PLoS Neglected Tropical Diseases Journal Impact Factor & Information

Publisher: Public Library of Science, Public Library of Science

Journal description

PLoS Neglected Tropical Diseases is the first open-access journal devoted to the world's most neglected tropical diseases (NTDs), such as elephantiasis, river blindness, leprosy, hookworm, schistosomiasis, and African sleeping sickness. The journal publishes high-quality, peer-reviewed research on all scientific, medical, and public-health aspects of these forgotten diseases affecting the world's forgotten people.

Current impact factor: 4.49

Impact Factor Rankings

2015 Impact Factor Available summer 2015
2013 / 2014 Impact Factor 4.489
2012 Impact Factor 4.569
2011 Impact Factor 4.716
2010 Impact Factor 4.752
2009 Impact Factor 4.693
2008 Impact Factor 4.172

Impact factor over time

Impact factor
Year

Additional details

5-year impact 4.96
Cited half-life 2.50
Immediacy index 0.78
Eigenfactor 0.03
Article influence 1.48
Website PLoS Neglected Tropical Diseases website
Other titles PLoS neglected tropical diseases (Online), PLoS neglected tropical diseases
ISSN 1935-2735
OCLC 77500770
Material type Document, Periodical, Internet resource
Document type Internet Resource, Computer File, Journal / Magazine / Newspaper

Publisher details

Public Library of Science

  • Pre-print
    • Author can archive a pre-print version
  • Post-print
    • Author can archive a post-print version
  • Conditions
    • Creative Commons Attribution License
    • Eligible UK authors may deposit in OpenDepot
    • Publisher's version/PDF may be used
    • All titles are open access journals
  • Classification
    ​ green

Publications in this journal

  • [Show abstract] [Hide abstract]
    ABSTRACT: Inflammation plays an important role in the pathophysiology of Chagas disease, caused by Trypanosoma cruzi. Prostanoids are regulators of homeostasis and inflammation and are produced mainly by myeloid cells, being cyclooxygenases, COX-1 and COX-2, the key enzymes in their biosynthesis from arachidonic acid (AA). Here, we have investigated the expression of enzymes involved in AA metabolism during T. cruzi infection. Our results show an increase in the expression of several of these enzymes in acute T. cruzi infected heart. Interestingly, COX-2 was expressed by CD68+ myeloid heart-infiltrating cells. In addition, infiltrating myeloid CD11b+Ly6G- cells purified from infected heart tissue express COX-2 and produce prostaglandin E2 (PGE2) ex vivo. T. cruzi infections in COX-2 or PGE2-dependent prostaglandin receptor EP-2 deficient mice indicate that both, COX-2 and EP-2 signaling contribute significantly to the heart leukocyte infiltration and to the release of chemokines and inflammatory cytokines in the heart of T. cruzi infected mice. In conclusion, COX-2 plays a detrimental role in acute Chagas disease myocarditis and points to COX-2 as a potential target for immune intervention.
    PLoS Neglected Tropical Diseases 08/2015; 9(8):e0004025. DOI:10.1371/journal.pntd.0004025
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Enterotoxigenic Escherichia coli (ETEC) is an endemic health threat in underdeveloped nations. Despite the significant effort extended to vaccine trials using ETEC colonization factors, these approaches have generally not been especially effective in mediating cross-protective immunity. We used quantitative proteomics to identify 24 proteins that differed in abundance in membrane protein preparations derived from wild-type vs. a type II secretion system mutant of ETEC. We expressed and purified a subset of these proteins and identified nine antigens that generated significant immune responses in mice. Sera from mice immunized with either the MltA-interacting protein MipA, the periplasmic chaperone seventeen kilodalton protein, Skp, or a long-chain fatty acid outer membrane transporter, ETEC_2479, reduced the adherence of multiple ETEC strains differing in colonization factor expression to human intestinal epithelial cells. In intranasal challenge assays of mice, immunization with ETEC_2479 protected 88% of mice from an otherwise lethal challenge with ETEC H10407. Immunization with either Skp or MipA provided an intermediate degree of protection, 68 and 64%, respectively. Protection was significantly correlated with the induction of a secretory immunoglobulin A response. This study has identified several proteins that are conserved among heterologous ETEC strains and may thus potentially improve cross-protective efficacy if incorporated into future vaccine designs.
    PLoS Neglected Tropical Diseases 08/2015; 9(8):e0003924. DOI:10.1371/journal.pntd.0003924