bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multi-Virulence-Locus Sequence Typing Identifies Single Nucleotide Polymorphisms Which Differentiate Epidemic Clones and Outbreak Strains ofListeria monocytogenes
Authors: Chen Yi , Zhang Wei , Knabel Stephen J. 
Published: January 2007

ABSTRACTA recently developed multi-virulence-locus sequence typing (MVLST) method showed improved discriminatory power for subtyping genetically diverseListeria monocytogenesisolates and identified epidemic clone II isolates associated with two recent U.S. multistate listeriosis outbreaks. To evaluate the ability of MVLST to distinguish other epidemic clones and outbreak strains ofL. monocytogenes, 58 outbreak-related isolates from 14 outbreaks and 49 unrelated isolates were analyzed. Results showed that MVLST provided very high discriminatory power (0.99), epidemiological concordance (1.0), stability, and typeability. MVLST accurately identified three previously known epidemic clones (epidemic clones I, II, and III) and redefined another epidemic clone (epidemic clone IV) in serotype 4b ofL. monocytogenes. A set of 28 single nucleotide polymorphisms (SNPs) differentiated all epidemiologically unrelated isolates. A subset of 16 SNPs differentiated all epidemic clones and outbreak strains. Phylogenetic analysis showed congruence between MVLST clusters, serotypes, and previously defined genetic lineages ofL. monocytogenes. SNPs in virulence genes appear to be excellent molecular markers for the epidemiological investigation of epidemics and outbreaks caused byL. monocytogenes.
High Prevalence of Human Bocavirus Detected in Young Children with Severe Acute Lower Respiratory Tract Disease by Use of a Standard PCR Protocol and a Novel Real-Time PCR Protocol
Authors: Kleines Michael , Scheithauer Simone , Rackowitz Annette , Ritter Klaus , Häusler Martin 
Published: January 2007

ABSTRACT

The human bocavirus (HBoV) was recently isolated from respiratory tract samples. Within a study collective of children with severe lower respiratory tract disease, the patients testing positive for HBoV (12.8%) had a higher rate of underlying cardiopulmonary disease. Viral loads in respiratory tract specimens varied from 10
2
to 10
10
genome equivalents/ml.
Correlation of Neo-Sensitabs Tablet Diffusion Assay Results on Three Different Agar Media with CLSI Broth Microdilution M27-A2 and Disk Diffusion M44-A Results for Testing Susceptibilities of
Candida
spp. and
Cryptococcus neoformans
to Amphotericin B, Caspofungin, Fluconazole, Itraconazole, and Voriconazole
Authors: Espinel-Ingroff A. , Canton E. , Gibbs D. , Wang A. 
Published: January 2007

ABSTRACT

We compared the Neo-Sensitabs tablet assay to both reference M27-A2 broth microdilution and M44-A disk diffusion methods for testing susceptibilities of 110 isolates of
Candida
spp. and
Cryptococcus neoformans
to amphotericin B, caspofungin, fluconazole, itraconazole, and voriconazole. Neo-Sensitabs assay inhibition zone diameters in millimeters on three agars (Mueller-Hinton agar supplemented with 2% dextrose and 0.5 μg/ml methylene blue [MGM], Shadomy [SHA], and RPMI 1640 [RPMI, 2% dextrose]) were obtained at 24 to 72 h. The correlation coefficient of Neo-Sensitabs results with MICs was similar to that of the disk method for most of the five agents on MGM (
R
, 0.80 to 0.89 versus 0.76 to 0.89, respectively). Overall, superior correlation was observed at 24 h for most agents. The exception was amphotericin B (
R
values of 0.68 and 0.5 for disk and tablet, respectively, at 48 h versus 0.68 and 0.48, respectively, at 24 h). In general, Neo-Sensitabs results were less consistent on SHA and RPMI agars. Although agreement by breakpoint category of Neo-Sensitabs and disk results with CLSI method M27-A2 was also similar on MGM (92.7 to 98.2% versus 95.5 to 100%, respectively), the Neo-Sensitabs method failed to identify two of the six isolates with high amphotericin B MICs. These data suggest the potential value of the Neo-Sensitabs assay for testing at least four of the five agents against yeasts evaluated in the clinical laboratory.
Activity of Dalbavancin Tested against
Staphylococcus
spp. and β-Hemolytic
Streptococcus
spp. Isolated from 52 Geographically Diverse Medical Centers in the United States
Authors: Biedenbach Douglas J. , Ross James E. , Fritsche Thomas R. , Sader Helio S. , Jones Ronald N. 
Published: January 2007

ABSTRACT

Dalbavancin is a lipoglycopeptide antimicrobial agent with a potency significantly better than that of vancomycin when tested against staphylococci and streptococci. These two pathogens are common causes of skin and skin structure infections (SSSIs), and dalbavancin has been approved for the treatment of moderate to severe SSSIs. This study generated susceptibility data for staphylococci and β-hemolytic streptococci from 52 U.S. medical centers that locally tested dalbavancin, vancomycin, and other antimicrobial class representatives to assess the potency of dalbavancin and the overall contemporary activities of commonly prescribed agents. Locally generated data showed that oxacillin-resistant staphylococci (57.0% overall) had slightly higher dalbavancin MIC
90
values (0.19 μg/ml) than oxacillin-susceptible strains (0.125 μg/ml). This potency was 8- to 16-fold greater than that for vancomycin. β-Hemolytic streptococci had MIC
90
values ranging between ≤0.016 and 0.064 μg/ml (highest for group B isolates). Levofloxacin, gentamicin, and tetracycline were active against oxacillin-susceptible staphylococci (82 to 99% susceptible), with lower susceptibility rates seen for the oxacillin-resistant strains. Linezolid coverage was >98% against staphylococci. Erythromycin resistance was high for staphylococci (30.6 to 94.1%) with inducible clindamycin resistance rates of 26.0% and 55.0% for oxacillin-susceptible and -resistant
Staphylococcus aureus
, respectively. β-Hemolytic streptococci had a 20.2% erythromycin resistance rate and a 60% inducible clindamycin resistance rate but were highly susceptible to other tested agents. Etest reading errors were apparent and skewed results towards slightly higher dalbavancin MICs, requiring further education on how to interpret Etest method results for this compound. Current disk diffusion breakpoint criteria for oxacillin susceptibility for
S. aureus
showed a very-major-error rate of 2.3% and only a 0.9% minor-error rate when cefoxitin was used to predict oxacillin susceptibility. Dalbavancin demonstrated excellent potency and activity (100% susceptibility at proposed breakpoints) against common causes of SSSI pathogens in this U.S. multicenter study sample.
UL20 Protein Functions Precede and Are Required for the UL11 Functions of Herpes Simplex Virus Type 1 Cytoplasmic Virion Envelopment
Authors: Fulmer Preston A. , Melancon Jeffrey M. , Baines Joel D. , Kousoulas Konstantin G. 
Published: January 2007

ABSTRACT
Egress of herpes simplex virus type 1 (HSV-1) from the nucleus of the infected cell to extracellular spaces involves a number of distinct steps, including primary envelopment by budding into the perinuclear space, de-envelopment into the cytoplasm, cytoplasmic reenvelopment, and translocation of enveloped virions to extracellular spaces. UL20/gK-null viruses are blocked in cytoplasmic virion envelopment and egress, as indicated by an accumulation of unenveloped or partially enveloped capsids in the cytoplasm. Similarly, UL11-null mutants accumulate unenveloped capsids in the cytoplasm. To assess whether UL11 and UL20/gK function independently or synergistically in cytoplasmic envelopment, recombinant viruses having either the UL20 or UL11 gene deleted were generated. In addition, a recombinant virus containing a deletion of both UL20 and UL11 genes was constructed using the HSV-1(F) genome cloned into a bacterial artificial chromosome. Ultrastructural examination of virus-infected cells showed that both UL20- and UL11-null viruses accumulated unenveloped capsids in the cytoplasm. However, the morphology and distribution of the accumulated capsids appeared to be distinct, with the UL11-null virions forming aggregates of capsids having diffuse tegument-derived material and the UL20-null virus producing individual capsids in close juxtaposition to cytoplasmic membranes. The UL20/UL11 double-null virions appeared morphologically similar to the UL20-null viruses. Experiments on the kinetics of viral replication revealed that the UL20/UL11 double-null virus replicated in a manner similar to the UL20-null virus. Additional experiments revealed that transiently expressed UL11 localized to the trans-Golgi network (TGN) independently of either gK or UL20. Furthermore, virus infection with the UL11/UL20 double-null virus did not alter the TGN localization of transiently expressed UL11 or UL20 proteins, indicating that these proteins did not interact. Taken together, these results show that the intracellular transport and TGN localization of UL11 is independent of UL20/gK functions, and that UL20/gK are required and function prior to UL11 protein in virion cytoplasmic envelopment.
Phosphoacceptor Site S173 in the Regulatory Domain of Epstein-Barr Virus ZEBRA Protein Is Required for Lytic DNA Replication but Not for Activation of Viral Early Genes
Authors: El-Guindy Ayman , Heston Lee , Delecluse Henri-Jacques , Miller George 
Published: January 2007

ABSTRACT
The Epstein-Barr virus ZEBRA protein controls the viral lytic cycle. ZEBRA activates the transcription of viral genes required for replication. ZEBRA also binds to oriLyt and interacts with components of the viral replication machinery. The mechanism that differentiates the roles of ZEBRA in regulation of transcription and initiation of lytic replication is unknown. Here we show that S173, a residue in the regulatory domain, is obligatory for ZEBRA to function as an origin binding protein but is dispensable for its role as a transcriptional activator of early genes. Serine-to-alanine substitution of this residue, which prevents phosphorylation of S173, resulted in a threefold reduction in the DNA binding affinity of ZEBRA for oriLyt, as assessed by chromatin immunoprecipitation. An independent assay based on ZEBRA solubility demonstrated a marked defect in DNA binding by the Z(S173A) mutant. The phenotype of a phosphomimetic mutant, the Z(S173D) mutant, was similar to that of wild-type ZEBRA. Our findings suggest that phosphorylation of S173 promotes viral replication by enhancing ZEBRA's affinity for DNA. The results imply that stronger DNA binding is required for ZEBRA to activate replication than that required to activate transcription.
Heparan Sulfate Binding Can Contribute to the Neurovirulence of Neuroadapted and Nonneuroadapted Sindbis Viruses
Authors: Ryman Kate D. , Gardner Christina L. , Burke Crystal W. , Meier Kathryn C. , Thompson Joseph M. , Klimstra William B. 
Published: January 2007

ABSTRACTCell culture-adapted laboratory strains of Sindbis virus (SB) exhibit efficient initial attachment to cell surface heparan sulfate (HS) receptors. In contrast, non-cell-adapted strains, such as the SB consensus sequence virus TR339, interact weakly with HS and cell surfaces. Regardless of their HS binding phenotype, most SB strains do not cause fatal disease in adult mice, whether inoculated subcutaneously (s.c.) or intracranially (i.c.). However, laboratory strains of SB can be rendered neurovirulent for adult mice by introduction of a glutamine (Gln)-to-histidine (His) mutation at position 55 of the E2 envelope glycoprotein. In the current work, we have determined that E2 His 55-containing viruses require a second-site mutation (Glu to Lys) at E2 position 70 that confers efficient HS binding in order to exhibit virulence for adult mice and that virulence is correlated with very high infectivity for many cell types. Furthermore, introduction of E2 Lys 70 or certain other HS-binding mutations alone also increased morbidity and/or mortality over that of TR339 for older mice inoculated i.c. However, all viruses containing single HS-binding mutations were attenuated in s.c. inoculated suckling mice in comparison with TR339. These results suggest that HS binding may attenuate viral disease that is dependent on high-titer viremia; however, efficient cell attachment through HS binding can increase virulence, presumably through enhancing the replication of SB within specific host tissues such as the brain.
Electron Tomography of Nascent Herpes Simplex Virus Virions
Authors: Baines Joel D. , Hsieh Chyong-Ere , Wills Elizabeth , Mannella Carmen , Marko Michael 
Published: January 2007

ABSTRACT
Cells infected with herpes simplex virus type 1 (HSV-1) were conventionally embedded or freeze substituted after high-pressure freezing and stained with uranyl acetate. Electron tomograms of capsids attached to or undergoing envelopment at the inner nuclear membrane (INM), capsids within cytoplasmic vesicles near the nuclear membrane, and extracellular virions revealed the following phenomena. (i) Nucleocapsids undergoing envelopment at the INM, or B capsids abutting the INM, were connected to thickened patches of the INM by fibers 8 to 19 nm in length and ≤5 nm in width. The fibers contacted both fivefold symmetrical vertices (pentons) and sixfold symmetrical faces (hexons) of the nucleocapsid, although relative to the respective frequencies of these subunits in the capsid, fibers engaged pentons more frequently than hexons. (ii) Fibers of similar dimensions bridged the virion envelope and surface of the nucleocapsid in perinuclear virions. (iii) The tegument of perinuclear virions was considerably less dense than that of extracellular virions; connecting fibers were observed in the former case but not in the latter. (iv) The prominent external spikes emanating from the envelope of extracellular virions were absent from perinuclear virions. (v) The virion envelope of perinuclear virions appeared denser and thicker than that of extracellular virions. (vi) Vesicles near, but apparently distinct from, the nuclear membrane in single sections were derived from extensions of the perinuclear space as seen in the electron tomograms. These observations suggest very different mechanisms of tegumentation and envelopment in extracellular compared with perinuclear virions and are consistent with application of the final tegument to unenveloped nucleocapsids in a compartment(s) distinct from the perinuclear space.
Importance of the Anti-Interferon Capacity of Sendai Virus C Protein for Pathogenicity in Mice
Authors: Kato Atsushi , Kiyotani Katsuhiro , Kubota Toru , Yoshida Tetsuya , Tashiro Masato , Nagai Yoshiyuki 
Published: January 2007

ABSTRACT

The Sendai virus (SeV) C protein blocks signal transduction of interferon (IFN), thereby counteracting the antiviral actions of IFN. Using HeLa cell lines expressing truncated or mutated SeV C proteins, we found that the C-terminal half has anti-IFN capacity, and that K
151
A, E
153
A, and R
154
A substitutions in the C protein eliminated this capacity. Here, we further created the mutant virus SeV Cm*, in which K
151
A, E
153
K, and R
157
L substitutions in the C protein were introduced without changing the amino acid sequence of overlapped P, V, and W proteins. SeV Cm* was found to lack anti-IFN capacity, as expected. While the growth rate and final yield of SeV Cm* were inferior to those of the wild-type SeV in IFN-responsive, STAT1-positive 2fTGH cells, SeV Cm* grew equivalently to the wild-type SeV in IFN-nonresponsive, STAT1-deficient U3A cells. SeV Cm* was thus shown to maintain multiplication capacity, except that it lacked anti-IFN capacity. Intranasally inoculated SeV Cm* could propagate in the lungs of STAT1
−/−
mice but was cleared from those of STAT1
+/+
mice without propagation. It was found that the anti-IFN capacity of the SeV C protein was indispensable for pathogenicity in mice. Conversely, the results show that the innate immunity contributed to elimination of SeV in early stages of infection in the absence of anti-IFN capacity.
Inhibition of human and rabbit arterial smooth muscle cell migration mediated by the kinin B1 receptor: role of receptor density and released mediators
Authors: Morissette Guillaume , Sabourin Thierry , Adam Albert , Marceau François 
Published: January 2007

Bradykinin (BK)-related peptides are suspected to negatively influence diverse functions in vascular smooth muscle cells (SMCs), notably via stimulation of the inducible B1 receptor (B1R), and have been shown to inhibit the migration of rat SMCs. The present study had several objectives: (i) to test whether B1R mediates the inhibition of migration of arterial SMCs from additional species (the human and the rabbit); (ii) whether B1R density influences this action and whether autocrine NO or prostanoid release modulate it; and (iii) the possible signaling interaction between the B1R and phosphatidylinositol-3 kinase (PI-3K) has been addressed. The peptidase resistant B1R agonist Sar-[D-Phe8]des-Arg9-BK (10 nmol/L – 1 μmol/L) was an inhibitor of migration in human or rabbit arterial SMCs in a wound closure assay, more effectively if the medium composition allowed a high B1R expression (20% fetal bovine serum (FBS) + interleukin-1β (IL-1β) in human SMCs, 10% FBS in rabbit cells). The effect of the B1R agonist on motility was abrogated by a B1R antagonist, B-9858, but not by the B2R antagonist Hoe 140; a peptidase-resistant B2R agonist, [Phe8Ψ(CH2-NH)-Arg9]BK, had a marginal or no effect on migration. Sar-[D-Phe8]des-Arg9-BK (1 μmol/L) did not significantly influence SMC proliferation. The B1R-mediated inhibition of SMC migration was not affected by pharmacological inhibition of the nitric oxide synthases or cyclooxygenases-1 or -2, but was correlated to an inhibition of PI-3K in both types of SMCs. The inhibition of SMC migration mediated by the kinin B1R is likely independent from NO or prostanoid release, applicable to several species, and correlated to receptor density and the inhibition of PI-3K.
Field stimulation-induced tetrodotoxin-resistant vasorelaxation is mediated by sodium hypochlorite
Authors: Varma Daya R. , Xia Zhicheng , Ozgoli Mehran , Chemtob Sylvain , Mulay Shree 
Published: January 2007

This study was done to determine the mechanism of field stimulation-induced tetrodotoxin (TTX)- and NG- nitro-l-arginine (LNA)-resistant vasorelaxation. Field stimulation with platinum and carbon, but not with silver, electrodes (30 V, 30 HZ, 2–5 ms pulse width) as well as electrically stimulated salt (0.9% NaCl) solution (ESSS) or Krebs solution caused 100% relaxation of phenylephrine-contracted rat aortic strips, which was TTX and LNA resistant and endothelium independent. ESSS also relaxed other vascular preparations (rabbit aorta and renal artery, dog coronary artery, pig ductus arteriosus, and rat portal vein). The electric current generated hypochlorite (OCl–) and H2O2 from the salt solution; however, vasorelaxation was caused by NaOCl and not by H2O2. ESSS and NaOCl caused contraction failure of spontaneously beating right atria of rats and did not affect uterine contractions, vascular cAMP, cGMP, or the pH of the tissue bath. Field stimulation, ESSS, and NaOCl did not relax aortic preparations contracted by 32 mmol/L potassium and their vasorelaxant effects on phenylephrine-contracted rat aortic strips and rings were completely reversed by tetraethylammonium and partially by glibenclamide and iberiotoxin. We conclude that electric pulses generate the oxidant OCl– from the salt solution, which causes vasorelaxation by increasing K+ conductance.
Intrahepatic adenosine-mediated activation of hepatorenal reflex is via A1receptors in rats
Authors: Ming Zhi , Lautt W. Wayne 
Published: January 2007

Previous studies have shown that intrahepatic adenosine is involved in activation of the hepatorenal reflex that regulates renal sodium and water excretion. The present study aims to determine which subtype of adenosine receptors is implicated in the process. Mean arterial pressure, portal venous pressure and flow, and renal arterial flow were monitored in pentobarbital anesthetized rats. Urine was collected from the bladder. Intraportal administration of 8-cyclopentyl-1,3-dipropylxanthine (DPCPX), a selective adenosine A1receptor antagonist, increased urine flow by 24%, 89%, and 143% at the dose of 0.01, 0.03, and 0.1 mg·kg–1, respectively; in contrast, DPCPX, when administered intravenously at the same doses, only increased urine flow by 0%, 18%, and 36%. The increases in urine flow induced by intraportal administration of DPCPX were abolished in rats with liver denervation. Intrahepatic infusion of adenosine significantly decreased urine flow and this response was abolished by intraportal administration of DPCPX. Neither intraportal nor intravenous administration of 3,7-dimethyl-1-propargylxanthine, a selective adenosine A2receptor antagonist, showed significant influence on urine flow. Systemic arterial pressure, renal blood flow and glomerular filtration rate were unaltered by the administration of any of the drugs. In conclusion, intrahepatic adenosine A1receptors are responsible for the adenosine-mediated hepatorenal reflex that regulates renal water and sodium excretion.
Acute hemorrhage causes hepatic insulin sensitizing substance (HISS)-dependent insulin resistance
Authors: Seredycz Larissa I. , Ming Zhi , Lautt W. Wayne 
Published: January 2007

Hepatic insulin sensitizing substance (HISS) has been shown to account for 55% of the action of insulin in the fed state. HISS blockade leads to HISS-dependent insulin resistance (HDIR). The objective of this study was to test the hypothesis that insulin resistance produced by hemorrhage was HDIR. Insulin sensitivity was measured using the rapid insulin sensitivity test (RIST), which can identify HISS-dependent and independent components. Hemorrhage was performed in anesthetized rats by removing blood to reduce mean arterial pressure to 50 mmHg. Subsequent to blood removal, a RIST was performed. The results show that hemorrhage caused complete HDIR as subsequent administration of atropine failed to further reduce insulin sensitivity. However, the posthemorrhage RIST was reduced by 34% and not the anticipated 55%. The lesser reduction of the RIST index by hemorrhage was related to reduced apparent volume of distribution and clearance of insulin, since occlusion of the superior mesenteric artery, which caused a similar decrease in portal venous flow as did hemorrhage, resulted in a similar degree of reduction of insulin clearance. The response to administered insulin was confounded by the impact of reduced hepatic blood flow on insulin metabolism that resulted in an increase in the HISS independent (direct) action of injected insulin against a background of complete HDIR. HDIR represents a useful hormonal response to assure a hyperglycemic response to hemorrhage.