bluuebunny/crossref_metadata_2025_split huggingface dataset:
Identification of DysI, the Immunity Factor of the Streptococcal Bacteriocin Dysgalacticin
Authors: Swe Pearl M. , Heng Nicholas C. K. , Cook Gregory M. , Tagg John R. , Jack Ralph W. 
Published: October 2010

ABSTRACT

DysI is identified as the protein that confers specific immunity to dysgalacticin, a plasmid-encoded streptococcal bacteriocin.
dysI
is transcribed as part of the
copG
-
repB
-
dysI
replication-associated operon. DysI appears to function at the membrane level to prevent the inhibitory effects of dysgalacticin on glucose transport, membrane integrity, and intracellular ATP content.
Functional Characterization of Replication and Stability Factors of an Incompatibility Group P-1 Plasmid from
Xylella fastidiosa
Authors: Lee Min Woo , Rogers Elizabeth E. , Stenger Drake C. 
Published: October 2010

ABSTRACT

Xylella fastidiosa
strain riv11 harbors a 25-kbp plasmid (pXF-RIV11) belonging to the IncP-1 incompatibility group. Replication and stability factors of pXF-RIV11 were identified and used to construct plasmids able to replicate in
X. fastidiosa
and
Escherichia coli
. Replication in
X. fastidiosa
required a 1.4-kbp region from pXF-RIV11 containing a replication initiation gene (
trfA
) and the adjacent origin of DNA replication (
oriV
). Constructs containing
trfA
and
oriV
from pVEIS01, a related IncP-1 plasmid of the earthworm symbiont
Verminephrobacter eiseniae
, also were competent for replication in
X. fastidiosa
. Constructs derived from pXF-RIV11 but not pVEIS01 replicated in
Agrobacterium tumefaciens
,
Xanthomonas campestris
, and
Pseudomonas syringae
. Although plasmids bearing replication elements from pXF-RIV11 or pVEIS01 could be maintained in
X. fastidiosa
under antibiotic selection, removal of selection resulted in plasmid extinction after 3 weekly passages. Addition of a toxin-antitoxin addiction system (
pemI
/
pemK
) from pXF-RIV11 improved plasmid stability such that >80 to 90% of
X. fastidiosa
cells retained plasmid after 5 weekly passages in the absence of antibiotic selection. Expression of PemK in
E. coli
was toxic for cell growth, but toxicity was nullified by coexpression of PemI antitoxin. Deletion of N-terminal sequences of PemK containing the conserved motif RGD abolished toxicity.
In vitro
assays revealed a direct interaction of PemI with PemK, suggesting that antitoxin activity of PemI is mediated by toxin sequestration. IncP-1 plasmid replication and stability factors were added to an
E. coli
cloning vector to constitute a stable 6.0-kbp shuttle vector (pXF20-PEMIK) suitable for use in
X. fastidiosa
.
Antibody Responses in Mice Stimulated by Various Doses of the Potato-Derived Major Surface Antigen of Hepatitis B Virus
Authors: Youm Jung Won , Won Young Suk , Jeon Jae Heung , Moon Ki Beom , Kim Hyoung Chin , Shin Kee-Sun , Joung Hyouk , Kim Hyun Soon 
Published: October 2010

ABSTRACTThe ability of potato-derived major surface antigen of hepatitis B virus (P-HBsAg) to elicit antibody responses to different dosages of P-HBsAg ranging from 0.02 to 30 μg administered orally in mice was examined. All immunized groups produced specific serum IgG and fecal IgA antibodies against P-HBsAg, even at low levels (<5 μg), after administration of a 0.5-μg yeast-derived HBsAg (Y-HBsAg; LG Life Sciences, Republic of Korea) booster.
Evaluation of Gamma Interferon Release Assays Using
Mycobacterium tuberculosis
Antigens for Diagnosis of Latent and Active Tuberculosis in
Mycobacterium bovis
BCG-Vaccinated Populations
Authors: Zhang Shu , Shao Lingyun , Mo Ling , Chen Jiazhen , Wang Feifei , Meng Chengyan , Zhong Min , Qiu Lihua , Wu Meiying , Weng Xinhua , Zhang Wenhong 
Published: October 2010

ABSTRACT

T-cell-based gamma interferon (IFN-γ) release assays (IGRAs) using
Mycobacterium tuberculosis
-specific antigens have shown higher sensitivity and specificity than the routine tuberculin skin test (TST). However, the effects of
Mycobacterium bovis
BCG vaccination and anti-tuberculosis (TB) treatment on dynamic T-cell responses to
M. tuberculosis
-specific antigens in active TB cases have rarely been investigated in regions where TB is endemic. Eighty-nine patients with active pulmonary TB (ATB) and 57 healthy controls (HC) from China were recruited and tested by sputum smear and culture, TSTs, and IGRAs with
M. tuberculosis
-specific antigens ESAT-6 and CFP-10 (T-SPOT.TB) as well as purified protein derivative (PPD) stimulation. All 146 participants were screened by the T-SPOT.TB assay at recruitment. T-SPOT.TB-positive rates in ATB and HC groups were 87.6% (78/89) and 21.1% (12/57), respectively. Of 38 ATB patients who were both TST and T-SPOT.TB tested, the positive rates were 73.7% (28/38) and 94.7% (36/38), respectively (
P
= 0.0215), and those in the HC group were 62.3% (33/53) and 18.9% (10/53), respectively (
P
< 0.0001). The T-SPOT.TB-positive rates declined during TB treatment and were 94.4% (51/54), 86.4% (19/22), and 61.5% (8/13) for ATB patients receiving 0- to 1-month, 1- to 3-month, and 3- to 6-month anti-TB treatment, respectively. The IGRA is a most promising test for both active TB and latent TB infection (LTBI) diagnosis due to the improvement of its specificity and convenience, especially in the
Mycobacterium bovis
BCG-vaccinated population. Furthermore, the T-SPOT.TB assay using ESAT-6 and CFP-10 in ATB patients during anti-TB treatment could serve as a potential predictor of therapeutic efficacy.
FliZ Induces a Kinetic Switch in Flagellar Gene Expression
Authors: Saini Supreet , Koirala Santosh , Floess Emily , Mears Patrick J. , Chemla Yann R. , Golding Ido , Aldridge Christine , Aldridge Phillip D. , Rao Christopher V. 
Published: October 2010

ABSTRACTFliZ is an activator of class 2 flagellar gene expression inSalmonella enterica. To understand its role in flagellar assembly, we investigated how FliZ affects gene expression dynamics. We demonstrate that FliZ participates in a positive-feedback loop that induces a kinetic switch in class 2 gene expression.
Shadowing the Actions of a Predator: Backlit Fluorescent Microscopy Reveals Synchronous Nonbinary Septation of Predatory
Bdellovibrio
inside Prey and Exit through Discrete Bdelloplast Pores
Authors: Fenton A. K. , Kanna M. , Woods R. D. , Aizawa S.-I. , Sockett R. E. 
Published: October 2010

ABSTRACT

The
Bdellovibrio
are miniature “living antibiotic” predatory bacteria which invade, reseal, and digest other larger Gram-negative bacteria, including pathogens. Nutrients for the replication of
Bdellovibrio
bacteria come entirely from the digestion of the single invaded bacterium, now called a bdelloplast, which is bound by the original prey outer membrane.
Bdellovibrio
bacteria are efficient digesters of prey cells, yielding on average 4 to 6 progeny from digestion of a single prey cell of a genome size similar to that of the
Bdellovibrio
cell itself. The developmental intrabacterial cycle of
Bdellovibrio
is largely unknown and has never been visualized “live.” Using the latest motorized
xy
stage with a very defined
z
-axis control and engineered periplasmically fluorescent prey allows, for the first time, accurate return and visualization without prey bleaching of developing
Bdellovibrio
cells using solely the inner resources of a prey cell over several hours. We show that
Bdellovibrio
bacteria do not follow the familiar pattern of bacterial cell division by binary fission. Instead, they septate synchronously to produce both odd and even numbers of progeny, even when two separate
Bdellovibrio
cells have invaded and develop within a single prey bacterium, producing two different amounts of progeny. Evolution of this novel septation pattern, allowing odd progeny yields, allows optimal use of the finite prey cell resources to produce maximal replicated, predatory bacteria. When replication is complete,
Bdellovibrio
cells exit the exhausted prey and are seen leaving via discrete pores rather than by breakdown of the entire outer membrane of the prey.
Influence of Extraction Protocol on Physical Properties of Parvovirus B19 DNA
Authors: Matz Bertfried , Kupfer Bernd , Kreil Thomas R. , Eis-Hübinger Anna Maria 
Published: October 2010

ABSTRACT
While establishing a quantification standard for parvovirus B19 diagnostics, we extracted viral DNA from a high-titered human plasma by using three commercial kits. Despite similar viral DNA yields being obtained, striking differences in electrophoretic mobilities of the extracted nucleic acids were observed.
First Report of
Salmonella enterica
Serotype Paratyphi A Azithromycin Resistance Leading to Treatment Failure
Authors: Molloy Aoife , Nair Satheesh , Cooke Fiona J. , Wain John , Farrington Mark , Lehner Paul J. , Torok M. Estee 
Published: October 2010

ABSTRACT

The prevalence of
Salmonella enterica
serotype Paratyphi A infection is increasing, and multidrug resistance is a well-recognized problem. Resistance to fluoroquinolones is common and leads to more frequent use of newer agents like azithromycin. We report the first case of azithromycin resistance and treatment failure in a patient with
S
. Paratyphi A infection.
TROCAI (Tropism Coreceptor Assay Information): a New Phenotypic Tropism Test and Its Correlation with Trofile Enhanced Sensitivity and Genotypic Approaches
Authors: Gonzalez-Serna Alejandro , Leal Manuel , Genebat Miguel , Abad Maria Antonia , Garcia-Perganeda Antonio , Ferrando-Martinez Sara , Ruiz-Mateos Ezequiel 
Published: October 2010

ABSTRACT
The only clinically validated assay available to determine HIV tropism is Trofile, an assay that possesses some limitations. Our first aim was to develop a new phenotypic tropism test (TROCAI [tropism coreceptor assay information]) and to categorize results generated by this test according to the virological response to a short-term exposure to the CCR5 receptor antagonist maraviroc (maraviroc clinical test). Our second aim was to compare TROCAI results to those obtained by Trofile enhanced sensitivity (ES) and to different genotypic algorithms. TROCAI assayed HIV tropism in 33 HIV-infected patient viral isolates obtained from a modified coculture, followed by multiple infection cycles of indicator cells. TROCAI obtained a reportable result in all patients with viral loads of >500 HIV RNA copies/ml and in 3/6 patients with <500 HIV RNA copies/ml (30/33 patients, 91.9%). Patients who responded to maraviroc had an X4-using virus proportion in indicator cell supernatant of 0 to 0.41%. Hence, we used the threshold of 0.5% to categorize TROCAI results as R5 (<0.5%) or dual/mixed (>0.5%). The concordance between TROCAI and Trofile (ES) was 22/24 (91.6%), and with genotypic approaches it was 22/26 (84.6%). TROCAI results, which were categorized in this study by the maraviroc clinical test, could be used as a test in addition to those currently used to select patients for treatment with CCR5 antagonists.
Complete Nucleotide Sequence Analysis of Plasmids in Strains of
Staphylococcus aureus
Clone USA300 Reveals a High Level of Identity among Isolates with Closely Related Core Genome Sequences
Authors: Kennedy Adam D. , Porcella Stephen F. , Martens Craig , Whitney Adeline R. , Braughton Kevin R. , Chen Liang , Craig Carly T. , Tenover Fred C. , Kreiswirth Barry N. , Musser James M. , DeLeo Frank R. 
Published: October 2010

ABSTRACT

A community-associated methicillin-resistant
Staphylococcus aureus
(CA-MRSA) strain known as pulsed-field type USA300 (USA300) is epidemic in the United States. Previous comparative whole-genome sequencing studies demonstrated that there has been recent clonal emergence of a subset of USA300 isolates, which comprise the epidemic clone. Although the core genomes of these isolates are closely related, the level of diversity among USA300 plasmids was not resolved. Inasmuch as these plasmids might contribute to significant gene diversity among otherwise closely related USA300 isolates, we performed
de novo
sequencing of endogenous plasmids from 10 previously characterized USA300 clinical isolates obtained from different geographic locations in the United States. All isolates tested contained small (2- to 3-kb) and/or large (27- to 30-kb) plasmids. The large plasmids encoded heavy metal and/or antimicrobial resistance elements, including those that confer resistance to cadmium, bacitracin, macrolides, penicillin, kanamycin, and streptothricin, although all isolates were sensitive to minocycline, doxycycline, trimethoprim-sulfamethoxazole, vancomycin, teicoplanin, and linezolid. One of the USA300 isolates contained an archaic plasmid that encoded staphylococcal enterotoxins R, J, and P. Notably, the large plasmids (27 to 28 kb) from 8 USA300 isolates—those that comprise the epidemic USA300 clone—were virtually identical (99% identity) and similar to a large plasmid from strain USA300_TCH1516 (a previously sequenced USA300 strain from Houston, TX). These plasmids are largely divergent from the 37-kb plasmid of FPR3757, the first sequenced USA300 strain. The high level of plasmid sequence identity among the majority of closely related USA300 isolates is consistent with the recent clonal emergence hypothesis for USA300.
Clinical Features of Infections and Colonization by
Acinetobacter
Genospecies 3
Authors: Molina José , Cisneros José Miguel , Fernández-Cuenca Felipe , Rodríguez-Baño Jesús , Ribera Anna , Beceiro Alejandro , Martínez-Martínez Luis , Pascual Álvaro , Bou Germán , Vila Jordi , Pachón Jerónimo 
Published: October 2010

ABSTRACT

Two hundred twenty-one isolates of
Acinetobacter baumannii
and 15 of
Acinetobacter
genospecies 3 (AG3) were consecutively collected in a 30-day period during the nationwide project GEIH-Ab2000. Nosocomial acquisition (
P
= 0.01), intensive care unit admission (
P
= 0.02), and antibiotic pressure (
P
= 0.03) were observed to be lower in the AG3 group. AG3 isolates were more frequently implied in wound infections (
P
= 0.05), while
A. baumannii
tended to be recovered from respiratory samples (
P
= 0.08). To our knowledge, this is the first report analyzing the clinical differences among
Acinetobacter
genospecies, with our findings suggesting that clinical features of AG3 may not be equivalent to those traditionally described for
A. baumannii
.
Differential Circulation of
Streptococcus pneumoniae
Serotype 6C Clones in Two Israeli Pediatric Populations
Authors: Porat Nurith , Park In Ho , Nahm Moon H. , Dagan Ron 
Published: October 2010

ABSTRACT

We genotyped
Streptococcus pneumoniae
serotype 6C (Sp6C) isolates collected from Jewish and Bedouin children in southern Israel during the decade before vaccination. Sp6C constituted 8.2% of the presumed Sp6A isolates. All of the Sp6C clonal clusters were associated with serogroup 6, mainly Sp6A. Different clonal distributions were found in the two subpopulations.
Roles of Vaccinia Virus Genes E3L and K3L and Host Genes PKR and RNase L during Intratracheal Infection of C57BL/6 Mice
Authors: Rice Amanda D. , Turner Peter C. , Embury Jennifer E. , Moldawer Lyle L. , Baker Henry V. , Moyer Richard W. 
Published: October 2010

ABSTRACT

The importance of the 2′-5′ oligoadenylate synthetase (OAS)/RNase L and double-stranded RNA (dsRNA)-dependent protein kinase (PKR) pathways in host interferon induction resulting from virus infection in response to dsRNA has been well documented. In poxvirus infections, the interactions between the vaccinia virus (VV) genes E3L and K3L, which target RNase L and PKR, respectively, serve to prevent the induction of the dsRNA-dependent induced interferon response in cell culture. To determine the importance of these host genes in controlling VV infections, mouse single-gene knockouts of RNase L and PKR and double-knockout mice were studied following intratracheal infection with VV, VVΔK3L, or VVΔE3L. VV caused lethal disease in all mouse strains. The single-knockout animals were more susceptible than wild-type animals, while the RNase L
−/−
PKR
−/−
mice were the most susceptible. VVΔE3L infections of wild-type mice were asymptomatic, demonstrating that E3L plays a critical role in controlling the host immune response. RNase L
−/−
mice showed no disease, whereas 20% of the PKR
−/−
mice succumbed at a dose of 10
8
PFU. Lethal disease was routinely observed in RNase L
−/−
PKR
−/−
mice inoculated with 10
8
PFU of VVΔE3L, with a distinct pathology. VVΔK3L infections exhibited no differences in virulence among any of the mouse constructs, suggesting that PKR is not the exclusive target of K3L. Surprisingly, VVΔK3L did not disseminate to other tissues from the lung. Hence, the cause of death in this model is respiratory disease. These results also suggest that an unanticipated role of the K3L gene is to facilitate virus dissemination.
NFAT and CREB Regulate Kaposi's Sarcoma-Associated Herpesvirus-Induced Cyclooxygenase 2 (COX-2)
Authors: Sharma-Walia Neelam , George Paul Arun , Patel Kinjan , Chandran Karthic , Ahmad Waseem , Chandran Bala 
Published: October 2010

ABSTRACTCOX-2 has been implicated in Kaposi's sarcoma-associated herpesvirus (KSHV) latency and pathogenesis (A. George Paul, N. Sharma-Walia, N. Kerur, C. White, and B. Chandran, Cancer Res. 70:3697-3708, 2010; P. P. Naranatt, H. H. Krishnan, S. R. Svojanovsky, C. Bloomer, S. Mathur, and B. Chandran, Cancer Res. 64:72-84, 2004; N. Sharma-Walia, A. G. Paul, V. Bottero, S. Sadagopan, M. V. Veettil, N. Kerur, and B. Chandran, PLoS Pathog. 6:e1000777, 2010; N. Sharma-Walia, H. Raghu, S. Sadagopan, R. Sivakumar, M. V. Veettil, P. P. Naranatt, M. M. Smith, and B. Chandran, J. Virol. 80:6534-6552, 2006). However, the precise regulatory mechanisms involved in COX-2 induction during KSHV infection have never been explored. Here, we identifiedcis-acting elements involved in the transcriptional regulation of COX-2 upon KSHVdenovoinfection. Promoter analysis using human COX-2 promoter deletion and mutation reporter constructs revealed that nuclear factor of activated T cells (NFAT) and the cyclic AMP (cAMP) response element (CRE) modulate KSHV-mediated transcriptional regulation of COX-2. Along with multiple KSHV-induced signaling pathways, infection-induced prostaglandin E2(PGE2) also augmented COX-2 transcription. Infection of endothelial cells markedly induced COX-2 expression via a cyclosporine A-sensitive, calcineurin/NFAT-dependent pathway. KSHV infection increased intracellular cAMP levels and activated protein kinase A (PKA), which phosphorylated the CRE-binding protein (CREB) at serine 133, which probably led to interaction with CRE in the COX-2 promoter, thereby enhancing COX-2 transcription. PKA selective inhibitor H-89 pretreatment strongly inhibited CREB serine 133, indicating the involvement of a cAMP-PKA-CREB-CRE loop in COX-2 transcriptional regulation. In contrast to phosphatidylinositol 3-kinase and protein kinase C, inhibition of FAK and Src effectively reduced KSHV infection-induced COX-2 transcription and protein levels. Collectively, our study indicates that mediation of COX-2 transcription upon KSHV infection is a paradigm of a complex regulatory milieu involving the interplay of multiple signal cascades and transcription factors. Intervention at each step of COX-2/PGE2induction can be used as a potential therapeutic target to treat KSHV-associated neoplasm and control inflammatory sequels of KSHV infection.
The Early Whole-Blood Transcriptional Signature of Dengue Virus and Features Associated with Progression to Dengue Shock Syndrome in Vietnamese Children and Young Adults
Authors: Hoang Long Truong , Lynn David J. , Henn Matt , Birren Bruce W. , Lennon Niall J. , Le Phuong Thi , Duong Kien Thi Hue , Nguyen Tham Thi Hong , Mai Lanh Ngoc , Farrar Jeremy J. , Hibberd Martin L. , Simmons Cameron P. 
Published: October 2010

ABSTRACT

Dengue is a pantropic public health problem. In children, dengue shock syndrome (DSS) is the most common life-threatening complication. The ability to predict which patients may develop DSS may improve triage and treatment. To this end, we conducted a nested case-control comparison of the early host transcriptional features in 24 DSS patients and 56 sex-, age-, and virus serotype-matched uncomplicated (UC) dengue patients. In the first instance, we defined the “early dengue” profile. The transcriptional signature in acute rather than convalescent samples (≤72 h post-illness onset) was defined by an overabundance of interferon-inducible transcripts (31% of the 551 overabundant transcripts) and canonical gene ontology terms that included the following: response to virus, immune response, innate immune response, and inflammatory response. Pathway and network analyses identified STAT1, STAT2, STAT3, IRF7, IRF9, IRF1, CEBPB, and SP1 as key transcriptional factors mediating the early response. Strikingly, the only difference in the transcriptional signatures of early DSS and UC dengue cases was the greater abundance of several neutrophil-associated transcripts in patients who progressed to DSS, a finding supported by higher plasma concentrations of several canonical proteins associated with neutrophil degranulation (bactericidal/permeability-increasing protein [BPI], elastase 2 [ELA2], and defensin 1 alpha [DEF1A]). Elevated levels of neutrophil-associated transcripts were independent of the neutrophil count and also of the genotype of the infecting virus, as genome-length sequences of dengue virus serotype 1 (DENV-1) (
n
= 15) and DENV-2 (
n
= 3) sampled from DSS patients were phylogenetically indistinguishable from those sampled from uncomplicated dengue patients (32 DENV-1 and 9 DENV-2 sequences). Collectively, these data suggest a hitherto unrecognized association between neutrophil activation, pathogenesis, and the development of DSS and point to future strategies for guiding prognosis.
Determinants of Strain-Specific Differences in Efficiency of Reovirus Entry
Authors: Sarkar Payel , Danthi Pranav 
Published: October 2010

ABSTRACT
Cell entry of reovirus requires a series of ordered steps, which include conformational changes in outer capsid protein μ1 and its autocleavage. The μ1N fragment released as a consequence of these events interacts with host cell membranes and mediates their disruption, leading to delivery of the viral core into the cytoplasm. The prototype reovirus strains T1L and T3D exhibit differences in the efficiency of autocleavage, in the propensity to undergo conformational changes required for membrane penetration, and in the capacity for penetrating host cell membranes. To better understand how polymorphic differences in μ1 influence reovirus entry events, we generated recombinant viruses that express chimeric T1L-T3D μ1 proteins and characterized them for the capacity to efficiently complete each step required for membrane penetration. Our studies revealed two important functions for the central δ region of μ1. First, we found that μ1 autocleavage is regulated by the N-terminal portion of δ, which forms an α-helical pedestal structure. Second, we observed that the C-terminal portion of δ, which forms a jelly-roll β barrel structure, regulates membrane penetration by influencing the efficiency of ISVP* formation. Thus, our studies highlight the molecular basis for differences in the membrane penetration efficiency displayed by prototype reovirus strains and suggest that distinct portions of the reovirus δ domain influence different steps during entry.