bluuebunny/crossref_metadata_2025_split huggingface dataset:
Well-Characterized Monoclonal Antibodies against Cell Wall Antigen of
Aspergillus
Species Improve Immunoassay Specificity and Sensitivity
Authors: Hao Wei , Pan Yu-Xian , Ding Yan-Qing , Xiao Sha , Yin Kai , Wang Ya-Di , Qiu Li-Wen , Zhang Qing-Lin , Woo Patrick C. Y. , Lau Susanna K. P. , Yuen Kwok-Yung , Che Xiao-Yan 
Published: November 2007

ABSTRACT

The diagnosis of invasive aspergillosis (IA) based on the detection of
Aspergillus
galactomannan (GM) is complicated by the presence of cross-reactive GM epitopes in patient specimens. We have developed a novel and specific
Aspergillus
antigen-capture enzyme-linked immunosorbent assay (ELISA) by the selection of two well-characterized monoclonal antibodies from 17 candidate antibodies. The epitopes recognized by the monoclonal antibodies were present on the cell walls of the hyphae and the conidia of
Aspergillus
species, which were circulating or excreted as immunodominant antigens during the acute phase of IA established in the animal models. The detection of experimental
Aspergillus
-mediated antigenemia was suitably sensitive, and the sensitivity was comparable to that of a commercial GM detection ELISA kit (the Platelia
Aspergillus
assay). Moreover, the specificity of this assay was 100% when it was used to test 382 serum specimens and 120 urine specimens from healthy individuals. Cross-reactivity with other common opportunistic fungi, such as
Penicillium
and
Candida
species, and with purified GM protein derived from
Aspergillus
was not evident. Therefore, the chemical nature of the epitopes captured in this assay is most likely not associated with the GM structure, indicating that this newly developed
Aspergillus
antigen-capture ELISA is a promising tool for the diagnosis of IA without the risk of the false-positive results that are problematic with current GM antigen assays.
Rapid and Highly Sensitive Coxsackievirus A Indirect Immunofluorescence Assay Typing Kit for Enterovirus Serotyping
Authors: Lin Tsuey-Li , Li Yi-Syue , Huang Chiao-Wei , Hsu Chiu-Chu , Wu Ho-Sheng , Tseng Tsan-Chang , Yang Chen-Fu 
Published: November 2007

ABSTRACT
We describe the development and evaluation of an indirect immunofluorescence assay (IFA) kit for rapid and sensitive detection of coxsackievirus A2, -4, -5, -6, and -10. This IFA kit was determined to have 95.9 to 100% sensitivity and 95.8 to 97.2% specificity. It also proved to be beneficial in reducing the number of enteroviruses that are untypeable in the clinical virology laboratory.
Hidden VIM-1 Metallo-β-Lactamase Phenotypes among
Acinetobacter baumannii
Clinical Isolates
Authors: Ikonomidis Alexandros , Ntokou Eleni , Maniatis Antonios N. , Tsakris Athanassios , Pournaras Spyros 
Published: November 2007

ABSTRACT

A total of 87
Acinetobacter baumannii
nonrepetitive consecutive clinical isolates were tested for the presence of metallo-β-lactamases (MBLs). Results of phenotypic assays (MBL Etest, imipenem/imipenem-EDTA combined-disk test, and imipenem/EDTA double-disk synergy test) were negative in all cases, but molecular testing revealed the presence of two
bla
VIM-1
-carrying isolates. One isolate had
bla
VIM-1
preceded by a weak P1 promoter, and both had inactivated P2 promoters and reduced
bla
VIM-1
expression, partially justifying the results revealing hidden MBL phenotypes.
Elucidating Global Epidemiology of
Burkholderia multivorans
in Cases of Cystic Fibrosis by Multilocus Sequence Typing
Authors: Baldwin Adam , Mahenthiralingam Eshwar , Drevinek Pavel , Pope Chris , Waine David J. , Henry Deborah A. , Speert David P. , Carter Phil , Vandamme Peter , LiPuma John J. , Dowson Chris G. 
Published: November 2007

ABSTRACT

Burkholderia multivorans
is a prominent
B. cepacia
complex (BCC) species causing infection in people with cystic fibrosis. Despite infection control measures being introduced to reduce the spread of BCC there is a continued emergence of infections by
B. multivorans
. Our objective was to analyze a global collection of
B. multivorans
isolates, comparing those from environmental and clinical sources with those from reported outbreaks. Multilocus sequence typing (MLST) was performed on 107
B. multivorans
isolates to provide a detailed analysis of the global population biology of this species. MLST resolved 64
B. multivorans
sequence types. Twelve of these were globally distributed and associated with human infection; two of these (ST-21 and ST-375) were also composed of environmental isolates. These global lineages included strains previously linked to large outbreaks (e.g., French epidemic clone ST-16). Though few environmental isolates of
B. multivorans
were available for analysis, of six strains identified, three were identical to strains recovered from cystic fibrosis (CF) infection. Although the ability of
B. multivorans
to cause CF outbreaks is known, our report here concerning the existence of globally distributed
B. multivorans
CF strains is a new observation for this emerging
B. cepacia
complex pathogen and suggests that certain strain types may be better adapted to human infection than others. Common transmission-associated risk factors were not obviously linked to the globally distributed strains; however, the overlap in strains recovered from water environments, industrial products, and human infection suggests that environmental sources may be an important reservoir for infection with
B. multivorans
.
Identification of Residues Required for RNA Replication in Domains II and III of the Hepatitis C Virus NS5A Protein
Authors: Tellinghuisen Timothy L. , Foss Katie L. , Treadaway Jason C. , Rice Charles M. 
Published: November 2007

ABSTRACTThe NS5A protein of hepatitis C virus (HCV) plays an important but undefined role in viral RNA replication. NS5A has been proposed to be a three-domain protein, and the crystal structure of the well-conserved amino-terminal domain I has been determined. The remaining two domains of NS5A, designated domains II and III, and their corresponding interdomain regions are poorly understood. We have conducted a detailed mutagenesis analysis of NS5A domains II and III using the genotype 1b HCV replicon system. The majority of the mutants containing 15 small (8- to 15-amino-acid) deletions analyzed were capable of efficient RNA replication. Only five deletion mutations yielded lethal phenotypes, and these were colinear, spanning a 56-amino-acid region within domain II. This region was further analyzed by combining triple and single alanine scanning mutagenesis to identify individual residues required for RNA replication. Based upon this analysis, 23 amino acids were identified that were found to be essential. In addition, two residues were identified that yielded a small colony phenotype while possessing only a moderate defect in RNA replication. These results indicate that the entire domain III region and large portions of domain II of the NS5A protein are not required for the function of NS5A in HCV RNA replication.
Early Divergence in Lymphoid Tissue Apoptosis between Pathogenic and Nonpathogenic Simian Immunodeficiency Virus Infections of Nonhuman Primates
Authors: Cumont M.-C. , Diop O. , Vaslin B. , Elbim C. , Viollet L. , Monceaux V. , Lay S. , Silvestri G. , Le Grand R. , Müller-Trutwin M. , Hurtrel B. , Estaquier J. 
Published: November 2007

ABSTRACTThe events that contribute to the progression to AIDS during the acute phase of a primate lentiviral infection are still poorly understood. In this study, we used pathogenic and nonpathogenic simian models of simian immunodeficiency virus (SIV) infection of rhesus macaques (RMs) and African green monkeys (AGMs), respectively, to investigate the relationship between apoptosis in lymph nodes and the extent of viral replication, immune activation, and disease outcome. Here, we show that, in SIVmac251-infected RMs, a marked increased in lymphocyte apoptosis is evident during primary infection at the level of lymph nodes. Interestingly, the levels of apoptosis correlated with the extent of viral replication and the rate of disease progression to AIDS, with higher apoptosis in RMs of Indian genetic background than in those of Chinese origin. In stark contrast, no changes in the levels of lymphocyte apoptosis were observed during primary infection in the nonpathogenic model of SIVagm-sab infection of AGMs, despite similarly high rates of viral replication. A further and early divergence between SIV-infected RMs and AGMs was observed in terms of the dynamics of T- and B-cell proliferation in lymph nodes, with RMs showing significantly higher levels of cycling cells (Ki67+) in the T-cell zones in association with relatively low levels of Ki67+in the B-cell zones, whereas AGMs displayed a low frequency of Ki67+in the T-cell area but a high proportion of Ki67+cells in the B-cell area. As such, this study suggests that species-specific host factors determine an early immune response to SIV that predominantly involves either cellular or humoral immunity in RMs and AGMs, respectively. Taken together, these data are consistent with the hypotheses that (i) high levels of T-cell activation and lymphocyte apoptosis are key pathogenic factors during pathogenic SIV infection of RMs and (ii) low T-cell activation and apoptosis are determinants of the AIDS resistance of SIVagm-infected AGMs, despite high levels of SIVagm replication.
The UL14 Tegument Protein of Herpes Simplex Virus Type 1 Is Required for Efficient Nuclear Transport of the Alpha Transinducing Factor VP16 and Viral Capsids
Authors: Yamauchi Yohei , Kiriyama Kazuya , Kubota Naomi , Kimura Hiroshi , Usukura Jiro , Nishiyama Yukihiro 
Published: November 2007

ABSTRACT
The protein encoded by the UL14 gene of herpes simplex virus type 1 (HSV-1) and HSV-2 is expressed late in infection and is a minor component of the virion tegument. An UL14-deficient HSV-1 mutant (UL14D) forms small plaques and exhibits an extended growth cycle at low multiplicities of infection (MOI) compared to wild-type virus. Although UL14 is likely to be involved in the process of viral maturation and egress, its precise role in viral replication is still enigmatic. In this study, we found that immediate-early viral mRNA expression was decreased in UL14D-infected cells. Transient coexpression of UL14 and VP16 in the absence of infection stimulated the nuclear accumulation of both proteins. We intended to visualize the fate of VP16 released from the infected virion and constructed UL14-null (14D-VP16G) and rescued (14R-VP16G) viruses that expressed a VP16-green fluorescent protein (GFP) fusion protein. Synchronous high-multiplicity infection of the viruses was performed at 4°C in the absence of de novo protein synthesis. We found that the presence of UL14 in the virion had an enhancing effect on the nuclear accumulation of VP16-GFP. The lack of UL14 did not significantly alter virus internalization but affected incoming capsid transport to the nuclear pore. These observations suggested that UL14 (i) enhanced VP16 nuclear localization at the immediately early phase, thus indirectly regulating the expression of immediate-early genes, and (ii) was associated with efficient nuclear targeting of capsids. The tegument protein UL14 could be part of the machinery that regulates HSV-1 replication.
Inhibition of Endosome-Lysosome System Acidification Enhances Porcine Circovirus 2 Infection of Porcine Epithelial Cells
Authors: Misinzo Gerald , Delputte Peter L. , Nauwynck Hans J. 
Published: November 2007

ABSTRACT

Recently, Misinzo et al. (G. Misinzo, P. Meerts, M. Bublot, J. Mast, H. M. Weingartl, and H. J. Nauwynck, J. Gen. Virol.
86
:2057-2068, 2005) reported that inhibiting endosome-lysosome system acidification reduced porcine circovirus 2 (PCV2) infection of monocytic 3D4/31 cells. The present study examined the effect of inhibiting endosome-lysosome system acidification in epithelial cells, since epithelial cells support PCV2 infection in vivo and are used in culturing PCV2 in vitro. Ammonium chloride (NH
4
Cl), chloroquine diphosphate (CQ), and monensin were used to inhibit endosome-lysosome system acidification. NH
4
Cl, CQ, or monensin increased PCV2 (Stoon-1010) infection by 726% ± 110%, 1,212% ± 34%, and 1,100% ± 179%, respectively, in porcine kidney (PK-15) cells; by 128% ± 7%, 158% ± 3%, and 142% ± 11% in swine kidney cells; by 160% ± 28%, 446% ± 50%, and 162% ± 56% in swine testicle (ST) cells; and by 313% ± 25%, 611% ± 86%, and 352% ± 44% in primary kidney epithelial cells. Similarly, increased PCV2 infection was observed with six other PCV2 strains in PK-15 cells treated with endosome-lysosome system acidification inhibitors. The mechanism behind increased PCV2 infection was further investigated in PK-15 cells using CQ. PCV2 infection of PK-15 cells was increased only when CQ was added early during PCV2 infection. CQ did not affect PCV2 virus-like particle (VLP) attachment to PK-15 cells but increased the disassembly of internalized PCV2 VLPs. In untreated PK-15 cells, internalized PCV2 VLPs localized within the endosome-lysosome system. PCV2 infection of untreated 3D4/31 and PK-15 cells and CQ-treated PK-15 cells was blocked by a serine protease inhibitor [4-(2-aminoethyl) benzenesulfonyl fluoride hydrochloride] but not by aspartyl protease (pepstatin A), cysteine protease (E-64), and metalloprotease (phosphoramidon) inhibitors. These results suggest that serine protease-mediated PCV2 disassembly is enhanced in porcine epithelial cells but inhibited in monocytic cells after inhibition of endosome-lysosome system acidification.
Species-Specific Restriction of Apobec3-Mediated Hypermutation
Authors: Browne Edward P. , Littman Dan R. 
Published: November 2007

ABSTRACT
Apobec proteins are a family of cellular cytidine deaminases, among which several members have been shown to have potent antiviral properties. This antiviral activity is associated with the ability to cause hypermutation of retroviral cDNA. However, recent research has indicated that Apobec proteins are also able to inhibit retroviruses by other mechanisms that are independent of their deaminase activity. We have compared the antiviral activities of human and murine Apobec3 (A3) proteins, and we have found that, consistent with previous reports, human immunodeficiency virus (HIV) is able to resist human A3G but is sensitive to murine A3, whereas murine leukemia virus (MLV) is relatively resistant to murine A3 (mA3) but sensitive to human A3G. In contrast to previous studies, we observed that mA3 is packaged efficiently into MLV particles. The C-terminal cytidine deaminase domain (CDD2) is required for packaging of mA3 into MLV particles, and packaging did not depend on the MLV viral RNA. However, mA3 packed into MLV particles failed to cause hypermutation of viral DNA, indicating that its deaminase activity is blocked or inhibited. hA3G also caused significantly less hypermutation of MLV than of HIV DNA. Both mA3 and the splice variant mA3Δ5 exhibited some residual antiviral activity against MLV and caused a reduction in the ability of MLV particles to generate reverse transcription products. These results suggest that MLV has evolved specific mechanisms to block the ability of Apobec proteins to mediate deaminase-dependent hypermutation.
Replication-Coupled Packaging Mechanism in Positive-Strand RNA Viruses: Synchronized Coexpression of Functional Multigenome RNA Components of an Animal and a Plant Virus in
Nicotiana benthamiana
Cells by Agroinfiltration
Authors: Annamalai Padmanaban , Rofail Fady , DeMason Darleen A. , Rao A. L. N. 
Published: November 2007

ABSTRACT

Flock house virus (FHV), a bipartite RNA virus of insects and a member of the
Nodaviridae
family, shares viral replication features with the tripartite brome mosaic virus (BMV), an RNA virus that infects plants and is a member of the
Bromoviridae
family. In BMV and FHV, genome packaging is coupled to replication, a widely conserved mechanism among positive-strand RNA viruses of diverse origin. To unravel the events that modulate the mechanism of replication-coupled packaging, in this study, we have extended the transfer DNA (T-DNA)-based agroinfiltration system to express functional genome components of FHV in plant cells (
Nicotiana benthamiana
). Replication, intracellular membrane localization, and packaging characteristics in agroinfiltrated plant cells revealed that T-DNA plasmids of FHV were biologically active and faithfully mimicked complete replication and packaging behavior similar to that observed for insect cells. Synchronized coexpression of wild-type BMV and FHV genome components in plant cells resulted in the assembly of virions packaging the respective viral progeny RNA. To further elucidate the link between replication and packaging, coat protein (CP) open reading frames were precisely exchanged between BMV RNA 3 (B3) and FHV RNA 2 (F2), creating chimeric RNAs expressing heterologous CP genes (B3/FCP and F2/BCP). Coinfiltration of each chimera with its corresponding genome counterpart to provide viral replicase (B1+B2+B3/FCP and F1+F2/BCP) resulted in the expected progeny profiles, but virions exhibited a nonspecific packaging phenotype. Complementation with homologous replicase (with respect to CP) failed to enhance packaging specificity. Taken together, we propose that the transcription of CP mRNA from homologous replication and its translation must be synchronized to confer packaging specificity.
A Diacidic Motif in Human Immunodeficiency Virus Type 1 Nef Is a Novel Determinant of Binding to AP-2
Authors: Lindwasser O. Wolf , Smith William J. , Chaudhuri Rittik , Yang Peter , Hurley James H. , Bonifacino Juan S. 
Published: November 2007

ABSTRACT
A key function of the Nef protein of immunodeficiency viruses is the downregulation of the T-cell and macrophage coreceptor, CD4, from the surfaces of infected cells. CD4 downregulation depends on a conserved (D/E)XXXL(L/I)-type dileucine motif in the C-terminal, flexible loop of Nef, which mediates binding to the clathrin adaptor complexes AP-1, AP-2, and AP-3. We now report the identification of a consensus (D/E)D motif within this loop as a second, conserved determinant of interaction of Nef with AP-2, though not with AP-1 and AP-3. Mutations in this diacidic motif abrogate both AP-2 binding and CD4 downregulation. We also show that a dileucine motif from tyrosinase, both in its native context and in the context of Nef, can bind to AP-2 independently of a diacidic motif. These results thus identify a novel type of AP-2 interaction determinant, support the notion that AP-2 is the key clathrin adaptor for the downregulation of CD4 by Nef, and reveal a previously unrecognized diversity among dileucine sorting signals.
DO RECENT SUPERNOVAE Ia OBSERVATIONS TEND TO RULE OUT ALL THE COSMOLOGIES?
Authors: VISHWAKARMA RAM GOPAL 
Published: November 2007

Dark energy and the accelerated expansion of the universe have been the direct predictions of the distant supernovae Ia observations which are also supported, indirectly, by the observations of the CMB anisotropies, gravitational lensing and the studies of galaxy clusters. Today these results are accommodated in what has become the concordance cosmology: a universe with flat spatial sections t = constant with about 70% of its energy in the form of Einstein's cosmological constant Λ and about 25% in the form of dark matter (made of perhaps weakly-interacting massive particles). Though the composition is weird, the theory has shown remarkable successes at many fronts. However, we find that as more and more supernovae Ia are observed, more accurately and towards higher redshift, the probability that the data are well-explained by the cosmological models decreases alarmingly, finally ruling out the concordance model at more than 95% confidence level. This raises doubts against the "standard candle"-hypothesis of the supernovae Ia and their use in constraining the cosmological models. We need a better understanding of the entire SN Ia phenomenon in order to extract cosmological consequences from them.
Lentiviral (HIV)-based RNA interference screen in human B-cell receptor regulatory networks reveals MCL1-induced oncogenic pathways
Authors: Ruiz-Vela Antonio , Aggarwal Mohit , de la Cueva Paloma , Treda Cezary , Herreros Beatriz , Martín-Pérez Daniel , Dominguez Orlando , Piris Miguel A. 
Published: November 2007

AbstractAberrant inhibition of B-cell receptor (BCR)-induced programmed cell death pathways is frequently associated with the development of human auto-reactive B-cell lymphomas. Here, we integrated loss-of-function, genomic, and bioinformatics approaches for the identification of oncogenic mechanisms linked to the inhibition of BCR-induced clonal deletion pathways in human B-cell lymphomas. Lentiviral (HIV)-based RNA interference screen identified MCL1 as a key survival molecule linked to BCR signaling. Loss of MCL1 by RNA interference rendered human B-cell lymphomas sensitive to BCR-induced programmed cell death. Conversely, MCL1 overexpression blocked programmed cell death on BCR stimulation. To get insight into the mechanisms of MCL1-induced survival and transformation, we screened 41 000 human genes in a genome-wide gene expression profile analysis of MCL1-overexpressing B-cell lymphomas. Bioinformatic gene network reconstruction illustrated reprogramming of relevant oncoproteins within β-catenin–T-cell factor signaling pathways induced by enforced MCL1 expression. Overall, our findings not only illustrate MCL1 as an aberrantly expressed reprogramming oncoprotein in follicular lymphomas but also highlight MCL1 as key therapeutic target.
Exercise training reduces pulmonary ischaemia–reperfusion-induced inflammatory responses
Authors: Mussi R. K. , Camargo E. A. , Ferreira T. , De Moraes C. , Delbin M. A. , Toro I. F. C. , Brancher S. , Landucci E. C. T. , Zanesco A. , Antunes E. 
Published: November 2007

Physical exercise reduces the deleterious effects of cardiovascular and inflammatory disorders. The purpose of the present study was to evaluate the beneficial effects of physical training on the inflammatory responses following lung ischaemia–reperfusion (IR) in rats.Male Wistar rats were divided into sham-operated animals and sedentary and trained animals submitted to lung IR. The run training programme consisted of 5 sessions·week−1, each lasting 60 min·day−1, at 66% of maximal oxygen consumption for 8 weeks. The left pulmonary artery, bronchus and pulmonary vein were occluded for 90 min and reperfused for 2 h. Lung protein extravasation was measured as125I-human albumin accumulation, whereas lung neutrophil infiltration was measured as myeloperoxidase activity.Lung IR in sedentary rats resulted in marked increases in protein extravasation and neutrophil influx, and in significant elevations of serum tumour necrosis factor (TNF)-α and interleukin (IL)-1β levels. Physical preconditioning attenuated the increased IR-induced protein leakage without affecting neutrophil influx. It also reduced serum TNF-α (and IL-1β) levels, but had no effect on IL-10 levels. Plasma superoxide dismutase activity was significantly increased in trained IR rats.The present data show that physical preconditioning protects the rat lung from ischaemia–reperfusion injury by attenuating the pulmonary vascular permeability that may be a consequence of reduced levels of tumour necrosis factor-α and interleukin-1β and elevated superoxide dismutase activity.