bluuebunny/crossref_metadata_2025_split huggingface dataset:
Bursopentine as a Novel Immunoadjuvant Enhances both Humoral and Cell-Mediated Immune Responses to Inactivated H9N2 Avian Influenza Virus in Chickens
Authors: Li Deyuan , Xue Maoyun , Wang Chen , Wang Junbao , Chen Puyan 
Published: July 2011

ABSTRACTThere is an urgent need for identification of a new adjuvant capable of selectively promoting an efficient immune response for use with vaccines and especially subunit vaccines. Our pervious study showed that Bursopentine (BP5) is a novel immunomodulatory peptide and has the ability to significantly stimulate an antigen-specific immune response in mice. In this study, the potential adjuvant activities of BP5 were examined in chickens by coinjection of BP5 and an inactivated avian influenza virus (AIV) (A/Duck/Jiangsu/NJ08/05 [AIV H9N2 subtype]). The results suggested that BP5 markedly elevated serum hemagglutination inhibition (HI) titers and antigen-specific antihemagglutinin (anti-HA) antibody (IgG) levels, induced both Th1 (interleukin 2 [IL-2] and gamma interferon [IFN-γ])- and Th2 (IL-4)-type cytokines, promoted the proliferation of peripheral blood lymphocytes, and increased populations of CD3+T cells and their subsets CD4+(CD3+CD4+) T cells and CD8+(CD3+CD8+) T cells. Furthermore, a virus challenge experiment revealed that BP5 contributes to protection against homologous avian influenza virus challenge by reducing viral replication in chicken lungs. This study indicates that the combination of inactivated AIVs and BP5 gives a strong immune response at both the humoral and cellular levels and implies that BP5 is a novel immunoadjuvant suitable for vaccine design.
Diverse Cytokine Profile from Mesenteric Lymph Node Cells of Cull Cows Severely Affected with Johne's Disease
Authors: Shu Dairu , Subharat Supatsak , Wedlock D. Neil , Luo Dongwen , de Lisle Geoffrey W. , Buddle Bryce M. 
Published: July 2011

ABSTRACTMycobacterium aviumsubsp.paratuberculosis, the causative agent of Johne's disease, is able to dampen or distort immune responses at the mucosal sites and coexist with a massive infiltration of immune cells in the gastrointestinal tract. Knowledge of the mechanism by whichM. aviumsubsp.paratuberculosissubverts the immune response at the mucosal level in cattle is important for the development of improved disease control strategies, including new vaccines and diagnostic tests. In this study, 38 cull cows from herds infected withM. aviumsubsp.paratuberculosiswere divided into four groups, based onM. aviumsubsp.paratuberculosisculture from gut tissues and histopathological lesion scores. Cytokine gene expression and secretion fromM. aviumsubsp.paratuberculosissonicate-stimulated peripheral blood mononuclear cell (PBMC) and mesenteric lymph node (MLN) cultures of the animals were compared. Antigen stimulation of MLN cells from the severely lesioned group resulted in significant upregulation of the mRNA expression of five cytokines, gamma interferon (IFN-γ), interleukin-10 (IL-10), IL-13, IL-17A, and tumor necrosis factor alpha (TNF-α), which have a diverse range of functions, while there was no significant upregulation of these cytokines by the other groups. There were major differences between the responses of the PBMC and MLN cultures, with higher levels of secreted IFN-γ released from the MLN cultures and, conversely, higher levels of IL-10 released from the PBMC cultures. The upregulation of all five cytokines from cells at the site of infection in the severely lesioned animals suggested a dysregulated immune response, contributing to a failure to clear infection in this group of animals.
Adhesin-Encoding Genes from Shiga Toxin-Producing Escherichia coli Are More Prevalent in Atypical than in Typical Enteropathogenic E. coli
Authors: Gomes Tânia A. T. , Hernandes Rodrigo T. , Torres Alfredo G. , Salvador Fábia A. , Guth Beatriz E. C. , Vaz Tânia M. I. , Irino Kinue , Silva Rosa M. , Vieira Mônica A. M. 
Published: July 2011

ABSTRACT

Four of six adhesin-encoding genes (
lpfA
,
paa
,
iha
, and
toxB
) from Shiga toxin-producing
Escherichia coli
strains were detected in typical and atypical enteropathogenic
E. coli
(EPEC) strains of various serotypes. Although the most prevalent gene was
lpfA
in both groups,
paa
was the only potential diarrhea-associated gene in atypical EPEC.
Native Valve Endocarditis Due to a Novel Strain of Legionella
Authors: Pearce Meghan M. , Theodoropoulos Nicole , Noskin Gary A. , Flaherty John P. , Stemper Mary E. , Aspeslet Teresa , Cianciotto Nicholas P. , Reed Kurt D. 
Published: July 2011

ABSTRACT

Legionellae are Gram-negative bacteria which are capable of causing disease, most commonly in the form of pneumonia. We describe a case of native valve endocarditis caused by a
Legionella
strain which by genotypic (16S rRNA and
mip
gene sequencing) and phenotypic analyses is unlike previously described strains of
Legionella
.
Rapid Identification of Staphylococcus aureus and Methicillin Resistance by Flow Cytometry Using a Peptide Nucleic Acid Probe
Authors: Shrestha Nabin K. , Scalera Nikole M. , Wilson Deborah A. , Brehm-Stecher Byron , Procop Gary W. 
Published: July 2011

ABSTRACT

A total of 56
Staphylococcus aureus
isolates incubated for 2 h in the presence or absence of oxacillin were analyzed by flow cytometry after labeling with an
S. aureus
-specific peptide nucleic acid (PNA) probe. Two defined ratios, the paired signal count ratio (PSCR) and the gate signal count ratio (GSCR), differentiated methicillin-resistant
S. aureus
(MRSA) and methicillin-susceptible
S. aureus
(MSSA) with sensitivities of 100% each and specificities of 96% and 100%, respectively.
Genotypic Characterization of Ureaplasma Serovars from Clinical Isolates by Pulsed-Field Gel Electrophoresis
Authors: Xiao Li , Crabb Donna M. , Moser Stephen A. , Duffy Lynn B. , Glass John I. , Paralanov Vanya , Waites Ken B. 
Published: July 2011

ABSTRACT

Genetic relationships within ureaplasma serovars were investigated by pulsed-field gel electrophoresis (PFGE). One hundred thirteen
Ureaplasma parvum
isolates and 78
Ureaplasma urealyticum
isolates were different from their ATCC serovar type strains and different within the same serovars. The organisms were geographically widespread. No unique patterns were associated with invasive disease.
Multiple-Locus Variable-Number Tandem-Repeat Analysis Genotyping of Human Brucella Isolates from Turkey
Authors: Kılıç Selçuk , Ivanov Ivan N. , Durmaz Rıza , Bayraktar Mehmet Refik , Ayaşlıoğlu Ergin , Uyanık M. Hamidullah , Alışkan Hikmet , Yaşar Ekrem , Bayramoğlu Gülçin , Arslantürk Ahmet , Vergnaud Gilles , Kantardjiev Todor V. 
Published: July 2011

ABSTRACT

A multiple-locus variable-number tandem-repeat analysis (MLVA) was applied to investigate the epidemiological relationship and genetic diversity among 162 human
Brucella
isolates collected from all geographic regions of Turkey in an 8-year period (2001 to 2008). The isolates were genotyped by using an MLVA assay developed in Orsay, France (MLVA-16
Orsay
) including eight minisatellite (panel 1) and eight microsatellite (panel 2, subdivided into 2A and 2B) markers. Panels 1 and 2A distinguish 14 genotypes; two of these represented 85% of the strains. Panel 2B displayed a very high discriminatory power. Three loci from panel 2B had diversity index values higher than 0.74. MLVA-16
Orsay
yielded 105 genotypes; 73 were represented by a unique isolate, and 32 included two to eight isolates. The isolates from different patients within the same outbreak or from the same patient before first-line therapy and after relapse showed identical genotypes. A number of MLVA genotypes appeared to be partially restricted to some geographic areas and displayed no annual variation, possibly reflecting persistence of genotypes in certain areas for a time span of at least a decade. This study, representing the first molecular typing results of human
Brucella
isolates from Turkey, indicated that Turkish human
Brucella melitensis
isolates were most closely related to the neighboring countries' isolates included in the East Mediterranean group.
Evaluation of Quantitative Antibiotic Susceptibility Testing by Vitek 2 as a Routine Method To Predict Strain Relatedness of Coagulase-Negative Staphylococci Isolated from Blood Cultures
Authors: Camerer Antonia , Kohlenberg Anke , Stefanik Danuta , Seifert Harald 
Published: July 2011

ABSTRACT
To test the hypothesis that the strain relatedness of coagulase-negative staphylococci (CoNS) recovered from blood cultures can be inferred from automated antibiotic susceptibility testing (AST) results generated by Vitek 2, concordant or discordant AST results were compared with pulsed-field gel electrophoresis (PFGE) typing results for 119 CoNS blood culture isolate pairs. Concordant AST results were highly predictive of the strain relatedness of CoNS isolates.
Deletion of Kaposi's Sarcoma-Associated Herpesvirus FLICE Inhibitory Protein, vFLIP, from the Viral Genome Compromises the Activation of STAT1-Responsive Cellular Genes and Spindle Cell Formation in Endothelial Cells
Authors: Alkharsah Khaled R. , Singh Vivek Vikram , Bosco Raffaella , Santag Susann , Grundhoff Adam , Konrad Andreas , Stürzl Michael , Wirth Dagmar , Dittrich-Breiholz Oliver , Kracht Michael , Schulz Thomas F. 
Published: July 2011

ABSTRACT
Kaposi's sarcoma herpesvirus (KSHV) Fas-associated death domain (FADD)-like interleukin-1 beta-converting enzyme (FLICE)-inhibitory protein, vFLIP, has antiapoptotic properties, is a potent activator of the NF-κB pathway, and induces the formation of endothelial spindle cells, the hallmark of Kaposi's sarcoma, when overexpressed in primary endothelial cells. We used a reverse genetics approach to study several functions of KSHV vFLIP in the context of the whole viral genome. Deletion of the gene encoding vFLIP from a KSHV genome cloned in a bacterial artificial chromosome (BAC) reduced the ability of the virus to persist and induce spindle cell formation in primary human umbilical vein endothelial cells (HUVECs). Only a few, mainly interferon (IFN)-responsive, genes were expressed in wild-type KSHV (KSHV-wt)-infected endothelial cells at levels higher than those in KSHV-ΔFLIP-infected endothelial cells, in contrast to the plethora of cellular genes induced by overexpressed vFLIP. In keeping with this observation, vFLIP induces the phosphorylation of STAT1 and STAT2 in an NF-κB-dependent manner in endothelial cells. vFLIP-dependent phosphorylation of STAT1 and STAT2 could be demonstrated after endothelial cells were infected with KSHV-wt, KSHV-ΔFLIP, and a KSHV-vFLIP revertant virus. These findings document the impact of KSHV vFLIP on the transcriptome of primary endothelial cells during viral persistence and highlight the role of vFLIP in the activation of STAT1/STAT2 and STAT-responsive cellular genes by KSHV.
Mechanisms Controlling Virulence Thresholds of Mixed Viral Populations
Authors: Lancaster Karen Z. , Pfeiffer Julie K. 
Published: July 2011

ABSTRACT

The propensity of RNA viruses to revert attenuating mutations contributes to disease and complicates vaccine development. Despite the presence of virulent revertant viruses in some live-attenuated vaccines, disease from vaccination is rare. This suggests that in mixed viral populations, attenuated viruses may limit the pathogenesis of virulent viruses, thus establishing a virulence threshold. Here we examined virulence thresholds using mixtures of virulent and attenuated viruses in a transgenic mouse model of poliovirus infection. We determined that a 1,000-fold excess of the attenuated Sabin strain of poliovirus was protective against disease induced by the virulent Mahoney strain. Protection was induced locally, and inactivated virus conferred protection. Treatment with a poliovirus receptor-blocking antibody phenocopied the protective effect of inactivated viruses
in vitro
and
in vivo
, suggesting that one mechanism controlling virulence thresholds may be competition for a viral receptor. Additionally, the type I interferon response reduces poliovirus pathogenesis; therefore, we examined virulence thresholds in mice lacking the alpha/beta interferon receptor. We found that the attenuated virus was virulent in immunodeficient mice due to the enhanced replication and reversion of attenuating mutations. Therefore, while the type I interferon response limits the virulence of the attenuated strain by reducing replication, protection from disease conferred by the attenuated strain in immunocompetent mice can occur independently of replication. Our results identified mechanisms controlling the virulence of mixed viral populations and indicate that live-attenuated vaccines containing virulent virus may be safe, as long as virulent viruses are present at levels below a critical threshold.
Emergence of Avian Influenza Viruses with Enhanced Transcription Activity by a Single Amino Acid Substitution in the Nucleoprotein during Replication in Chicken Brains
Authors: Tada Tatsuya , Suzuki Koutaro , Sakurai Yu , Kubo Masanori , Okada Hironao , Itoh Toshihiro , Tsukamoto Kenji 
Published: July 2011

ABSTRACT

To explore the genetic basis of the pathogenesis and adaptation of avian influenza viruses (AIVs) to chickens, the A/duck/Yokohama/aq10/2003 (H5N1) (DkYK10) virus was passaged five times in the brains of chickens. The brain-passaged DkYK10-B5 caused quick death of chickens through rapid and efficient replication in tissues, accompanied by severe apoptosis. Genome sequence comparison of two viruses identified a single amino acid substitution at position 109 in NP from isoleucine to threonine (NP
I
109
T
). By analyzing viruses constructed by the reverse-genetic method, we established that the NP
I
109
T
substitution also contributed to increased viral replication and polymerase activity in chicken embryo fibroblasts, but not in duck embryo fibroblasts. Real-time RT-PCR analysis demonstrated that the NP
I
109
T
substitution enhances mRNA synthesis quickly and then cRNA and viral RNA (vRNA) synthesis slowly. Next, to determine the mechanism underlying the appearance of the NP
I
109
T
substitution during passages, four H5N1 highly pathogenic AIVs (HPAIVs) were passaged in the lungs and brains of chicken embryos. Single-nucleotide polymorphism analysis, together with a database search, suggests that the NP
I
109
T
mutation would be induced frequently during replication of HPAIVs in brains, but not in lungs. These results demonstrate that the amino acid at position 109 in NP enhances viral RNA synthesis and the pathogenicity of highly pathogenic avian influenza viruses in chickens and that the NP mutation emerges quickly during replication of the viruses in chicken brains.
Widespread Endogenization of Densoviruses and Parvoviruses in Animal and Human Genomes
Authors: Liu Huiquan , Fu Yanping , Xie Jiatao , Cheng Jiasen , Ghabrial Said A. , Li Guoqing , Peng Youliang , Yi Xianhong , Jiang Daohong 
Published: July 2011

ABSTRACT

Parvoviruses infect humans and a broad range of animals, from mammals to crustaceans, and generally are associated with a variety of acute and chronic diseases. However, many others cause persistent infections and are not known to be associated with any disease. Viral persistence is likely related to the ability to integrate into the chromosomal DNA and to establish a latent infection. However, there is little evidence for genome integration of parvoviral DNA except for
Adeno-associated virus
(AAV). Here we performed a systematic search for homologs of parvoviral proteins in publicly available eukaryotic genome databases followed by experimental verification and phylogenetic analysis. We conclude that parvoviruses have frequently invaded the germ lines of diverse animal species, including mammals, fishes, birds, tunicates, arthropods, and flatworms. The identification of orthologous endogenous parvovirus sequences in the genomes of humans and other mammals suggests that parvoviruses have coexisted with mammals for at least 98 million years. Furthermore, some of the endogenized parvoviral genes were expressed in eukaryotic organisms, suggesting that these viral genes are also functional in the host genomes. Our findings may provide novel insights into parvovirus biology, host interactions, and evolution.
The Major Determinant of Attenuation in Mice of the Candid1 Vaccine for Argentine Hemorrhagic Fever Is Located in the G2 Glycoprotein Transmembrane Domain
Authors: Albariño César G. , Bird Brian H. , Chakrabarti Ayan K. , Dodd Kimberly A. , Flint Mike , Bergeron Éric , White David M. , Nichol Stuart T. 
Published: July 2011

ABSTRACT
Candid1, a live-attenuated Junin virus vaccine strain, was developed during the early 1980s to control Argentine hemorrhagic fever, a severe and frequently fatal human disease. Six amino acid substitutions were found to be unique to this vaccine strain, and their role in virulence attenuation in mice was analyzed using a series of recombinant viruses. Our results indicate that Candid1 is attenuated in mice through a single amino acid substitution in the transmembrane domain of the G2 glycoprotein. This work provides insight into the molecular mechanisms of attenuation of the only arenavirus vaccine currently available.
Expression of Herpes Simplex Virus 1-Encoded MicroRNAs in Human Trigeminal Ganglia and Their Relation to Local T-Cell Infiltrates
Authors: Held Kathrin , Junker Andreas , Dornmair Klaus , Meinl Edgar , Sinicina Inga , Brandt Thomas , Theil Diethilde , Derfuss Tobias 
Published: July 2011

ABSTRACT

Herpes simplex type 1 (HSV-1) is a neurotropic virus which establishes lifelong latency in human trigeminal ganglia (TG). Currently, two nonexclusive control mechanisms of HSV-1 latency are discussed: antiviral CD8
+
T cells and viral microRNAs (miRNAs) encoded by the latency associated transcript (LAT). We investigate here to what extent these mechanisms may contribute to the maintenance of HSV-1 latency. We show that only a small proportion of LAT
+
neurons is surrounded by T cells in human TG. This indicates that viral latency in human TG might be controlled by other mechanisms such as viral miRNAs. Therefore, we assessed TG sections for the presence of HSV-1 miRNA, DNA, and mRNA by combining LAT
in situ
hybridization, T-cell immunohistochemistry, and single cell analysis of laser-microdissected sensory neurons. Quantitative reverse transcription-PCR (RT-PCR) revealed that LAT
+
neurons with or without surrounding T cells were always positive for HSV-1 miRNAs and DNA. Furthermore, ICP0 mRNA could rarely be detected only in LAT
+
neurons, as analyzed by single-cell RT-PCR. In contrast, in LAT
−
neurons that were surrounded by T cells, neither miRNAs nor the DNA of HSV-1, HSV-2, or varicella-zoster virus could be detected. These data indicate that the majority of LAT
+
neurons is not directly controlled by T cells. However, miRNA expression in every latently infected neuron would provide an additional checkpoint before viral replication is initiated.
The Fecal Viral Flora of California Sea Lions
Authors: Li Linlin , Shan Tongling , Wang Chunlin , Côté Colette , Kolman John , Onions David , Gulland Frances M. D. , Delwart Eric 
Published: July 2011

ABSTRACTCalifornia sea lions are one of the major marine mammal species along the Pacific coast of North America. Sea lions are susceptible to a wide variety of viruses, some of which can be transmitted to or from terrestrial mammals. Using an unbiased viral metagenomic approach, we surveyed the fecal virome in California sea lions of different ages and health statuses. Averages of 1.6 and 2.5 distinct mammalian viral species were shed by pups and juvenile sea lions, respectively. Previously undescribed mammalian viruses from four RNA virus families (Astroviridae,Picornaviridae,Caliciviridae, andReoviridae) and one DNA virus family (Parvoviridae) were characterized. The first complete or partial genomes of sapeloviruses, sapoviruses, noroviruses, and bocavirus in marine mammals are reported. Astroviruses and bocaviruses showed the highest prevalence and abundance in California sea lion feces. The diversity of bacteriophages was higher in unweaned sea lion pups than in juveniles and animals in rehabilitation, where the phage community consisted largely of phages related to the familyMicroviridae. This study increases our understanding of the viral diversity in marine mammals, highlights the high rate of enteric viral infections in these highly social carnivores, and may be used as a baseline viral survey for comparison with samples from California sea lions during unexplained disease outbreaks.
Epstein-Barr Virus Latent Membrane Protein 1 (LMP1) C-Terminal-Activating Region 3 Contributes to LMP1-Mediated Cellular Migration via Its Interaction with Ubc9
Authors: Bentz Gretchen L. , Whitehurst Christopher B. , Pagano Joseph S. 
Published: July 2011

ABSTRACT
Epstein-Barr virus (EBV) latent membrane protein 1 (LMP1), the principal viral oncoprotein and a member of the tumor necrosis factor receptor superfamily, is a constitutively active membrane signaling protein that regulates multiple signal transduction pathways via its C-terminal-activating region 1 (CTAR1) and CTAR2, and also the less-studied CTAR3. Because protein sumoylation among other posttranslational modifications may regulate many signaling pathways induced by LMP1, we investigated whether during EBV latency LMP1 regulates sumoylation processes that control cellular activation and cellular responses. By immunoprecipitation experiments, we show that LMP1 interacts with Ubc9, the single reported SUMO-conjugating enzyme. Requirements for LMP1-Ubc9 interactions include enzymatically active Ubc9: expression of inactive Ubc9 (Ubc9 C93S) inhibited the LMP1-Ubc9 interaction. LMP1 CTAR3, but not CTAR1 and CTAR2, participated in the LMP1-Ubc9 interaction, and amino acid sequences found in CTAR3, including the JAK-interacting motif, contributed to this interaction. Furthermore, LMP1 expression coincided with increased sumoylation of cellular proteins, and disruption of the Ubc9-LMP1 CTAR3 interaction almost completely abrogated LMP1-induced protein sumoylation, suggesting that this interaction promotes the sumoylation of downstream targets. Additional consequences of the disruption of the LMP1 CTAR3-Ubc9 interaction revealed effects on cellular migration, a hallmark of oncogenesis. Together, these data demonstrate that LMP1 CTAR3 does in fact function in intracellular signaling and leads to biological effects. We propose that LMP1, by interaction with Ubc9, modulates sumoylation processes, which regulate signal transduction pathways that affect phenotypic changes associated with oncogenesis.