bluuebunny/crossref_metadata_2025_split huggingface dataset:
Effects of Daptomycin, Linezolid, and Vancomycin on Establishment of Intestinal Colonization with Vancomycin-Resistant Enterococci and Extended-Spectrum-β-Lactamase-Producing
Klebsiella pneumoniae
in Mice
Authors: Pultz Nicole J. , Stiefel Usha , Donskey Curtis J. 
Published: July 2005

ABSTRACT

In mice, vancomycin and linezolid treatment disrupted the anaerobic intestinal microflora, based on denaturing gradient gel electrophoresis analysis, and promoted colonization by
Klebsiella pneumoniae
and vancomycin-resistant enterococci. However, the effects varied depending on dose and duration of treatment. Daptomycin treatment did not disrupt the anaerobic microflora or promote either pathogen.
Molecular Characterization of the First Telithromycin-Resistant
Streptococcus pneumoniae
Isolate in Germany
Authors: Reinert Ralf René , van der Linden Mark , Al-Lahham Adnan 
Published: July 2005

ABSTRACT

A total of 486
Streptococcus pneumoniae
isolates were collected in 2003 and 2004 in Germany and revealed the following resistance rates: penicillin G (7.2%) and erythromycin A (18.9%). Telithromycin exhibited good in vitro activity (MIC at which 90% of the isolates tested were inhibited, 0.125 μg/ml). However, one
erm
(B)-positive isolate was found to be telithromycin resistant (MIC, 8 μg/ml).
First Nosocomial Outbreak of
Pseudomonas aeruginosa
Producing an Integron-Borne Metallo-β-Lactamase (VIM-2) in the United States
Authors: Lolans K. , Queenan A. M. , Bush K. , Sahud A. , Quinn J. P. 
Published: July 2005

ABSTRACT

Carbapenemases are rare in the United States. This is the first report of a United States nosocomial outbreak of pan-resistant
Pseudomonas aeruginosa
infections due to an integron-borne metallo-β-lactamase, VIM-2. This emergence of carbapenemases on mobile genetic elements in the United States warrants surveillance.
IS
26
-Associated In4-Type Integrons Forming Multiresistance Loci in Enterobacterial Plasmids
Authors: Miriagou Vivi , Carattoli Alessandra , Tzelepi Eva , Villa Laura , Tzouvelekis Leonidas S. 
Published: July 2005

ABSTRACT

Three distinct multiresistant loci from enterobacterial plasmids each comprised an integron and an IS
26
-associated sequence. Sequence comparison suggested a common ancestral structure that derived from an IS
26
insertion into the 5′ conserved segment of an In4-type integron and evolved through acquisition of gene cassettes and IS
26
-mediated recruitment of additional resistance genes of diverse origin.
In Vitro Interaction of Posaconazole and Caspofungin against Clinical Isolates of
Candida glabrata
Authors: Oliveira E. R. , Fothergill A. W. , Kirkpatrick W. R. , Coco B. J. , Patterson T. F. , Redding S. W. 
Published: July 2005

ABSTRACT

Combinations of caspofungin and posaconazole were evaluated by fractional inhibitory concentration index against 119
Candida glabrata
isolates. Synergy was seen in 18% of all isolates and in 4% of fluconazole-resistant isolates at 48 h without evidence of antagonism. This antifungal combination may have utility against this organism.
Nystatin Induces Secretion of Interleukin (IL)-1β, IL-8, and Tumor Necrosis Factor Alpha by a Toll-Like Receptor-Dependent Mechanism
Authors: Razonable Raymund R. , Henault Martin , Watson Harold L. , Paya Carlos V. 
Published: July 2005

ABSTRACT
Nystatin is an antifungal compound with potent proinflammatory properties. Herein, we demonstrate that nystatin induces interleukin (IL)-1β, IL-8, and tumor necrosis factor alpha secretion through its activation of toll-like receptor 1 (TLR1) and TLR2. Hence, a TLR-dependent mechanism could serve as the molecular basis for the proinflammatory properties of nystatin.
Novel Mechanism of Resistance to Oxazolidinones, Macrolides, and Chloramphenicol in Ribosomal Protein L4 of the Pneumococcus
Authors: Wolter Nicole , Smith Anthony M. , Farrell David J. , Schaffner William , Moore Matthew , Whitney Cynthia G. , Jorgensen James H. , Klugman Keith P. 
Published: July 2005

ABSTRACT

Two clinical
Streptococcus pneumoniae
isolates, identified as resistant to macrolides and chloramphenicol and nonsusceptible to linezolid, were found to contain 6-bp deletions in the gene encoding riboprotein L4. The gene transformed susceptible strain R6 so that it exhibited such resistance, with the transformants also showing a fitness cost. We demonstrate a novel bacterial mechanism of resistance to chloramphenicol and nonsusceptibility to linezolid.
Pharmacokinetics of Nelfinavir and Efavirenz in Antiretroviral-Naïve, Human Immunodeficiency Virus-Infected Subjects when Administered Alone or in Combination with Nucleoside Analog Reverse Transcriptase Inhibitors
Authors: Smith Patrick F. , Robbins Gregory K. , Shafer Robert W. , Wu Hulin , Yu Song , Hirsch Martin S. , Merigan Thomas C. , Park Jeong-Gun , Forrest Alan , Fischl Margaret A. , Morse Gene D. ,   the ACTG 384-5006 Team
Published: July 2005

ABSTRACT
Pharmacokinetic studies were conducted with human immunodeficiency virus-infected patients receiving efavirenz, nelfinavir, or both agents at weeks 4 and 32. Reductions of 25% and 45% were observed in the mean nelfinavir area under the concentration-time curve and minimum concentration of the drug in serum, and there was a 31% more rapid half-life for patients receiving both drugs compared to patients receiving nelfinavir alone. There were no significant differences in efavirenz pharmacokinetics.
In Vivo Transfer of Plasmid-Encoded ACC-1 AmpC from
Klebsiella pneumoniae
to
Escherichia coli
in an Infant and Selection of Impermeability to Imipenem in
K. pneumoniae
Authors: Bidet Philippe , Burghoffer Béatrice , Gautier Valérie , Brahimi Naïma , Mariani-Kurkdjian Patricia , El-Ghoneimi Alaa , Bingen Edouard , Arlet Guillaume 
Published: July 2005

ABSTRACT

We describe in vivo selection of a
Klebsiella pneumoniae
strain with diminished imipenem susceptibility attributable to plasmid-encoded ACC-1 β-lactamase production and loss of a 36-kDa major outer membrane protein, together with transfer of this plasmid from
K. pneumoniae
to
Escherichia coli
in a Tunisian infant.
Isocratic High-Performance Liquid Chromatographic Method with Ultraviolet Detection for Simultaneous Determination of Levels of Voriconazole and Itraconazole and Its Hydroxy Metabolite in Human Serum
Authors: Khoschsorur GholamAli , Fruehwirth Franz , Zelzer Sieglinde 
Published: July 2005

ABSTRACT
A simple, specific method is presented for simultaneous determination of voriconazole and itraconazole and its metabolite, hydroxyitraconazole, in human serum using one-step liquid-liquid extraction and high-performance liquid chromatography. Linearity tests ranged from 0.1 to 8.0 μg/ml; the minimum detectable concentration was 0.03 μg/ml.
In Vitro Synergy Testing of Anidulafungin with Itraconazole, Voriconazole, and Amphotericin B against
Aspergillus
spp. and
Fusarium
spp
Authors: Philip Annie , Odabasi Zekaver , Rodriguez Jose , Paetznick Victor L. , Chen Enuo , Rex John H. , Ostrosky-Zeichner Luis 
Published: July 2005

ABSTRACT

The in vitro interactions of anidulafungin with itraconazole, voriconazole, and amphotericin B were evaluated by using the checkerboard method. For
Aspergillus
spp., anidulafungin with amphotericin B showed indifference for 16/26 isolates, while anidulafungin with either azole showed a synergy trend for 18/26 isolates. All drug combinations showed indifference for 7/7
Fusarium
sp. isolates.
Simple Histidine-Rich Protein 2 Double-Site Sandwich Enzyme-Linked Immunosorbent Assay for Use in Malaria Drug Sensitivity Testing
Authors: Noedl Harald , Bronnert Jan , Yingyuen Kritsanai , Attlmayr Bernhard , Kollaritsch Herwig , Fukuda Mark 
Published: July 2005

ABSTRACT

A simple double-site sandwich enzyme-linked immunosorbent assay (ELISA) for
Plasmodium falciparum
in vitro drug sensitivity tests based on measuring histidine-rich protein 2 (HRP2) is presented. The ELISA uses two commercial monoclonal antibodies and provides a drastically cheaper alternative to the test kits previously used in the HRP2 drug sensitivity test. The assay is simple to establish and perform. The sensitivity is comparable and the drug sensitivity results very closely match those obtained with the commercial ELISA kits (
R
2
= 0.979; P < 0.001; mean log difference at the 50% inhibitory concentration = 0.07).
Inducement and Reversal of Tetracycline Resistance in
Escherichia coli
K-12 and Expression of Proton Gradient-Dependent Multidrug Efflux Pump Genes
Authors: Viveiros Miguel , Jesus Ana , Brito Mafalda , Leandro Clara , Martins Marta , Ordway Diane , Molnar Ana Maria , Molnar Joseph , Amaral Leonard 
Published: July 2005

ABSTRACT

Expression of eight transporter genes of
Escherichia coli
K-12 and its Δ
acrAB
mutant prior to and after induction of both strains to tetracycline resistance and after reversal of induced resistance were analyzed by quantitative reverse transcriptase PCR. All transporter genes were overexpressed after induced resistance with
acrF
being 80-fold more expressed in the Δ
acrAB
tetracycline-induced strain.
Novel Genetic Structure Associated with an Extended-Spectrum β-Lactamase
bla
VEB
Gene in a
Providencia stuartii
Clinical Isolate from Algeria
Authors: Aubert Daniel , Naas Thierry , Lartigue Marie-Frédérique , Nordmann Patrice 
Published: July 2005

ABSTRACT

A ceftazidime-resistant
Providencia stuartii
isolate from Algeria harbored a ca. 160-kb conjugative plasmid that contained a truncated
bla
VEB-1b
gene flanked by three 135-bp repeated elements. This work gives further evidence of the worldwide spread of
bla
VEB
genes that are associated with genetic structures other than class 1 integrons.
Integron-Encoded GES-Type Extended-Spectrum β-Lactamase with Increased Activity toward Aztreonam in
Pseudomonas aeruginosa
Authors: Poirel Laurent , Brinas Laura , Fortineau Nicolas , Nordmann Patrice 
Published: July 2005

ABSTRACT

A
Pseudomonas aeruginosa
strain expresses an extended-spectrum β-lactamase, GES-9, which differs from GES-1 by a Gly243Ser substitution, is inhibited by clavulanic acid and imipenem, and hydrolyzes aztreonam. The
bla
GES-9
gene was located inside a class 1 integron structure containing two copies of a novel insertion sequence belonging to the IS
1111
family.
p38 Mitogen-Activated Protein Kinase-Dependent Hyperinduction of Tumor Necrosis Factor Alpha Expression in Response to Avian Influenza Virus H5N1
Authors: Lee Davy C. W. , Cheung Chung-Yan , Law Anna H. Y. , Mok Chris K. P. , Peiris Malik , Lau Allan S. Y. 
Published: July 2005

ABSTRACT
Avian influenza A virus subtype H5N1 can infect humans to cause a severe viral pneumonia with mortality rates of more than 30%. The biological basis for this unusual disease severity is not fully understood. We previously demonstrated that in contrast to human influenza A virus subtypes including H1N1 or H3N2, the H5N1 virus associated with the “bird flu” outbreak in Hong Kong in 1997 (H5N1/97) hyperinduces proinflammatory cytokines, including tumor necrosis factor alpha (TNF-α), in primary human macrophages in vitro. To delineate the molecular mechanisms involved, we analyzed the role of transcription factor NF-κB and cellular kinases in TNF-α dysregulation. H5N1 and H1N1 viruses did not differ in the activation of NF-κB or degradation of IκB-α in human macrophages. However, we demonstrated that unlike H1N1 virus, H5N1/97 strongly activates mitogen-activated protein kinase (MAPK), including p38 MAPK and extracellular signal-regulated kinases 1 and 2. Specific inhibitors of p38 MAPK significantly reduced the H5N1/97-induced TNF-α expression in macrophages. Taken together, our findings suggest that H5N1/97-mediated hyperinduction of cytokines involves the p38 MAPK signaling pathway. These results may provide insights into the pathogenesis of H5N1 disease and rationales for the development of novel therapeutic strategies.
Mutations That Abrogate Human Immunodeficiency Virus Type 1 Reverse Transcriptase Dimerization Affect Maturation of the Reverse Transcriptase Heterodimer
Authors: Wapling Johanna , Moore Katie L. , Sonza Secondo , Mak Johnson , Tachedjian Gilda 
Published: July 2005

ABSTRACT
The specific impact of mutations that abrogate human immunodeficiency virus type 1 (HIV-1) reverse transcriptase (RT) dimerization on virus replication is not known, as mutations shown previously to inhibit RT dimerization also impact Gag-Pol stability, resulting in pleiotropic effects on HIV-1 replication. We have previously characterized mutations at codon 401 in the HIV-1 RT tryptophan repeat motif that abrogate RT dimerization in vitro, leading to a loss in polymerase activity. The introduction of the RT dimerization-inhibiting mutations W401L and W401A into HIV-1 resulted in the formation of noninfectious viruses with reduced levels of both virion-associated and intracellular RT activity compared to the wild-type virus and the W401F mutant, which does not inhibit RT dimerization in vitro. Steady-state levels of the p66 and p51 RT subunits in viral lysates of the W401L and W401A mutants were reduced, but no significant decrease in Gag-Pol was observed compared to the wild type. In contrast, there was a decrease in processing of p66 to p51 in cell lysates for the dimerization-defective mutants compared to the wild type. The treatment of transfected cells with indinavir suggested that the HIV-1 protease contributed to the degradation of virion-associated RT subunits. These data demonstrate that mutations near the RT dimer interface that abrogate RT dimerization in vitro result in the production of replication-impaired viruses without detectable effects on Gag-Pol stability or virion incorporation. The inhibition of RT activity is most likely due to a defect in RT maturation, suggesting that RT dimerization represents a valid drug target for chemotherapeutic intervention.
Human Cytomegalovirus UL131 Open Reading Frame Is Required for Epithelial Cell Tropism
Authors: Wang Dai , Shenk Thomas 
Published: July 2005

ABSTRACT
Epithelial cells are one of the prominent cell types infected by human cytomegalovirus (HCMV) within its host. However, many cultured epithelial cells, such as ARPE-19 retinal pigmented epithelial cells, are poorly infected by laboratory-adapted strains in cell culture, and little is known about the viral factors that determine HCMV epithelial cell tropism. In this report, we demonstrate that the UL131 open reading frame (ORF), and likely the entire UL131-128 locus, is required for efficient infection of epithelial cells. Repair of the mutated UL131 gene in the AD169 laboratory strain of HCMV restored its ability to infect both epithelial and endothelial cells while compromising its ability to replicate in fibroblasts. ARPE-19 epithelial cells support replication of the repaired AD169 virus as well as clinical isolates of HCMV. Productive infection of cultured epithelial cells, endothelial cells, and fibroblasts with the repaired AD169 virus leads to extensive membrane fusion and syncytium formation, suggesting that the virus may spread through cell-cell fusion.
cis
-Acting Packaging Signals in the Influenza Virus PB1, PB2, and PA Genomic RNA Segments
Authors: Liang Yuying , Hong Ying , Parslow Tristram G. 
Published: July 2005

ABSTRACT

The influenza A virus genome consists of eight negative-sense RNA segments. The
cis
-acting signals that allow these viral RNA segments (vRNAs) to be packaged into influenza virus particles have not been fully elucidated, although the 5′ and 3′ untranslated regions (UTRs) of each vRNA are known to be required. Efficient packaging of the NA, HA, and NS segments also requires coding sequences immediately adjacent to the UTRs, but it is not yet known whether the same is true of other vRNAs. By assaying packaging of genetically tagged vRNA reporters during plasmid-directed influenza virus assembly in cells, we have now mapped
cis
-acting sequences that are sufficient for packaging of the PA, PB1, and PB2 segments. We find that each involves portions of the distal coding regions. Efficient packaging of the PA or PB1 vRNAs requires at least 40 bases of 5′ and 66 bases of 3′ coding sequences, whereas packaging of the PB2 segment requires at least 80 bases of 5′ coding region but is independent of coding sequences at the 3′ end. Interestingly, artificial reporter vRNAs carrying mismatched ends (i.e., whose 5′ and 3′ ends are derived from different vRNA segments) were poorly packaged, implying that the two ends of any given vRNA may collaborate in forming specific structures to be recognized by the viral packaging machinery.
The Receptor for the Subgroup C Avian Sarcoma and Leukosis Viruses, Tvc, Is Related to Mammalian Butyrophilins, Members of the Immunoglobulin Superfamily
Authors: Elleder Daniel , Stepanets Volodymir , Melder Deborah C. , Šenigl Filip , Geryk Josef , Pajer Petr , Plachý Jiří , Hejnar Jiří , Svoboda Jan , Federspiel Mark J. 
Published: July 2005

ABSTRACT

The five highly related envelope subgroups of the avian sarcoma and leukosis viruses (ASLVs), subgroup A [ASLV(A)] to ASLV(E), are thought to have evolved from an ancestral envelope glycoprotein yet utilize different cellular proteins as receptors. Alleles encoding the subgroup A ASLV receptors (Tva), members of the low-density lipoprotein receptor family, and the subgroup B, D, and E ASLV receptors (Tvb), members of the tumor necrosis factor receptor family, have been identified and cloned. However, alleles encoding the subgroup C ASLV receptors (Tvc) have not been cloned. Previously, we established a genetic linkage between
tvc
and several other nearby genetic markers on chicken chromosome 28, including
tva
. In this study, we used this information to clone the
tvc
gene and identify the Tvc receptor. A bacterial artificial chromosome containing a portion of chicken chromosome 28 that conferred susceptibility to ASLV(C) infection was identified. The
tvc
gene was identified on this genomic DNA fragment and encodes a 488-amino-acid protein most closely related to mammalian butyrophilins, members of the immunoglobulin protein family. We subsequently cloned cDNAs encoding Tvc that confer susceptibility to infection by subgroup C viruses in chicken cells resistant to ASLV(C) infection and in mammalian cells that do not normally express functional ASLV receptors. In addition, normally susceptible chicken DT40 cells were resistant to ASLV(C) infection after both
tvc
alleles were disrupted by homologous recombination. Tvc binds the ASLV(C) envelope glycoproteins with low-nanomolar affinity, an affinity similar to that of binding of Tva and Tvb with their respective envelope glycoproteins. We have also identified a mutation in the
tvc
gene in line L15 chickens that explains why this line is resistant to ASLV(C) infection.
The Complete Genome Sequence of J Virus Reveals a Unique Genome Structure in the Family
Paramyxoviridae
Authors: Jack Philippa J. M. , Boyle David B. , Eaton Bryan T. , Wang Lin-Fa 
Published: July 2005

ABSTRACT

J virus (J-V) was isolated from feral mice (
Mus musculus
) trapped in Queensland, Australia, during the early 1970s. Although studies undertaken at the time revealed that J-V was a new paramyxovirus, it remained unclassified beyond the family level. The complete genome sequence of J-V has now been determined, revealing a genome structure unique within the family
Paramyxoviridae
. At 18,954 nucleotides (nt), the J-V genome is the largest paramyxovirus genome sequenced to date, containing eight genes in the order 3′-N-P/V/C-M-F-SH-TM-G-L-5′. The two genes located between the fusion (F) and attachment (G) protein genes, which have been named the small hydrophobic (SH) protein gene and the transmembrane (TM) protein gene, encode putative proteins of 69 and 258 amino acids, respectively. The 4,401-nt J-V G gene, much larger than other paramyxovirus attachment protein genes sequenced to date, encodes a putative attachment protein of 709 amino acids and distally contains a second open reading frame (ORF) of 2,115 nt, referred to as ORF-X. Taken together, these novel features represent the most significant divergence to date from the common six-gene genome structure of
Paramyxovirinae
. Although genome analysis has confirmed that J-V can be classified as a member of the subfamily
Paramyxovirinae
, it cannot be assigned to any of the five existing genera within this subfamily. Interestingly, a recently isolated paramyxovirus appears to be closely related to J-V, and preliminary phylogenetic analyses based on putative matrix protein sequences indicate that these two viruses will likely represent a new genus within the subfamily
Paramyxovirinae
.
Epstein-Barr Virus Nuclear Antigen 2 (EBNA2) Gene Deletion Is Consistently Linked with EBNA3A, -3B, and -3C Expression in Burkitt's Lymphoma Cells and with Increased Resistance to Apoptosis
Authors: Kelly Gemma L. , Milner Anne E. , Tierney Rosemary J. , Croom-Carter Debbie S. G. , Altmann Markus , Hammerschmidt Wolfgang , Bell Andrew I. , Rickinson Alan B. 
Published: July 2005

ABSTRACT
Most Epstein-Barr virus (EBV)-positive Burkitt's lymphomas (BLs) carry a wild-type EBV genome and express EBV nuclear antigen 1 (EBNA1) selectively from the BamHI Q promoter (latency I). Recently we identified a distinct subset of BLs carrying both wild-type and EBNA2 gene-deleted (transformation-defective) viral genomes. The cells displayed an atypical “BamHI W promoter (Wp)-restricted” form of latency where Wp (rather than Qp) was active and EBNA1, -3A, -3B, -3C, and -LP were expressed in the absence of EBNA2 or latent membrane proteins 1 and 2. Here we present data strongly supporting the view that the EBNA2-deleted genome is transcriptionally active in these cells and the wild-type genome is silent. Single-cell cloning of three parental Wp-restricted BL lines generated clones carrying either both viral genomes or the EBNA2-deleted genome only, never clones with the wild-type genome only. All rescued clones displayed the Wp-restricted form of latency characteristic of the parent line and retained the original parent cell phenotype. Interestingly, Wp-restricted parent lines and derived clones were markedly more resistant to inducers of apoptosis than standard latency I BL lines. Furthermore, in vitro infection of EBV-negative BL lines with an EBNA2 gene-deleted virus generated EBV-positive converts with Wp-restricted latency and a similarly marked apoptosis resistance. We postulate that, in the subset of BLs displaying Wp-restricted latency, infection of a tumor progenitor cell with an EBNA2 gene-deleted virus has provided that cell with a survival advantage through broadening antigen expression to include the EBNA3 proteins.