bluuebunny/crossref_metadata_2025_split huggingface dataset:
Multisite virological influenza surveillance in India: 2004–2008
Authors: Chadha Mandeep S. , Broor Shobha , Gunasekaran Palani , Potdar Varsha A. , Krishnan Anand , Chawla‐Sarkar Mamta , Biswas Dipankar , Abraham Asha M. , Jalgaonkar Suresh V. , Kaur Harpreet , Klimov Alexander , Lal Renu B. , Moen Ann , Kant Lalit , Mishra Akhilesh C. 
Published: September 2011

Please cite this paper as: Chadha et al. (2011) Multi site Virological Influenza Surveillance in India: 2004–2008. Influenza and Other Respiratory Viruses 6(3), 196–203.Background  Influenza surveillance is important to identify circulating, emerging/reemerging strains and unusual epidemiological trends. With these objectives, a multisite human influenza surveillance network was initiated in India in 2004.Methods  Epidemiologic data and throat swabs for laboratory testing were collected from patients with influenza‐like illness (ILI) and severe acute respiratory infections (SARI). Virus isolation was carried out in Madin–Darby canine kidney cells and strains identified by hemagglutination inhibition assay. Meteorological data were collected.Results  From September 2004 to December 2008, 617 (4·43%) of 13928 cases yielded isolates: 27·8% were influenza A(H1N1), 29·8% were type A(H3N2), and 42·3% were type B. The yearly type and subtype distribution varied significantly from site to site. Peak influenza activity was observed from June to August in Delhi, Pune, and Kolkata and October to December in Chennai. Maximum influenza activity was seen during the rains in Delhi, Pune, Chennai, and Kolkata in correlation with virus isolations. Multivariate analysis of ILI cases showed chill/rigors, cough, fatigue, and ILI in family, correlated positively with isolation. Genetic analysis of Indian isolates revealed that viruses matched with vaccine strains by and large. Overlapping between circulating and vaccine component strains of consecutive years was also observed.Conclusions  Seasonal influenza A(H1N1), H3N2, and type B co‐circulated in all regions without any particular pattern of movement of any subtype. Year‐round limited influenza activity with peaks during rains was observed. Genetic drifts and varying seasonality in different parts of the country suggest that a staggered timing of vaccination may be appropriate for India.
No evidence of a link between influenza vaccines and Guillain–Barre syndrome–associated antiganglioside antibodies
Authors: Wang David J. , Boltz David A. , McElhaney Janet , McCullers Jonathan A. , Webby Richard J. , Webster Robert G. 
Published: September 2011

Please cite this paper as: Wang et al. (2011) No evidence of a link between influenza vaccines and Guillain–Barre syndrome–associated antiganglioside antibodies. Influenza and Other Respiratory Viruses 6(3), 159–166.Background  Guillain–Barre syndrome (GBS) is a rare autoimmune disease characterized by acute, progressive peripheral neuropathy and is commonly associated with the presence of antiganglioside antibodies. Previously, influenza vaccination was linked with the increased incidence of GBS; however, whether antiganglioside antibodies are subsequently induced remains unresolved.Methods  Sera from human subjects vaccinated with seasonal influenza vaccines from the 2007–2008, 2008–2009, or 1976–1977 influenza seasons were screened for the induction of immunity to influenza and the presence of antiganglioside antibodies pre‐ and post‐vaccination. Likewise, sera from mice vaccinated with seasonal influenza vaccines (1988–1989, 2007–2008) or “swine flu” pandemic vaccines (1976, 2009) were assessed in the same manner. Viruses were also screened for cross‐reacting ganglioside epitopes.Results  Antiganglioside antibodies were found to recognize influenza viruses; this reactivity correlated with virus glycosylation. Antibodies to influenza viruses were detected in human and mouse sera, but the prevalence of antiganglioside antibodies was extremely low.Conclusions  Although the correlation between antiganglioside antibody cross‐reactivity and glycosylation of viruses suggests the role of shared carbohydrate epitopes, no correlation was observed between hemagglutinin‐inhibition titers and the induction of antiganglioside antibodies after influenza vaccination.
A short clinical overview of Prader–Willi syndrome
Authors: McAllister C. J. , Whittington J. E. 
Published: September 2011

SummaryPrader–Willi syndrome (PWS) is a multifaceted developmental disorder most commonly associated with extreme hyperphagia and life‐threatening obesity. PWS is a genetic disorder of imprinting with almost all cases occurring spontaneously. Behavioural and imaging studies have shown that obesity in PWS arises from overeating driven by a faulty satiety mechanism which manifests as an almost permanent state similar to starvation. With no available treatments, management of the eating behaviour is the only option and has two main strategies: restrict access to food and distract thoughts from food. In this mini review, which we have aimed at clinicians, we outline the main aspects of PWS including genetics, development of the eating behaviour and best practice approaches to management.
Suppressed Type 1, Type 2, and Type 17 Cytokine Responses in Active Tuberculosis in Children
Authors: Kumar N. Pavan , Anuradha R. , Suresh R. , Ganesh R. , Shankar Janani , Kumaraswami V. , Nutman Thomas B. , Babu Subash 
Published: September 2011

ABSTRACTType 1 cytokine responses are known to play an important role in immunity to tuberculosis (TB) in children, although little is known about other factors that might be important. In addition, children are more prone to developing extrapulmonary manifestations of TB than adults. To identify the immune responses important both in control of infection and in extrapulmonary dissemination, we examined mycobacterium-specific cytokine responses of children with pulmonary TB (PTB) and extrapulmonary TB (ETB) and compared them with those of healthy control children (HC). No significant differences were found in the cytokine responses either with no stimulation or following mycobacterial-antigen (Ag) stimulation between children with PTB and ETB. On the other hand, children with active TB compared with HC showed markedly diminished production of type 1 (gamma interferon [IFN-γ] and tumor necrosis factor alpha [TNF-α]), 2 (interleukin 4 [IL-4] and IL-13), and 17 (IL-17A, IL-21, and IL-23)-associated cytokines with no stimulation and in response to mycobacterial antigens. This was not associated with significantly altered production of IL-10 or transforming growth factor β (TGF-β). Among children with ETB, those with neurologic involvement exhibited more significantly diminished Ag-driven IFN-γ and IL-17 production. Pediatric TB is characterized by diminished type 1, 2, and 17 cytokine responses, with the most profound diminution favoring development of neurologic TB, suggesting a crucial role for these cytokines in protection against pediatric tuberculosis.
The
N
-Acylneuraminate Cytidyltransferase Gene,
neuA
, Is Heterogenous in Legionella pneumophila Strains but Can Be Used as a Marker for Epidemiological Typing in the Consensus Sequence-Based Typing Scheme
Authors: Farhat Claudia , Mentasti Massimo , Jacobs Enno , Fry Norman K. , Lück Christian 
Published: September 2011

ABSTRACT

Sequence-based typing (SBT) is the internationally recognized standard method for genotyping
Legionella pneumophila
. To date all strains of serogroup 1 (SG1) and some of SGs 2 to 14 yield a seven-allele profile and can be assigned a sequence type (ST). However, for some strains belonging to SGs 2 to 14, the targeted region of the
neuA
gene could not be amplified using the published standard primers. We determined the DNA sequence of a
neuA
gene homolog located in the lipopolysaccharide synthesis locus of strain Dallas-1E. By using newly designed degenerate consensus primers based on the
neuA
homolog in strains Dallas-1E, Philadelphia-1, Paris, Lens, and Corby, we were able to obtain DNA sequences for all 48 non-SG1 strains which were untypeable by the standard method. Our data show that the
neuA
gene is present in all
L. pneumophila
strains but differs significantly in some non-SG1 strains at both the DNA and amino acid levels. The new primers can be used to amplify and sequence the
neuA
gene in all strains and can substitute for the standard primers. This offers the possibility of assigning an ST to all strains of
L. pneumophila
.
Lack of Association between Clinical Outcome of Clostridium difficile Infections, Strain Type, and Virulence-Associated Phenotypes
Authors: Sirard Stéphanie , Valiquette Louis , Fortier Louis-Charles 
Published: September 2011

ABSTRACT

Clostridium difficile
strain NAP1/027 (North American pulsed-field gel electrophoresis [PFGE] type 1 and PCR ribotype 027 [R027]) has been associated with recent outbreaks in North America and Europe. It has been associated with more severe disease symptoms, higher mortality rates, and greater risk of relapse. This strain is thought to produce more toxins and sporulate to higher levels. However, recent studies suggest that this may not always be the case. The objective of our study was to assess, in a nonoutbreak situation, whether specific strains, such as NAP1/027, were associated with more severe disease symptoms, higher toxin production, and/or greater sporulation
in vitro
. We isolated and characterized
C. difficile
strains from 21 patients with mild to moderate, severe, or complicated symptoms of
C. difficile
infection (CDI). The isolates were characterized by different molecular typing methods, including PCR ribotyping, tandem repeat sequence typing (TRST), and sequencing of the
tcdC
gene. Fourteen isolates were of PCR ribotype 027 with deletions in
tcdC
, but no association with severity or clinical outcome was found. We show by immunodot blot detection of toxins with monoclonal antibodies that all R027 isolates produced more TcdA and TcdB than other strains. On the other hand, they consistently produced fewer spores than non-R027 isolates. Taken together, our data suggest that NAP1/027 isolates are not always associated with more severe disease, even though they may produce larger amounts of toxins. Our study also suggests that current assertions regarding the NAP1/027 may not apply to all isolates and that other factors may come into play.
An Enhanced DNA Fingerprinting Service To Investigate Potential Clostridium difficile Infection Case Clusters Sharing the Same PCR Ribotype
Authors: Fawley Warren N. , Wilcox Mark H. 
Published: September 2011

ABSTRACT

Of 53 potential
Clostridium difficile
infection (CDI) case clusters/outbreaks, affecting 2 to 41 patients in 27 institutions, 19% comprised unrelated isolates and 34% had highly related and distinct isolates as shown by multilocus variable-number tandem-repeat analysis, despite sharing a common ribotype. These findings emphasize the value of enhanced fingerprinting to confirm or refute suspected CDI case clusters.
Targeting of the Influenza A Virus Polymerase PB1-PB2 Interface Indicates Strain-Specific Assembly Differences
Authors: Reuther Peter , Mänz Benjamin , Brunotte Linda , Schwemmle Martin , Wunderlich Kerstin 
Published: September 2011

ABSTRACT

Assembly of the heterotrimeric influenza virus polymerase complex from the individual subunits PB1, PA, and PB2 is a prerequisite for viral replication. The conserved protein-protein interaction sites have been suggested as potential drug targets. To characterize the PB1-PB2 interface, we fused the PB1-binding domain of PB2 to green fluorescent protein (PB2
1-37
-GFP) and determined its competitive inhibitory effect on the polymerase activity of influenza A virus strains. Coexpression of PB2
1-37
-GFP in a polymerase reconstitution system led to substantial inhibition of the polymerase of A/WSN/33 (H1N1). Surprisingly, polymerases of other strains, including A/SC35M (H7N7), A/Puerto Rico/8/34 (H1N1), A/Hamburg/4/2009 (H1N1), and A/Thailand/1(KAN-1)/2004 (H5N1), showed various degrees of resistance. Individual exchange of polymerase subunits and the nucleoprotein between the sensitive WSN polymerase and the insensitive SC35M polymerase mapped the resistance to both PB1 and PA of SC35M polymerase. While PB2
1-37
-GFP bound equally well to the PB1 subunits of both virus strains, PB1-PA dimers of SC35M polymerase showed impaired binding compared to PB1-PA dimers of WSN polymerase. The use of PA
SC35M/WSN
chimeras revealed that the reduced affinity of the SC35M PB1-PA dimer was mediated by the N-terminal 277 amino acids of PA. Based on these observations, we speculate that the PB1-PA dimer formation of resistant polymerases shields the PB2
1-37
binding site, whereas sensitive polymerases allow this interaction, suggesting different assembly strategies of the trimeric polymerase complex between different influenza A virus strains.
Glutamate Excitotoxicity Is Involved in the Induction of Paralysis in Mice after Infection by a Human Coronavirus with a Single Point Mutation in Its Spike Protein
Authors: Brison Elodie , Jacomy Hélène , Desforges Marc , Talbot Pierre J. 
Published: September 2011

ABSTRACT
Human coronaviruses (HCoV) are recognized respiratory pathogens, and some strains, including HCoV-OC43, can infect human neuronal and glial cells of the central nervous system (CNS) and activate neuroinflammatory mechanisms. Moreover, HCoV-OC43 is neuroinvasive, neurotropic, and neurovirulent in susceptible mice, where it induces chronic encephalitis. Herein, we show that a single point mutation in the viral spike (S) glycoprotein (Y241H), acquired during viral persistence in human neural cells, led to a hind-limb paralytic disease in infected mice. Inhibition of glutamate excitotoxicity using a 2-amino-3-(5-methyl-3-oxo-1,2-oxazol-4-yl)propranoic acid (AMPA) receptor antagonist (GYKI-52466) improved clinical scores related to the paralysis and motor disabilities in S mutant virus-infected mice, as well as protected the CNS from neuronal dysfunctions, as illustrated by restoration of the phosphorylation state of neurofilaments. Expression of the glial glutamate transporter GLT-1, responsible for glutamate homeostasis, was downregulated following infection, and GYKI-52466 also significantly restored its steady-state expression level. Finally, GYKI-52466 treatment of S mutant virus-infected mice led to reduced microglial activation, which may lead to improvement in the regulation of CNS glutamate homeostasis. Taken together, our results strongly suggest an involvement of excitotoxicity in the paralysis-associated neuropathology induced by an HCoV-OC43 mutant which harbors a single point mutation in its spike protein that is acquired upon persistent virus infection.
Avian Coronavirus in Wild Aquatic Birds
Authors: Chu Daniel K. W. , Leung Connie Y. H. , Gilbert Martin , Joyner Priscilla H. , Ng Erica M. , Tse Tsemay M. , Guan Yi , Peiris Joseph S. M. , Poon Leo L. M. 
Published: September 2011

ABSTRACT

We detected a high prevalence (12.5%) of novel avian coronaviruses in aquatic wild birds. Phylogenetic analyses of these coronaviruses suggest that there is a diversity of gammacoronaviruses and deltacoronaviruses circulating in birds. Gammacoronaviruses were found predominantly in
Anseriformes
birds, whereas deltacoronaviruses could be detected in
Ciconiiformes
,
Pelecaniformes
, and
Anseriformes
birds in this study. We observed that there are frequent interspecies transmissions of gammacoronaviruses between duck species. In contrast, deltacoronaviruses may have more stringent host specificities. Our analysis of these avian viral and host mitochondrial DNA sequences also suggests that some, but not all, coronaviruses may have coevolved with birds from the same order.
H5N1-SeroDetect EIA and Rapid Test: a Novel Differential Diagnostic Assay for Serodiagnosis of H5N1 Infections and Surveillance
Authors: Khurana Surender , Sasono Pretty , Fox Annette , Van Kinh Nguyen , Mai Le Quynh , Thai Pham Quang , Hien Nguyen Tran , Liem Nguyen Thanh , Horby Peter , Golding Hana 
Published: September 2011

ABSTRACT
Continuing evolution of highly pathogenic (HP) H5N1 influenza viruses in wild birds with transmission to domestic poultry and humans poses a pandemic threat. There is an urgent need for a simple and rapid serological diagnostic assay which can differentiate between antibodies to seasonal and H5N1 strains and that could provide surveillance tools not dependent on virus isolation and nucleic acid technologies. Here we describe the establishment of H5N1 SeroDetect enzyme-linked immunosorbent assay (ELISA) and rapid test assays based on three peptides in HA2 (488-516), PB1-F2 (2-75), and M2e (2-24) that are highly conserved within H5N1 strains. These peptides were identified by antibody repertoire analyses of H5N1 influenza survivors in Vietnam using whole-genome-fragment phage display libraries (GFPDLs). To date, both platforms have demonstrated high levels of sensitivity and specificity in detecting H5N1 infections (clade 1 and clade 2.3.4) in Vietnamese patients as early as 7 days and up to several years postinfection. H5N1 virus-uninfected individuals in Vietnam and the United States, including subjects vaccinated with seasonal influenza vaccines or with confirmed seasonal virus infections, did not react in the H5N1-SeroDetect assays. Moreover, sera from individuals vaccinated with H5N1 subunit vaccine with moderate anti-H5N1 neutralizing antibody titers did not react positively in the H5N1-SeroDetect ELISA or rapid test assays. The simple H5N1-SeroDetect ELISA and rapid tests could provide an important tool for large-scale surveillance for potential exposure to HP H5N1 strains in both humans and birds.
Growth of Esteya vermicola in media amended with nitrogen sources yields conidia with increased predacity and resistance to environmental stress
Authors: Wang Zhen , Wang Chun Yan , Gu Li Juan , Wang Yun Bo , Zhang Yong An , Sung Chang Keun 
Published: September 2011

Esteya vermicola , an endoparasitic fungus of pinewood nematode, exhibits great potential as a biological agent against nematodes. In this study to enhance the sporulation, predacity, and environmental resistance of E. vermicola, various nitrogen sources, such as glycine, l-leucine, and ammonium nitrate, were tested. The supplement of glycine and l-leucine had a significant influence on the growth rate of the colony, enhancing colony dry mass by 5-fold more than did ammonium nitrate or the control. Of the nitrogen sources tested, ammonium nitrate and l-leucine promoted sporulation, yielding more than 6 × 106 CFU/g, while glycine enhanced the proportion of lunate spores. Meanwhile, the supplement of nitrogen sources had a significant influence on adhesive rate and mortality rate against Bursaphelenchus xylophilus . Moreover, the supplement of glycine enhanced the survival rate against heat stress by more than 3-fold that of l-leucine, ammonium nitrate, and control. The spores produced in media amended with glycine, l-leucine, and ammonium nitrate had slightly but not significantly higher UV resistance and drought resistance than spores produced without nitrogen sources. These results suggested that the addition of glycine resulted in the production of E. vermicola conidia with increased predacity and resistance to environmental stress that may be more suitable for control of pine wilt disease.
AutoactivatedKlPDR1gene in the control of multidrug resistance inKluyveromyces lactis
Authors: Toth Hervay Nora , Hodurova Zuzana , Balazfyova Zuzana , Gbelska Yvetta 
Published: September 2011

The KlPDR1 gene encodes a zinc finger transcription factor that has recently been shown to be involved in the control of multidrug resistance of Kluyveromyces lactis . In this work, we provide evidence that the K. lactis KlPDR1 gene is under positive autoregulation by KlPdr1p, which plays a role in the activation of the main multidrug resistance transporter gene KlPDR5. Electrophoretic mobility shift assays, as well as the use of gusA reporter constructs, enabled us to identify the 5′-tataTCCGGGTAactt-3′ sequence motif in the KlPDR1 promoter (in the position –326 to –319 bp) as the PDRE (pleiotropic drug responsive element) for the binding of KlPdr1p. The drug sensitivity of Klpdr1Δ mutant cells was complemented by introducing the plasmid-born KlPDR1 gene. The KlPdr1p activated the expression of the PKlPDR1-gusA fusion gene, and the expression of the KlPDR1 gene was induced by fluconazole. The PDRE was also found in the promoter of KlPDR5, a gene encoding the ATP-dependent efflux pump responsible for the drug resistance phenomenon in K. lactis.
Molecular epidemiology and clinical characterization of group A rotavirus infections in Tunisian children with acute gastroenteritis
Authors: Sdiri-Loulizi Khira , Ambert-Balay Katia , Gharbi-Khelifi Hakima , Hassine Mouna , Chouchane Slaheddine , Sakly Nabil , Neji-Guédiche Mohamed , Pothier Pierre , Aouni Mahjoub 
Published: September 2011

Rotaviruses are the most common cause of severe viral gastroenteritis in early childhood worldwide. Thus, the objectives of our study were to determine the molecular epidemiology and the clinical features of rotavirus gastroenteritis in Tunisia. Between January 2003 and April 2007, a prospective study was conducted on 788 stool samples collected from children under 12 years of age who were suffering from acute gastroenteritis. Rotavirus was detected by multiplex RT-PCR in 27% (n = 213) of samples, among them 79.3% (n = 169) cases were monoinfections. The frequency of rotavirus infections was significantly higher among inpatients (29%) than among outpatients (13%) (P < 0.001). The seasonal distribution of rotavirus diarrhea showed a winter peak, with an unusual peak from June to September. The mean duration of hospitalization was 6.5 ± 8.1 days and the mean age was 15.8 ± 22.8 months for rotavirus monoinfections. Fever, vomiting, abdominal pain, and dehydration were observed in 88, 98, 13, and 80 cases, respectively, in children with rotavirus monoinfections. G3P[8] (45.6%) and G1P[8] (23.9%) were the most common genotypes found in our study. The determination of rotavirus infection prevalence and the characterization of the rotavirus strains circulating will help us to better understand the molecular biology and epidemiology of the disease in our country.
Functional characterization ofpfmin protein secretion and lung infection ofPseudomonas aeruginosa
Authors: Bai Fang , Xu Haijin , Zhang Qi , Qi Xizhen , Mou Rui , Bai Gang , Qiao Mingqiang 
Published: September 2011

Lung infections caused by Pseudomonas aeruginosa in cystic fibrosis (CF) patients cause progressive airway obstruction and tissue damage, which is the predominant cause of morbidity and mortality in patients with CF. This paper describes the functional characterization of the pfm gene (open reading frame PA2950) of P. aeruginosa. Using DNA microarrays, we found that the transcriptional levels of type II secretory system genes were significantly reduced in the pfm mutant strain. The type-II-dependent exoprotein LasB could not be secreted normally. The pfm gene was identified as a gene involved in bacterial protein secretion that was critical for the extracellular release of elastase in P. aeruginosa. The abilities to induce lung injury by wild-type and pfm mutant P. aeruginosa were evaluated in a murine acute lung infection model. The results showed that the pathogenicity and virulence of the pfm mutant strain was significantly reduced compared with that of the wild-type strain. The pfm gene and its expression product, as potential new drug targets against P. aeruginosa infection, have important research significance.