIV are poorly understood, but HIV-induced dysfunction in the anti-HCV humoral immune response may play a role. Methods. To define the effect of HIV coinfection on the anti-HCV antibody response, we measured anti-HCV envelope (E1E2) binding antibody titers, neutralizing antibody (nAb) titers, and neutralizing antibody breadth of serum from HCV-infected subjects isolated longitudinally before and after incident HIV infection. Results. A significant reduction in HCV envelope-specific binding antibody and neutralizing antibody titers was detected in subjects with CD4+ T cell counts of <350 cells/mm3 after HIV infection, and subjects with CD4+ T cell counts of <200 cells/mm3 also showed a reduction in nAb breadth. Subjects who maintained ≥350 CD4+ T cells/mm3 displayed little to no decline in antibody levels. Conclusions. Depletion of CD4+ T cells by HIV infection results in a global decline in the anti-HCV envelope antibody response, including binding antibody titers, neutralizing antibody titers, and neutralizing antibody breadth.
    The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv139
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    ABSTRACT: Background. HIV/hepatitis C virus (HCV) coinfection is associated with reduced bone mineral density (BMD) and increased fracture rates, particularly in women. The structural underpinnings for skeletal fragility in coinfected women have not been characterized. We used tibia peripheral quantitative computed tomography (pQCT) to evaluate skeletal parameters in women, by HIV/HCV status. Methods. We conducted a cross-sectional study among 50 HIV/HCV-coinfected, 51 HCV-monoinfected, and 50 HIV-monoinfected women. Tibial volumetric BMD and cortical dimensions were determined by pQCT. Race-specific Z-scores for age were generated using 263 female reference participants without HIV or liver disease. Results. Coinfected participants had lower mean trabecular volumetric BMD (-0.85), cortical volumetric BMD (-0.67), cortical area (-0.61), and cortical thickness (-0.77) Z-scores than reference participants (all p<0.001). The smaller cortical dimensions were due to greater mean endosteal circumference (+0.67; p<0.001) and comparable periosteal circumference (+0.04; p=0.87) Z-scores. Trabecular volumetric BMD was lower in coinfected than HCV- and HIV-monoinfected participants. HCV-infected women with stage 3-4 liver fibrosis had lower mean trabecular volumetric BMD, cortical thickness, and total hip BMD Z-scores than those with stage 0-2 fibrosis. Conclusions. Compared to healthy reference patients, HIV/HCV-coinfected women had decreased tibial trabecular volumetric BMD, diminished cortical dimensions, and significant endocortical bone loss.
    The Journal of Infectious Diseases 03/2015; DOI:10.1093/infdis/jiv147