bluuebunny/crossref_metadata_2025_split huggingface dataset:
TheclcElement ofPseudomonassp. Strain B13, a Genomic Island with Various Catabolic Properties
Authors: Gaillard Muriel , Vallaeys Tatiana , Vorhölter Frank Jörg , Minoia Marco , Werlen Christoph , Sentchilo Vladimir , Pühler Alfred , van der Meer Jan Roelof 
Published: February 2006

ABSTRACTPseudomonassp. strain B13 is a bacterium known to degrade chloroaromatic compounds. The properties to use 3- and 4-chlorocatechol are determined by a self-transferable DNA element, theclcelement, which normally resides at two locations in the cell's chromosome. Here we report the complete nucleotide sequence of theclcelement, demonstrating the unique catabolic properties while showing its relatedness to genomic islands and integrative and conjugative elements rather than to other known catabolic plasmids. As far as catabolic functions, theclcelement harbored, in addition to the genes for chlorocatechol degradation, a complete functional operon for 2-aminophenol degradation and genes for a putative aromatic compound transport protein and for a multicomponent aromatic ring dioxygenase similar to anthranilate hydroxylase. The genes for catabolic functions were inducible under various conditions, suggesting a network of catabolic pathway induction. For about half of the open reading frames (ORFs) on theclcelement, no clear functional prediction could be given, although some indications were found for functions that were similar to plasmid conjugation. The region in which these ORFs were situated displayed a high overall conservation of nucleotide sequence and gene order to genomic regions in other recently completed bacterial genomes or to other genomic islands. Most notably, except for two discrete regions, theclcelement was almost 100% identical over the whole length to a chromosomal region inBurkholderia xenovoransLB400. This indicates the dynamic evolution of this type of element and the continued transition between elements with a more pathogenic character and those with catabolic properties.
Herpes Simplex Virus Type 1 DNA-Packaging Protein UL17 Is Required for Efficient Binding of UL25 to Capsids
Authors: Thurlow Johanna K. , Murphy Mary , Stow Nigel D. , Preston Valerie G. 
Published: February 2006

ABSTRACT
Herpes simplex virus type 1 packages its DNA genome into a precursor capsid, referred to as the procapsid. Of the three capsid-associated DNA-packaging proteins, UL17, UL25, and UL6, only UL17 and UL6 appear to be components of the procapsid, with UL25 being added subsequently. To determine whether the association of UL17 or UL25 with capsids was dependent on the other two packaging proteins, B capsids, which lack viral DNA but retain the cleaved internal scaffold, were purified from nonpermissive cells infected with UL17, UL25, or UL6 null mutants and compared with wild-type (wt) B capsids. In the absence of UL17, the levels of UL25 in the mutant capsids were much lower than those in wt B capsids. These results suggest that UL17 is required for efficient incorporation of UL25 into B capsids. B capsids lacking UL25 contained about twofold-less UL17 than wt capsids, raising the possibilities that UL25 is important for stabilizing UL17 in capsids and that the two proteins interact in the capsid. The distribution of UL17 and UL25 on B capsids was examined using immunogold labeling. Both proteins appeared to bind to multiple sites on the capsid. The properties of the UL17 and UL25 proteins are consistent with the idea that the two proteins are important in stabilizing capsid-DNA structures rather than having a direct role in DNA packaging.
Vaccinia Virus Proteome: Identification of Proteins in Vaccinia Virus Intracellular Mature Virion Particles
Authors: Chung Che-Sheng , Chen Chein-Hung , Ho Ming-Yi , Huang Cheng-Yen , Liao Chung-Lin , Chang Wen 
Published: February 2006

ABSTRACTVaccinia virus is a large enveloped poxvirus with more than 200 genes in its genome. Although many poxvirus genomes have been sequenced, knowledge of the host and viral protein components of the virions remains incomplete. In this study, we used gel-free liquid chromatography and tandem mass spectroscopy to identify the viral and host proteins in purified vaccinia intracellular mature virions (IMV). Analysis of the proteins in the IMV showed that it contains 75 viral proteins, including structural proteins, enzymes, transcription factors, and predicted viral proteins not known to be expressed or present in the IMV. We also determined the relative abundances of the individual protein components in the IMV. Finally, 23 IMV-associated host proteins were also identified. This study provides the first comprehensive structural analysis of the infectious vaccinia virus IMV.
Matrix Protein Mutant of Vesicular Stomatitis Virus Stimulates Maturation of Myeloid Dendritic Cells
Authors: Ahmed Maryam , Brzoza Kristina L. , Hiltbold Elizabeth M. 
Published: February 2006

ABSTRACTMatrix (M) protein mutants of vesicular stomatitis virus have recently been used as oncolytic viruses for tumor therapies and are being developed as vaccine vectors for heterologous antigens. Because dendritic cell (DC) maturation is an important correlate of tumor immunosurveillance and vaccine efficacy, we sought to determine the ability of a recombinant M protein mutant virus (rM51R-M virus) to mature DC in vitro. We have previously shown that rM51R-M virus is defective at inhibiting host gene expression in several cell lines compared to its recombinant wild-type counterpart, rwt virus. Therefore, rM51R-M virus allows the expression of genes involved in antiviral responses, such as the type I interferon (IFN) gene. Our results demonstrate that, in contrast to the rwt virus, rM51R-M virus induced the maturation of myeloid DC (mDC) populations, as indicated by an increase in the surface expression of CD40, CD80, and CD86 as well as the secretion of interleukin-12 (IL-12), IL-6, and type I IFN. In addition, mDC infected with rM51R-M virus effectively activated naïve T cells in vitro, whereas rwt virus-infected mDC were defective in antigen presentation. The inability of rwt virus to induce mDC maturation was correlated with the inhibition of host gene expression in rwt virus-infected cells. Our studies also indicated that the production of costimulatory molecules on mDC by rM51R-M virus was dependent on the type I IFN receptor, while maturation induced by this virus was largely independent of MyD88. These data indicate that rM51R-M virus effectively stimulates the maturation of mDC and has the potential to promote effective T-cell responses to vector-expressed antigens, activate DC at tumor sites during therapy, and aid in tumor immunosurveillance and destruction.
A Single Amino Acid Substitution in the West Nile Virus Nonstructural Protein NS2A Disables Its Ability To Inhibit Alpha/Beta Interferon Induction and Attenuates Virus Virulence in Mice
Authors: Liu Wen Jun , Wang Xiang Ju , Clark David C. , Lobigs Mario , Hall Roy A. , Khromykh Alexander A. 
Published: February 2006

ABSTRACT

Alpha/beta interferons (IFN-α/β) are key mediators of the innate immune response against viral infection. The ability of viruses to circumvent IFN-α/β responses plays a crucial role in determining the outcome of infection. In a previous study using subgenomic replicons of the Kunjin subtype of West Nile virus (WNV
KUN
), we demonstrated that the nonstructural protein NS2A is a major inhibitor of IFN-β promoter-driven transcription and that a single amino acid substitution in NS2A (Ala30 to Pro [A30P]) dramatically reduced its inhibitory effect (W. J. Liu, H. B. Chen, X. J. Wang, H. Huang, and A. A. Khromykh, J. Virol.
78:
12225-12235). Here we show that incorporation of the A30P mutation into the WNV
KUN
genome results in a mutant virus which elicits more rapid induction and higher levels of synthesis of IFN-α/β in infected human A549 cells than that detected following wild-type WNV
KUN
infection. Consequently, replication of the WNV
KUN
NS2A/A30P mutant virus in these cells known to be high producers of IFN-α/β was abortive. In contrast, both the mutant and the wild-type WNV
KUN
produced similar-size plaques and replicated with similar efficiency in BHK cells which are known to be deficient in IFN-α/β production. The mutant virus was highly attenuated in neuroinvasiveness and also attenuated in neurovirulence in 3-week-old mice. Surprisingly, the mutant virus was also partially attenuated in IFN-α/βγ receptor knockout mice, suggesting that the A30P mutation may also play a role in more efficient activation of other antiviral pathways in addition to the IFN response. Immunization of wild-type mice with the mutant virus resulted in induction of an antibody response of similar magnitude to that observed in mice immunized with wild-type WNV
KUN
and gave complete protection against challenge with a lethal dose of the highly virulent New York 99 strain of WNV. The results confirm and extend our previous original findings on the role of the flavivirus NS2A protein in inhibition of a host antiviral response and demonstrate that the targeted disabling of a viral mechanism for evading the IFN response can be applied to the development of live attenuated flavivirus vaccine candidates.
Host Species-Dependent Population Structure of a Pollen-Borne Plant Virus,
Cherry Leaf Roll Virus
Authors: Rebenstorf Kathrin , Candresse Thierry , Dulucq Marie Josée , Büttner Carmen , Obermeier Christian 
Published: February 2006

ABSTRACT

Cherry
leaf roll virus
(CLRV) belongs to the
Nepovirus
genus
within the family
Comoviridae
. It has a host range which
includes a number of wild tree and shrub species. The serological and
molecular diversity of CLRV was assessed using a collection of isolates
and samples recovered from woody and herbaceous host plants from
different geographical origins. Molecular diversity was assessed by
sequencing a short (375-bp) region of the 3′ noncoding region
(NCR) of the genomic RNAs while serological diversity was assessed
using a panel of seven monoclonal antibodies raised initially against a
walnut isolate of CLRV. The genomic region analyzed was shown to
exhibit a significant degree of molecular variability with an average
pairwise divergence of 8.5% (nucleotide identity). Similarly,
serological variability proved to be high, with no single monoclonal
antibody being able to recognize all isolates analyzed. Serological and
molecular phylogenetic reconstructions showed a strong correlation.
Remarkably, the diversity of CLRV populations is to a large extent
defined by the host plant from which the viral samples are originally
obtained. There are relatively few reports of plant viruses for which
the genetic diversity is structured by the host plant. In the case of
CLRV, we hypothesize that this situation may reflect the exclusive mode
of transmission in natural plant populations by pollen and by seeds.
These modes of transmission are likely to impose barriers to host
change by the virus, leading to rapid biological and genetic separation
of CLRV variants coevolving with different plant host
species.
Extensive Recombination among Human Immunodeficiency Virus Type 1 Quasispecies Makes an Important Contribution to Viral Diversity in Individual Patients
Authors: Charpentier Charlotte , Nora Tamara , Tenaillon Olivier , Clavel François , Hance Allan J. 
Published: February 2006

ABSTRACT

Although recombination during human immunodeficiency virus type 1 (HIV-1) replication in vitro and in vivo has been documented, little information is available concerning the extent that recombination contributes to the diversity of HIV-1 quasispecies in the course of infection in individual patents. To investigate the impact of recombination on viral diversity, we developed a technique that permits the isolation of contemporaneous clonal viral populations resulting from single infectious events by plasma-derived viruses, thereby permitting the assessment of recombination throughout the viral genomes, including widely separated loci, from individual patients. A comparison of the genomic sequences of clonal viruses from six patients, including patients failing treatment with antiretroviral therapy, demonstrated strong evidence for extensive recombination. Recombination increased viral diversity through two distinct mechanisms. First, evolutionary bottlenecks appeared to be restricted to minimal segments of the genome required to obtain selective advantage, thereby preserving diversity in adjacent regions. Second, recombination between adjacent gene segments appeared to generate diversity in both
pol
and
env
genes. Thus, the shuffling of resistance mutations within the genes coding for the protease and reverse transcriptase, as well as recombination between these regions, could increase the diversity of drug resistance genotypes. These findings demonstrate that recombination in HIV-1 contributes to the diversity of viral quasispecies by restricting evolutionary bottlenecks to gene segments and by generating novel genotypes in
pol
and
env
, supporting the idea that recombination may be critical to adaptive evolution of HIV in the face of constantly moving selective pressures, whether exerted by the immune system or antiretroviral therapy.
A comparison of stent-induced stenosis in coronary and peripheral arteries
Authors: Krueger K D , Mitra A K , DelCore M G , Hunter W J , Agrawal D K 
Published: February 2006

Background and objectives:Restenosis is a complication of interventional procedures such as angioplasty and stenting, often limiting the success of these procedures. Knowledge regarding the relative behaviour of different arteries after these procedures is limited, despite the extensive use of different vascular models. Although the results from studies using different vessels are analysed to predict the behaviour of coronary arteries and other vasculature, direct controlled comparisons between different arteries are necessary for a better understanding of the differential response to restenosis.Methods:This study examines the response to stenting in coronary and internal iliac arteries as characterised by intimal hyperplasia and restenosis. In a swine model of in-stent stenosis, coronary arteries exhibited higher levels of intimal hyperplasia and per cent stenosis than internal iliac arteries.Results:After normalisation for injury score, coronary arteries were found to undergo 47% more intimal hyperplasia (p<0.05), whereas per cent stenosis normalised for injury score tended to be higher (p = 0.01). Other measurements reflecting post-stenting intimal hyperplasia (maximal intimal thickness, medial area) did not exhibit significant differences between the artery groups.Conclusions:These results show that coronary vessels are more prone to develop significant intimal hyperplasia and subsequent restenosis than internal iliac vessels. A better insight into how different arteries and arterial components behave is important in understanding and developing newer and better therapeutic measures for restenosis.
Meiji Japan as a Model for Africa's Economic Development
Authors: Nafziger E. Wayne 
Published: February 2006

AbstractThis paper examines the major ways in which the economic development model of Meiji Japan, 1868-1912, applies to contemporary Africa. The focus is on capital formation and technology policies that contributed to Meiji Japan's rapid industrial capitalist growth: self-directed strategies, technological borrowing, taking advantage of shifts in comparative advantage from the product cycle, educational policy, business assistance, financial institutions, transfer of agricultural savings to industry, low wages policy, industrial dualistic complementarity, and foreign-exchange rate policies conducive to export expansion. For each of these policies, the author analyzes the extent to which African countries can emulate Meiji Japan's approaches or whether changing circumstances require modification of the Japanese model.
Education and Modernization: An Examination of the Experiences of Japan and Ethiopia
Authors: Felleke Getachew 
Published: February 2006

AbstractJapan has cultivated an immensely positive image among countries in the Sub-Saharan Region of Africa. Its industrial prowess, its post-war image as champion of peace, and its generous contributions of aid through its ODA lie behind this image. Beyond this, it also has long been regarded as a model of how a non-western and non-European country can successfully undertake a fast paced process of modernization. It is especially appealing as a model for African states to emulate in that the country managed to achieve its modernization without having to bear an undue cost of erosion of sovereignty and cultural integrity. This paper is a comparative examination of the early and divergent approaches to modernization that were adopted by Japan and Ethiopia.
Clonal restriction of the expansion of antigen-specific CD8+ memory T cells by transforming growth factor-β
Authors: Cheng Mei-Lien , Chen Hsin-Wei , Tsai Jy-Ping , Lee Yi-Ping , Shih Yan-Chung , Chang Chung-Ming , Ting Chou-Chik 
Published: February 2006

Abstract
Recent evidence showed that transforming growth factor-β (TGF-β) regulates the global expansion of CD8+ T cells, which are CD44hi, a marker for memory cells. However, it is not clear whether this regulatory mechanism also applies to the antigen-specific CD8+ memory cells. By using a murine mixed lymphocyte culture (MLC) model, we examined the effect of TGF-β on antigen-specific CD8+ memory cells [cytotoxic T lymphocyte (CTL)]. We found that the secondary CTL response in CD8+ memory cells from untreated MLC was not affected by TGF-β but augmented by interleukin (IL)-2, whereas the CD8+ memory cells from TGF-β-pretreated MLC (MLC-TGF-β) failed to mount a significant, secondary CTL response, even when IL-2 was added. In exploring this dichotomy, in combination with flow cytometry analysis, we found that prolonged exposure to TGF-β reduces the CTL activity in CD8+ memory cells. The increase by IL-2 and the reduction by TGF-β of the CTL responses were clonal-specific. TGF-β did not affect the CTL response to a third-party antigen or polyclonal T cell activation. Experiments performed with transgenic 2C cells gave similar results. Cell-cycle study performed with adoptive transfer of the cell tracker-labeled MLC cells revealed that the in vivo expansion of CD8+ memory cells from MLC-TGF-β was restricted severely, and the restriction was clonal-specific, thus offering direct evidence to show that TGF-β induces clonal restriction of CD8+ memory cell expansion.
Ethanol affects the generation, cosignaling molecule expression, and function of plasmacytoid and myeloid dendritic cell subsets in vitro and in vivo
Authors: Lau Audrey H , Abe Masanori , Thomson Angus W 
Published: February 2006

Abstract
The influence of ethanol (EtOH) on multiple dendritic cell (DC) subsets, in the steady state or following their mobilization in vivo, has not been characterized. Herein, generation of mouse bone marrow-derived DC (BMDC) in response to fms-like tyrosine kinase 3 ligand was inhibited by physiologically relevant concentrations of EtOH with selective suppression of plasmacytoid (p)DC. EtOH reduced surface expression of costimulatory molecules (CD40, CD80, CD86) but not that of coinhibitory CD274 (B7-H1) on resting or CpG-stimulated DC subsets. Interleukin (IL)-12p70 production by activated DC was impaired. Consistent with these findings, EtOH-exposed BMDC exhibited a reduced capacity to induce naïve, allogeneic T cell proliferation and impaired ability to prime T cells in vivo. DC subsets freshly isolated from EtOH-fed mice were also examined. Liver DC, inherently immature and resistant to maturation, exhibited little change in their low surface cosignaling molecule expression, whereas splenic DC showed reduced expression of surface costimulatory molecules in response to CpG stimulation in vivo. These splenic DC elicited reduced naïve, allogeneic T cell proliferation in vitro, and the stimulatory capacity of resting but not CpG-activated liver DC was reduced by chronic EtOH administration. T cells from animals primed with EtOH-exposed DC produced elevated levels of IL-10 following ex vivo challenge with donor alloantigen. Thus, EtOH impairs cytokine-driven differentiation and function of myeloid DC and pDC in vitro. Hepatic DC from chronic EtOH-fed mice are less affected than splenic DC, which exhibit impaired functional maturation following CpG stimulation. These results indicate a potential mechanism by which alcohol consumption is associated with immunosuppression.
Matrix metalloproteinase-9 modulates intestinal injury in rats with transmural colitis
Authors: Medina Carlos , Santana Alfredo , Paz Maria Cristina , Díaz-Gonzalez Federico , Farre Esther , Salas Antonio , Radomski Marek W , Quintero Enriquie 
Published: February 2006

AbstractProteolysis and degradation of extracellular matrix by metalloproteinases (MMPs) may contribute to intestinal injury in inflammatory bowel disease. In the present study, we investigated the pathogenic role of gelatinases (MMP-9 and MMP-2) on transmural colonic injury in a rat model of chronic colitis, which was induced by intracolonic instillation of trinitrobenzene sulfonic acid (TNBS). The activity and expression of MMP-2 and MMP-9 were measured in colonic tissue and peripheral neutrophils by fluorescence, zymography, Western blot, or immunohistochemistry at different time-points. Furthermore, myeloperoxidase content in colonic homogenates was analyzed to evaluate inflammation. Finally, morphological changes were assessed following early or delayed administration of CGS-27023-A, a synthetic inhibitor of MMPs. We found that the induction of colitis led to a significant up-regulation in tissue gelatinase concentration, whereas no changes in collagenase activity were observed. In addition, up-regulation of pro-MMP-9, but not of pro-MMP-2, was found on Days 7 and 10 following the induction of colitis. Furthermore, transmural MMP-9 was detected by immunofluorescent staining in the inflamed tissue. Consistent with tissue samples, neutrophils from colitic rats showed a significantly increased activity of pro-MMP-9. Finally, early but not delayed treatment with CGS-27023-A attenuated colonic mucosal injury in rats with TNBS-induced colitis. In conclusion, up-regulation of MMP-9 in peripheral and colonic neutrophils modulates transmural colonic injury in rats with TNBS-induced colitis.