bluuebunny/crossref_metadata_2025_split huggingface dataset:
Distribution of
emm
Types and Genetic Characterization of the
mgc
Locus in Group G
Streptococcus dysgalactiae
subsp.
equisimilis
from a Hospital in Northern Taiwan
Authors: Tseng Sung-Pin , Lin Yu-Yin , Tsai Jui-Chang , Hsueh Po-Ren , Chen Hsiao-Jan , Hung Wei-Chun , Teng Lee-Jene 
Published: June 2010

ABSTRACT

A total of 274
Streptococcus dysgalactiae
subsp.
equisimilis
isolates was analyzed by
emm
typing and by determining the organization of their
mgrC
loci. Three of the most frequent
emm
types were
stG485.0
(45/274, 16.4%),
stG6.1
(43/274, 15.7%), and
stC839.0
(32/274, 11.7%), in decreasing order. The
cpdB
-positive
mgrC
locus appears to be predominant in some
emm
types.
Low Specificities of HIV Diagnostic Tests Caused by
Trypanosoma brucei gambiense
Sleeping Sickness
Authors: Lejon V. , Ngoyi D. Mumba , Ilunga M. , Beelaert G. , Maes I. , Büscher P. , Fransen K. 
Published: June 2010

ABSTRACT

The accuracy of diagnostic tests for HIV in patients with tropical infections is poorly documented. Human African trypanosomiasis (HAT) is characterized by a polyclonal B-cell activation, constituting a risk for false-positive reactions to diagnostic tests, including HIV tests. A retrospective study of the accuracy of HIV diagnostic tests was performed with 360 human African HAT patients infected with
Trypanosoma brucei gambiense
before treatment and 163
T. b. gambiense
-infected patients 2 years after successful treatment in Mbuji Mayi, East Kasai, Democratic Republic of the Congo. The sensitivities, specificities, and positive predictive values (PPVs) of individual tests and algorithms consisting of 3 rapid tests were determined. The sensitivity of all tests was 100% (11/11). The low specificity (96.3%, 335/348) and PPV (45.8%, 11/24) of a classical seroconfirmation strategy (Vironostika enzyme-linked immunosorbent assay [ELISA] followed by line immunoassay) complicated the determination of HIV status, which had to be determined by PCR. The specificities of the rapid diagnostic tests were 39.1% for Determine (136/348); 85.3 to 92.8% (297/348 to 323/348) for Vikia, ImmunoFlow, DoubleCheck, and Bioline; and 96.6 to 98.3% (336/348 to 342/348) for Uni-Gold, OraQuick, and Stat-Pak. The specificity of Vironostika was 67.5% (235/348). PPVs ranged between 4.9 and 64.7%. Combining 3 different rapid tests resulted in specificities of 98.3 to 100% (342/348 to 348/348) and PPVs of 64.7 to 100% (11/17 to 11/11). For cured HAT patients, specificities were significantly higher for Vironostika, Determine, Uni-Gold, and ImmunoFlow.
T. b. gambiense
infection decreases the specificities of antibody detection tests for HIV diagnosis. Unless tests have been validated for interference with HAT, HIV diagnosis using classical algorithms in untreated HAT patients should be avoided. Specific, validated combinations of 3 HIV rapid tests can increase specificity.
Peptide Nucleic Acid Array for Detection of Point Mutations in Hepatitis B Virus Associated with Antiviral Resistance
Authors: Jang Hyunjung , Kim Jihyun , Choi Jae-jin , Son Yeojin , Park Heekyung 
Published: June 2010

ABSTRACT

The detection of antiviral-resistant hepatitis B virus (HBV) mutations is important for monitoring the response to treatment and for effective treatment decisions. We have developed an array using peptide nucleic acid (PNA) probes to detect point mutations in HBV associated with antiviral resistance. PNA probes were designed to detect mutations associated with resistance to lamivudine, adefovir, and entecavir. The PNA array assay was sensitive enough to detect 10
2
copies/ml. The PNA array assay was able to detect mutants present in more than 5% of the virus population when the total HBV DNA concentration was greater than 10
4
copies/ml. We analyzed a total of 68 clinical samples by this assay and validated its usefulness by comparing results to those of the sequencing method. The PNA array correctly identified viral mutants and has high concordance (98.3%) with direct sequencing in detecting antiviral-resistant mutations. Our results showed that the PNA array is a rapid, sensitive, and easily applicable assay for the detection of antiviral-resistant mutation in HBV. Thus, the PNA array is a useful and powerful diagnostic tool for the detection of point mutations or polymorphisms.
The Herpes Simplex Virus Type 1 UL20 Protein and the Amino Terminus of Glycoprotein K (gK) Physically Interact with gB
Authors: Chouljenko Vladimir N. , Iyer Arun V. , Chowdhury Sona , Kim Joohyun , Kousoulas Konstantin G. 
Published: June 2010

ABSTRACT
Herpes simplex virus type 1 (HSV-1) glycoprotein K (gK) and the UL20 protein (UL20p) are strictly required for virus-induced cell fusion, and mutations within either the gK or UL20 gene cause extensive cell fusion (syncytium formation). We have shown that gK forms a functional protein complex with UL20p, which is required for all gK and UL20p-associated functions in the HSV-1 life cycle. Recently, we showed that the amino-terminal 82 amino acids (aa) of gK (gKa) were required for the expression of the syncytial phenotype of the mutant virus gBΔ28 lacking the carboxyl-terminal 28 amino acids of gB (V. N. Chouljenko, A. V. Iyer, S. Chowdhury, D. V. Chouljenko, and K. G. Kousoulas, J. Virol. 83:12301-12313, 2009). This work suggested that the amino terminus of gK may directly or indirectly interact with gB and/or other viral glycoproteins. Two-way coimmunoprecipitation experiments revealed that UL20p interacted with gB in infected cells. Furthermore, the gKa peptide was coimmunoprecipitated with gB but not gD. Three recombinant baculoviruses were constructed, expressing the amino-terminal 82 aa of gKa together with either the extracellular portion of gB (30 to 748 aa), gD (1 to 340 aa), or gH (1 to 792 aa), respectively. Coimmunoprecipitation experiments revealed that gKa physically interacted with the extracellular portions of gB and gH but not gD. Three additional recombinant baculoviruses expressing gKa and truncated gBs encompassing aa 30 to 154, 30 to 364, and 30 to 500 were constructed. Coimmunoprecipitation experiments showed that gKa physically interacted with all three truncated gBs. Computer-assisted prediction of possible gKa binding sites on gB suggested that gKa may interact predominantly with gB domain I (E. E. Heldwein, H. Lou, F. C. Bender, G. H. Cohen, R. J. Eisenberg, and S. C. Harrison, Science 313:217-220, 2006). These results imply that the gK/UL20p protein complex modulates the fusogenic properties of gB and gH via direct physical interactions.
Temporal and Spatial Resolution of Type I and III Interferon ResponsesIn Vivo
Authors: Pulverer Julia Elisabeth , Rand Ulfert , Lienenklaus Stefan , Kugel Daniela , Ziętara Natalia , Kochs Georg , Naumann Ronald , Weiss Siegfried , Staeheli Peter , Hauser Hansjörg , Köster Mario 
Published: June 2010

ABSTRACTAlthough the action of interferons (IFNs) has been extensively studiedin vitro, limited information is available on the spatial and temporal activation pattern of IFN-induced genesin vivo. We created BAC transgenic mice expressing firefly luciferase under transcriptional control of the Mx2 gene promoter. Expression of the reporter with regard to onset and kinetics of induction parallels that of Mx2 and is thus a hallmark for the host response. Substantial constitutive expression of the reporter gene was observed in the liver and most other tissues of transgenic mice, whereas this expression was strongly reduced in animals lacking functional type I IFN receptors. As expected, the reporter gene was induced not only in response to type I (α and β) and type III (λ) IFNs but also in response to a variety of IFN inducers such as double-stranded RNA, lipopolysaccharide (LPS), and viruses.In vivoIFN subtypes show clear differences with respect to their kinetics of action and to their spatial activation pattern: while the type I IFN response was strong in liver, spleen, and kidney, type III IFN reactivity was most prominent in organs with mucosal surfaces. Infection of reporter mice with virus strains that differ in their pathogenicity shows that the IFN response is significantly altered in the strength of IFN action at sites which are not primarily infected as well as by the onset and duration of gene induction.
Delaying the Expression of Herpes Simplex Virus Type 1 Glycoprotein B (gB) to a True Late Gene Alters Neurovirulence and Inhibits the gB-CD8
+
T-Cell Response in the Trigeminal Ganglion
Authors: Ramachandran Srividya , Davoli Katherine A. , Yee Michael B. , Hendricks Robert L. , Kinchington Paul R. 
Published: June 2010

ABSTRACT

Following herpes simplex virus type 1 (HSV-1) ocular infection of C57BL/6 mice, activated CD8
+
T cells specific for an immunodominant epitope on HSV-1 glycoprotein B (gB-CD8 cells) establish a stable memory population in HSV-1 latently infected trigeminal ganglia (TG), whereas non-HSV-specific CD8
+
T cells are lost over time. The retention and activation of gB-CD8 cells appear to be influenced by persistent viral antigenic exposure within the latently infected TG. We hypothesized that the low-level expression of gB from its native promoter before viral DNA synthesis is critical for the retention and activation of gB-CD8 cells in the TG during HSV-1 latency and for their ability to block HSV-1 reactivation from latency. To test this, we created a recombinant HSV-1 in which gB is expressed only after viral DNA synthesis from the true late gC promoter (gCp-gB). Despite minor growth differences compared to its rescuant in infected corneas, gCp-gB was significantly growth impaired in the TG and produced a reduced latent genome load. The gCp-gB- and rescuant-infected mice mounted similar gB-CD8 effector responses, but the size and activation phenotypes of the memory gB-CD8 cells were diminished in gCp-gB latently infected TG, suggesting that the stimulation of gB-CD8 cells requires gB expression before viral DNA synthesis. Surprisingly, late gB expression did not compromise the capacity of gB-CD8 cells to inhibit HSV-1 reactivation from latency in
ex vivo
TG cultures, suggesting that gB-CD8 cells can block HSV-1 reactivation at a very late stage in the viral life cycle. These data have implications for designing better immunogens for vaccines to prevent HSV-1 reactivation.
A Single Asparagine-Linked Glycosylation Site of the Severe Acute Respiratory Syndrome Coronavirus Spike Glycoprotein Facilitates Inhibition by Mannose-Binding Lectin through Multiple Mechanisms
Authors: Zhou Yanchen , Lu Kai , Pfefferle Susanne , Bertram Stephanie , Glowacka Ilona , Drosten Christian , Pöhlmann Stefan , Simmons Graham 
Published: June 2010

ABSTRACTMannose-binding lectin (MBL) is a serum protein that plays an important role in host defenses as an opsonin and through activation of the complement system. The objective of this study was to assess the interactions between MBL and severe acute respiratory syndrome-coronavirus (SARS-CoV) spike (S) glycoprotein (SARS-S). MBL was found to selectively bind to retroviral particles pseudotyped with SARS-S. Unlike several other viral envelopes to which MBL can bind, both recombinant and plasma-derived human MBL directly inhibited SARS-S-mediated viral infection. Moreover, the interaction between MBL and SARS-S blocked viral binding to the C-type lectin, DC-SIGN. Mutagenesis indicated that a single N-linked glycosylation site, N330, was critical for the specific interactions between MBL and SARS-S. Despite the proximity of N330 to the receptor-binding motif of SARS-S, MBL did not affect interactions with the ACE2 receptor or cathepsin L-mediated activation of SARS-S-driven membrane fusion. Thus, binding of MBL to SARS-S may interfere with other early pre- or postreceptor-binding events necessary for efficient viral entry.
Vα14iNKT Cells Promote Liver Pathology during Adenovirus Infection by Inducing CCL5 Production: Implications for Gene Therapy
Authors: Ajuebor Maureen N. , Chen Qingling , Strieter Robert M. , Adegboyega Patrick A. , Aw Tak Yee 
Published: June 2010

ABSTRACTReplication-defective recombinant adenoviruses are the most widely studied replication-defective vectors for the potential treatment of inherited human diseases. However, broad clinical application of replication-defective adenoviruses in gene therapy is being hindered by the induction of vigorous innate and adaptive immune responses against the vector that cause deleterious effects in the liver. Vα14 invariant natural killer T cells (Vα14iNKT cells) are thymus-derived innate T cells at the interface between the two arms of the immune response and provide full engagement of host defense. The pathophysiological role of intrahepatic Vα14iNKT cells during replication-defective adenovirus infection is not known and is the main focus of our study. Our data showed that intrahepatic Vα14iNKT cells were activated in response to adenovirus infection to induce significant levels of hepatic chemokine (C-C motif) ligand 5 (CCL5) and subsequent liver toxicity. Moreover, intrahepatic CCL5 production was selectively reduced by Vα14iNKT cell deficiency.In vivostudies utilizing CCL5-deficient mice or Vα14iNKT cell-deficient mice demonstrated that CCL5 deficiency or Vα14iNKT cell deficiency was associated with reduced liver pathology. Similar results were seen after blocking the biological effects of the CCL5 receptors. In conclusion, we have identified an important proinflammatory role for activated intrahepatic Vα14iNKT cells in positively influencing hepatic CCL5 production to promote acute liver inflammation and injury. Therefore, our findings highlight the blockade of CCL5 interaction with a cognate receptor(s) as an important potential strategy to alleviate liver pathology associated with replication-defective adenovirus infection.
Poly(A)-Binding Protein 1 Partially Relocalizes to the Nucleus during Herpes Simplex Virus Type 1 Infection in an ICP27-Independent Manner and Does Not Inhibit Virus Replication
Authors: Salaun C. , MacDonald A. I. , Larralde O. , Howard L. , Lochtie K. , Burgess H. M. , Brook M. , Malik P. , Gray N. K. , Graham S. V. 
Published: June 2010

ABSTRACT
Infection of cells by herpes simplex virus type 1 (HSV-1) triggers host cell shutoff whereby mRNAs are degraded and cellular protein synthesis is diminished. However, virus protein translation continues because the translational apparatus in HSV-infected cells is maintained in an active state. Surprisingly, poly(A)-binding protein 1 (PABP1), a predominantly cytoplasmic protein that is required for efficient translation initiation, is partially relocated to the nucleus during HSV-1 infection. This relocalization occurred in a time-dependent manner with respect to virus infection. Since HSV-1 infection causes cell stress, we examined other cell stress inducers and found that oxidative stress similarly relocated PABP1. An examination of stress-induced kinases revealed similarities in HSV-1 infection and oxidative stress activation of JNK and p38 mitogen-activated protein (MAP) kinases. Importantly, PABP relocalization in infection was found to be independent of the viral protein ICP27. The depletion of PABP1 by small interfering RNA (siRNA) knockdown had no significant effect on viral replication or the expression of selected virus late proteins, suggesting that reduced levels of cytoplasmic PABP1 are tolerated during infection.
Association of the Influenza Virus RNA Polymerase Subunit PB2 with the Host Chaperonin CCT
Authors: Fislová Tatiana , Thomas Benjamin , Graef Katy M. , Fodor Ervin 
Published: June 2010

ABSTRACT
The RNA polymerase of influenza A virus is a host range determinant and virulence factor. In particular, the PB2 subunit of the RNA polymerase has been implicated as a crucial factor that affects cell tropism as well as virulence in animal models. These findings suggest that host factors associating with the PB2 protein may play an important role during viral replication. In order to identify host factors that associate with the PB2 protein, we purified recombinant PB2 from transiently transfected mammalian cells and identified copurifying host proteins by mass spectrometry. We found that the PB2 protein associates with the cytosolic chaperonin containing TCP-1 (CCT), stress-induced phosphoprotein 1 (STIP1), FK506 binding protein 5 (FKBP5), α- and β-tubulin, Hsp60, and mitochondrial protein p32. Some of these binding partners associate with each other, suggesting that PB2 might interact with these proteins in multimeric complexes. More detailed analysis of the interaction of the PB2 protein with CCT revealed that PB2 associates with CCT as a monomer and that the CCT binding site is located in a central region of the PB2 protein. PB2 proteins from various influenza virus subtypes and origins can associate with CCT. Silencing of CCT resulted in reduced viral replication and reduced PB2 protein and viral RNA accumulation in a ribonucleoprotein reconstitution assay, suggesting an important function for CCT during the influenza virus life cycle. We propose that CCT might be acting as a chaperone for PB2 to aid its folding and possibly its incorporation into the trimeric RNA polymerase complex.
PDZD8 Is a Novel Gag-Interacting Factor That Promotes Retroviral Infection
Authors: Henning Matthew S. , Morham Scott G. , Goff Stephen P. , Naghavi Mojgan H. 
Published: June 2010

ABSTRACT
In a yeast two-hybrid screen for cellular factors that could interact with human immunodeficiency virus type 1 (HIV-1) Gag protein, we identified PDZD8 and confirmed the interaction by coimmunoprecipitation (co-IP). PDZD8 overexpression promoted the initiation of reverse transcription and increased infection by pseudotyped retroviruses independent of the route of viral entry, while transient knockdown of endogenous levels decreased HIV-1 infection. A mutant of PDZD8 lacking a predicted coiled-coil domain in its Gag-interacting region failed to bind Gag and promote HIV-1 infection, identifying the domain of PDZD8 required for mediating these effects. As such, we identify PDZD8 as a novel positive mediator of retroviral infection.
Visualizing the Replication Cycle of Bunyamwera Orthobunyavirus Expressing Fluorescent Protein-Tagged Gc Glycoprotein
Authors: Shi Xiaohong , van Mierlo Joël T. , French Andrew , Elliott Richard M. 
Published: June 2010

ABSTRACT

The virion glycoproteins Gn and Gc of Bunyamwera virus (BUNV), the prototype of the
Bunyaviridae
family and also of the
Orthobunyavirus
genus, are encoded by the medium (M) RNA genome segment and are involved in both viral attachment and entry. After their synthesis Gn and Gc form a heterodimer in the endoplasmic reticulum (ER) and transit to the Golgi compartment for virus assembly. The N-terminal half of the Gc ectodomain was previously shown to be dispensable for virus replication in cell culture (X. Shi, J. Goli, G. Clark, K. Brauburger, and R. M. Elliott, J. Gen. Virol. 90:2483-2492, 2009.). In this study, the coding sequence for a fluorescent protein, either enhanced green fluorescent protein (eGFP) or mCherry fluorescent protein, was fused to the N terminus of truncated Gc, and two recombinant BUNVs (rBUNGc-eGFP and rBUNGc-mCherry) were rescued by reverse genetics. The recombinant viruses showed bright autofluorescence under UV light and were competent for replication in various mammalian cell lines. rBUNGc-mCherry was completely stable over 10 passages, whereas internal, in-frame deletions occurred in the chimeric Gc-eGFP protein of rBUNGc-eGFP, resulting in loss of fluorescence between passages 5 and 7. Autofluorescence of the recombinant viruses allowed visualization of different stages of the infection cycle, including virus attachment to the cell surface, budding of virus particles in Golgi membranes, and virus-induced morphological changes to the Golgi compartment at later stages of infection. The fluorescent protein-tagged viruses will be valuable reagents for live-cell imaging studies to investigate virus entry, budding, and morphogenesis in real time.
Tinnitus and mobile phone use
Authors: Hutter Hans-Peter , Moshammer Hanns , Wallner Peter , Cartellieri Monika , Denk-Linnert Doris-Maria , Katzinger Michaela , Ehrenberger Klaus , Kundi Michael 
Published: June 2010

ObjectivesThe mechanisms that produce tinnitus are not fully understood. While tinnitus can be associated with diseases and disorders of the ear, retrocochlear diseases and vascular pathologies, there are few known risk factors for tinnitus apart from these conditions. There is anecdotal evidence of an link between mobile phone use and tinnitus, but so far there have been no systematic investigations into this possible association.Methods100 consecutive patients presenting with tinnitus were enrolled in an individually matched case–control study. For each case a control subject was randomly selected from visiting outpatients matched for sex and age. The patient's history was obtained and clinical examinations were conducted to exclude patients with known underlying causes of tinnitus. Mobile phone use was assessed based on the Interphone Study protocol. ORs were computed by conditional logistic regression with years of education and living in an urban area as covariates.ResultsMobile phone use up to the index date (onset of tinnitus) on the same side as the tinnitus did not have significantly elevated ORs for regular use and intensity or for cumulative hours of use. The risk estimate was significantly elevated for prolonged use (≥4 years) of a mobile phone (OR 1.95; CI 1.00 to 3.80).ConclusionsMobile phone use should be included in future investigations as a potential risk factor for developing tinnitus.
Work-related mortality in England and Wales, 1979–2000
Authors: Coggon David , Harris E Clare , Brown Terry , Rice Simon , Palmer Keith T 
Published: June 2010

BackgroundTo explore time trends in deaths attributable to work in England and Wales, and identify priorities for prevention, we conducted a proportional analysis of mortality by occupation over a 22-year period.MethodsAnalysis was based on deaths in men aged 20–74 years during 1979–1980 and 1982–2000 with a recorded occupation. Proportional mortality ratios, standardised for age and social class, were calculated for pre-specified combinations of occupation and cause of death, for which excess mortality could reasonably be attributed to work. Differences between observed and expected numbers of deaths by cause and occupation were expressed as annual excess death rates.ResultsMortality attributable to work declined substantially over the period of study, with total excess death rates of 733.2 per year during 1979–1990 and 471.7 per year during 1991–2000. The largest contributing hazards were chronic obstructive pulmonary disease and pneumoconiosis in coal miners, pleural cancer from asbestos, and motor vehicle accidents in lorry drivers. In contrast to most other hazards, there was no clear decline in excess mortality attributable to asbestos, or in deaths from sino-nasal cancer associated with exposure to wood dust.ConclusionsThe overall decline in mortality attributable to work is likely to reflect reduced employment in more hazardous occupations, as well as improvements in working conditions. It is imperative to ensure that occupational exposures to asbestos and wood dust are now adequately controlled. Further research is needed on accidents involving lorries with the aim of developing more effective strategies for the prevention of injury.
Hybrid Viscosity Iterative Method for Fixed Point, Variational Inequality and Equilibrium Problems
Authors: Chen Yi-An , Zhang Yi-Ping 
Published: June 2010

AbstractWe introduce an iterative scheme by the viscosity iterative method for finding a common element of the solution set of an equilibrium problem, the solution set of the variational inequality, and the fixed points set of infinitely many nonexpansive mappings in a Hilbert space. Then we prove our main result under some suitable conditions.