bluuebunny/crossref_metadata_2025_split huggingface dataset:
Chicken Cells Sense Influenza A Virus Infection through MDA5 and CARDIF Signaling Involving LGP2
Authors: Liniger Matthias , Summerfield Artur , Zimmer Gert , McCullough Kenneth C. , Ruggli Nicolas 
Published: November 2011

ABSTRACT
Avian influenza viruses (AIV) raise worldwide veterinary and public health concerns due to their potential for zoonotic transmission. While infection with highly pathogenic AIV results in high mortality in chickens, this is not necessarily the case in wild birds and ducks. It is known that innate immune factors can contribute to the outcome of infection. In this context, retinoic acid-inducible gene I (RIG-I) is the main cytosolic pattern recognition receptor known for detecting influenza A virus infection in mammalian cells. Chickens, unlike ducks, lack RIG-I, yet chicken cells do produce type I interferon (IFN) in response to AIV infection. Consequently, we sought to identify the cytosolic recognition elements in chicken cells. Chicken mRNA encoding the putative chicken analogs of CARDIF and LGP2 (chCARDIF and chLGP2, respectively) were identified. HT7-tagged chCARDIF was observed to associate with mitochondria in chicken DF-1 fibroblasts. The exogenous expression of chCARDIF, as well as of the caspase activation and recruitment domains (CARDs) of the chicken melanoma differentiation-associated protein 5 (chMDA5), strongly activated the chicken IFN-β (chIFN-β) promoter. The silencing of chMDA5, chCARDIF, and chIRF3 reduced chIFN-β levels induced by AIV, indicating their involvement in AIV sensing. As with mammalian cells, chLGP2 had opposing effects. While overexpression decreased the activation of the chIFN-β promoter, the silencing of endogenous chLGP2 reduced chIFN-β induced by AIV. We finally demonstrate that the chMDA5 signaling pathway is inhibited by the viral nonstructural protein 1. In conclusion, chicken cells, including DF-1 fibroblasts and HD-11 macrophage-like cells, employ chMDA5 for sensing AIV.
Crystallographic Analysis Reveals Octamerization of Viroplasm Matrix Protein P9-1 of Rice Black Streaked Dwarf Virus
Authors: Akita Fusamichi , Higashiura Akifumi , Shimizu Takumi , Pu Yingying , Suzuki Mamoru , Uehara-Ichiki Tamaki , Sasaya Takahide , Kanamaru Shuji , Arisaka Fumio , Tsukihara Tomitake , Nakagawa Atsushi , Omura Toshihiro 
Published: November 2011

ABSTRACT

The P9-1 protein of
Rice black streaked dwarf virus
accumulates in viroplasm inclusions, which are structures that appear to play an important role in viral morphogenesis and are commonly found in viruses in the family
Reoviridae
. Crystallographic analysis of P9-1 revealed structural features that allow the protein to form dimers via hydrophobic interactions. Each dimer has carboxy-terminal regions, resembling arms, that extend to neighboring dimers, thereby uniting sets of four dimers via lateral hydrophobic interactions, to yield cylindrical octamers. The importance of these regions for the formation of viroplasm-like inclusions was confirmed by the absence of such inclusions when P9-1 was expressed without its carboxy-terminal arm. The octamers are vertically elongated cylinders resembling the structures formed by NSP2 of rotavirus, even though there are no significant similarities between the respective primary and secondary structures of the two proteins. Our results suggest that an octameric structure with an internal pore might be important for the functioning of the respective proteins in the events that occur in the viroplasm, which might include viral morphogenesis.
Direct Interaction of Baculovirus Capsid Proteins VP39 and EXON0 with Kinesin-1 in Insect Cells Determined by Fluorescence Resonance Energy Transfer-Fluorescence Lifetime Imaging Microscopy
Authors: Danquah John O. , Botchway Stanley , Jeshtadi Ananya , King Linda A. 
Published: November 2011

ABSTRACT

Autographa californica
multiple nucleopolyhedrovirus (AcMNPV) replicates in the nucleus of insect cells to produce nucleocapsids, which are transported from the nucleus to the plasma membrane for budding through GP64-enriched areas to form budded viruses. However, little is known about the anterograde trafficking of baculovirus nucleocapsids in insect cells. Preliminary confocal scanning laser microscopy studies showed that enhanced green fluorescent protein (EGFP)-tagged nucleocapsids and capsid proteins aligned and colocalized with the peripheral microtubules of virus-infected insect cells. A colchicine inhibition assay of virus-infected insect cells showed a significant reduction in budded virus production, providing further evidence for the involvement of microtubules and suggesting a possible role of kinesin in baculovirus anterograde trafficking. We investigated the interaction between AcMNPV nucleocapsids and kinesin-1 with fluorescence resonance energy transfer-fluorescence lifetime imaging microscopy (FRET-FLIM) and show for the first time that AcMNPV capsid proteins VP39 and EXON0, but not Orf1629, interact with the tetratricopeptide repeat (TPR) domain of kinesin. The excited-state fluorescence lifetime of EGFP fused to VP39 or EXON0 was quenched from 2.4 ± 1 ns to 2.1 ± 1 ns by monomeric fluorescent protein (mDsRed) fused to TPR (mDsRed-TPR). However, the excited-state fluorescence lifetime of an EGFP fusion of Orf1629 remained unquenched by mDsRed-TPR. These data indicate that kinesin-1 plays an important role in the anterograde trafficking of baculovirus in insect cells.
Role of Multiple Hosts in the Cross-Species Transmission and Emergence of a Pandemic Parvovirus
Authors: Allison Andrew B. , Harbison Carole E. , Pagan Israel , Stucker Karla M. , Kaelber Jason T. , Brown Justin D. , Ruder Mark G. , Keel M. Kevin , Dubovi Edward J. , Holmes Edward C. , Parrish Colin R. 
Published: November 2011

ABSTRACT
Understanding the mechanisms of cross-species virus transmission is critical to anticipating emerging infectious diseases. Canine parvovirus type 2 (CPV-2) emerged as a variant of a feline parvovirus when it acquired mutations that allowed binding to the canine transferrin receptor type 1 (TfR). However, CPV-2 was soon replaced by a variant virus (CPV-2a) that differed in antigenicity and receptor binding. Here we show that the emergence of CPV involved an additional host range variant virus that has circulated undetected in raccoons for at least 24 years, with transfers to and from dogs. Raccoon virus capsids showed little binding to the canine TfR, showed little infection of canine cells, and had altered antigenic structures. Remarkably, in capsid protein (VP2) phylogenies, most raccoon viruses fell as evolutionary intermediates between the CPV-2 and CPV-2a strains, suggesting that passage through raccoons assisted in the evolution of CPV-2a. This highlights the potential role of alternative hosts in viral emergence.
Activation of NF-κB in CD8
+
Dendritic Cells
Ex Vivo
by the γ
1
34.5 Null Mutant Correlates with Immunity against Herpes Simplex Virus 1
Authors: Jin Huali , Ma Yijie , Yan Zhipeng , Prabhakar Bellur S. , He Bin 
Published: November 2011

ABSTRACT

The γ
1
34.5 protein of herpes simplex viruses (HSV) is essential for virulence. Accordingly, an HSV mutant lacking γ
1
34.5 is attenuated
in vivo
. Despite its vaccine potential, the mechanism by which the γ
1
34.5 null mutant triggers protective immunity is unknown. In this report we show that vaccination with the γ
1
34.5 null mutant protects against lethal challenge from wild-type virus via IκB kinase in dendritic cells (DCs), which sense virus-associated molecular patterns. Unlike mock-treated DCs, DCs primed with the γ
1
34.5 null mutant
ex vivo
mediate resistance to wild-type HSV after adoptive transfer into naïve mice. Furthermore, the γ
1
34.5 null mutant activates IκB kinase, which facilitates p65/RelA phosphorylation and nuclear translocation, resulting in DC maturation. While unable to produce infectious virus in DCs, this mutant virus expresses early and late genes. In its abortive infection, the γ
1
34.5 null mutant induces protective immunity more effectively in CD8
+
DCs than in CD8
−
DCs. This is mirrored by a higher level of interleukin-6 (IL-6) and IL-12 secretion by CD8
+
DCs than CD8
−
DCs. Remarkably, inhibition of p65/RelA phosphorylation or nuclear translocation in CD8
+
DCs disrupts protective immunity. These results suggest that engagement of the γ
1
34.5 null mutant with CD8
+
DCs elicits innate immunity to activate NF-κB, which translates into protective immunity.
Human Pathogens and the Host Cell SUMOylation System
Authors: Wimmer Peter , Schreiner Sabrina , Dobner Thomas 
Published: November 2011

ABSTRACTSince posttranslational modification (PTM) by the small ubiquitin-related modifiers (SUMOs) was discovered over a decade ago, a huge number of cellular proteins have been found to be reversibly modified, resulting in alteration of differential cellular pathways. Although the molecular consequences of SUMO attachment are difficult to predict, the underlying principle of SUMOylation is altering inter- and/or intramolecular interactions of the modified substrate, changing localization, stability, and/or activity. Unsurprisingly, many different pathogens have evolved to exploit the cellular SUMO modification system due to its functional flexibility and far-reaching functional downstream consequences. Although the extensive knowledge gained so far is impressive, a definitive conclusion about the role of SUMO modification during virus infection in general remains elusive and is still restricted to a few, yet promising concepts. Based on the available data, this review aims, first, to provide a detailed overview of the current state of knowledge and, second, to evaluate the currently known common principles/molecular mechanisms of how human pathogenic microbes, especially viruses and their regulatory proteins, exploit the host cell SUMO modification system.
Structural Characterization of the Hemagglutinin Receptor Specificity from the 2009 H1N1 Influenza Pandemic
Authors: Xu Rui , McBride Ryan , Nycholat Corwin M. , Paulson James C. , Wilson Ian A. 
Published: November 2011

ABSTRACT
Influenza virus hemagglutinin (HA) is the viral envelope protein that mediates viral attachment to host cells and elicits membrane fusion. The HA receptor-binding specificity is a key determinant for the host range and transmissibility of influenza viruses. In human pandemics of the 20th century, the HA normally has acquired specificity for human-like receptors before widespread infection. Crystal structures of the H1 HA from the 2009 human pandemic (A/California/04/2009 [CA04]) in complex with human and avian receptor analogs reveal conserved recognition of the terminal sialic acid of the glycan ligands. However, favorable interactions beyond the sialic acid are found only for α2-6-linked glycans and are mediated by Asp190 and Asp225, which hydrogen bond with Gal-2 and GlcNAc-3. For α2-3-linked glycan receptors, no specific interactions beyond the terminal sialic acid are observed. Our structural and glycan microarray analyses, in the context of other high-resolution HA structures with α2-6- and α2-3-linked glycans, now elucidate the structural basis of receptor-binding specificity for H1 HAs in human and avian viruses and provide a structural explanation for the preference for α2-6 siaylated glycan receptors for the 2009 pandemic swine flu virus.
Prolonged dormancy in the geophyte Allium amplectens on Vancouver Island
Authors: Hawryzki Allan R. , Allen Geraldine A. , Antos Joseph A. 
Published: November 2011

Prolonged dormancy occurs when a plant fails to appear above ground during the growing season. Although it may be an important life history trait of many geophytes, studies focusing on prolonged dormancy are infrequent and are concentrated on the Orchidaceae even though the phenomenon occurs in many taxonomic groups. We tracked individual plants of Allium amplectens (Amaryllidaceae) in permanent plots on Vancouver Island, which allowed us to determine rates of prolonged dormancy during a 4-year period. Dormancy rates per year averaged 38% and differed substantially among years. Over 70% of plants had a dormant period during the study. Dormancy periods of 2 years were almost as frequent as 1-year periods, and 8% of plants were dormant for 3 years. Plant density, which included small plants that we could not track in the plots, varied much more among years than did dormancy of tracked plants, suggesting that small plants may be especially prone to dormancy. High rates of prolonged dormancy and frequent multiyear dormancy indicate that this is an important life history feature of A. amplectens. We suggest that prolonged dormancy contributes to the ability of this species, and probably other species, to persist in dry habitats with fluctuating resources.
Encapsulation and immobilization of a mycophagous nematode by two Sphaerobolus species
Authors: Tanney Joey B. , Hutchison Leonard J. 
Published: November 2011

A defence mechanism against nematodes produced by Sphaerobolus stellatus Tode and Sphaerobolus iowensis L.B. Walker is described for the first time. Within 24 h of introduction, some individuals of a mycophagous nematode ( Aphelenchoides sp.) exhibited lethargic behaviour marked by the cessation of feeding and a reduction in movement. The anterior portion of the affected nematodes appeared swollen and was encapsulated with an amorphous material of unknown composition. The nematode stylet could not penetrate this encapsulating matrix, preventing further hyphal grazing and subsequently leading to death of the nematodes, possibly due to starvation. Immobilized nematodes were not consumed by the fungi. It is hypothesized that when the feeding nematodes pierce a specialized structure found in Sphaerobolus cultures, referred to as a gloeocystidium, the contents are released and solidify on the nematode heads. It is proposed that the gloeocystidia function to protect the hyphal system and act as a general antifeedant mechanism against mycophagous nematodes and possibly other fungus-feeding microfauna.
The combination of four different clinical decision rules and an age-adjusted D-dimer cut-off increases the number of patients in whom acute pulmonary embolism can safely be excluded
Authors: Mos Inge , Douma Renée , Erkens Petra , Durian Marc , Nizet Tessa , van Houten Anja , Hofstee Herman , ten Cate Hugo , Ullmann Eric , Büller Harry , Huisman Menno , Kamphuisen P. W. , van Es Josien 
Published: November 2011

SummaryFour clinical decision rules (CDRs) (Wells score, Revised Geneva Score (RGS), simplified Wells score and simplified RGS) safely exclude pulmonary embolism (PE), when combined with a normal D-dimer test. Recently, an age-adjusted cut-off of the D-dimer (patient’s age x 10 μg/l) safely increased the number of patients above 50 years in whom PE could safely be excluded. We validated the age-adjusted D-dimer test and assessed its performance in combination with the four CDRs in patients with suspected PE. A total of 414 consecutive patients with suspected PE who were older than 50 years were included. The proportion of patients in whom PE could be excluded with an ‘unlikely’ clinical probability combined with a normal age-adjusted D-dimer test was calculated and compared with the proportion using the conventional D-dimer cut-off. We assessed venous thromboembolism (VTE) failure rates during three months follow-up. In patients above 50 years, a normal age-adjusted D-dimer level in combination with an ‘unlikely’ CDR substantially increased the number of patients in whom PE could be safely excluded: from 13–14% to 19–22% in all CDRs similarly. In patients over 70 years, the number of exclusions was nearly four-fold higher, and the original Wells score excluded most patients, with an increase from 6% to 21% combined with the conventional and age-adjusted D-dimer cut-off, respectively. The number of VTE failures was also comparable in all CDRs. In conclusion, irrespective of which CDR is used, the age-adjusted D-dimer substantially increases the number of patients above 50 years in whom PE can be safely excluded.
Music exposure and hearing health education: A review of knowledge, attitude, and behaviour in adolescents and young adults
Authors: Zhao Fei , French David , Manchaiah Vinaya KC , Liang Maojin , Price Sharon M 
Published: November 2011

Introduction: Adolescents and young adults have been shown to be the age group most at risk of music-induced hearing loss (MIHL), which is already evident and increasing among this group. Objective: The purpose of this review is to provide further insight into the effectiveness of education programmes on attitude and behaviour towards loud music exposure in adolescents and young adults, and to suggest positive and influential ways of delivering hearing health education. Methods: Literature searches were conducted using various databases, including PubMed, Google Scholar and Cumulative Index to Nursing and Allied Health Literature (CINAHL). Authors went through the abstracts of these articles to identify those which were potentially relevant; subsequently the full articles were retrieved. Results: This review highlights the dangers of significant exposure to music on hearing mechanics in adolescents and young adults, and shows that this danger continues to increase with modern music culture. Because the consequences are not immediate, it is difficult for the young to perceive the seriousness of a problem that may not present itself for many years. Conventional education may go a little way in helping to raise awareness but a raised awareness of consequences does not, in itself, change behaviour. There is a significant gap in literature regarding effective methods of education that will inspire attitude change, and have a bearing on actions. Conclusion: This review has concluded that there is a lack of understanding of how to best influence and educate adolescents and young adults in a way that will motivate and encourage a change in listening habits. It is of vital importance that these groups are made aware of the immediate and future dangers, and how changes in listening behaviour do not necessarily lower their enjoyment.
Exploring the everyday world of hate victimization through community mediation
Authors: Walters Mark Austin , Hoyle Carolyn 
Published: November 2011

For some time, hate crimes were conceptualized as acts of hatred committed by strangers – typically as violent attacks against people perceived to be different from the attacker. Considering hate as an aggravating feature resulted in increasingly punitive and exclusionary criminal justice and sentencing legislation. Left out of this picture were the messier, sometimes intractable disputes between people known to one another – neighbours, colleagues or other acquaintances – conflicts sometimes only partly motivated by prejudice. This article brings these under-researched conflicts to centre stage. Drawing on a study of community mediation in cases of ‘hate conflicts’, we explore the effects of prolonged processes of hate-motivated abuse on those involved – the main parties and often the wider community. We provide evidence of two distinct ‘types’ of hate crime cases. The first looks at the persistent targeted abuse of vulnerable victims, while the second is characterized by multi-layered conflicts involving numerous disputants. In these latter cases, we argue, it is not always helpful, and sometimes not even possible, to label one party the ‘perpetrator’ and one the ‘victim’. Indeed, we show that at times during long-term disputes, these roles are reversed and at other times they become meaningless. In both ‘types’ of hate conflict we explore the potential of community mediation to repair broken relationships and the harms caused by acts of hatred.
Alveolar bone regeneration using poly-(lactic acid-co-glycolic acid-co-ε-caprolactone) porous membrane with collagen sponge containing basic fibroblast growth factor: An experimental study in the dog
Authors: Matsumoto Goichi , Hoshino Jyunichi , Kinoshita Yasuhiko , Sugita Yoshihiko , Kubo Katsutoshi , Maeda Hatsuhiko , Ikada Yoshito , Kinoshita Yukihiko 
Published: November 2011

The aim of this study was to evaluate the effects of combining porous poly-lactic acid-co-glycolic acid-co-ε-caprolactone (PLGC) as a barrier membrane and collagen sponge containing basic fibroblast growth factor (bFGF) to promote bone regeneration in the canine mandible. In six beagle dogs, two lateral bone defects per side were created in the mandible. The lateral bone defects on the left side were treated with a PLGC membrane plus a collagen sponge containing bFGF. In half of these, the collagen sponge contained 50 µg of bFGF. In the other half, it contained 250 µg of bFGF. As a control, we treated the right-side bone defects in each animal with the same PLGC membrane but with a collagen sponge containing phosphate buffered saline. Computed tomography (CT) images were recorded at 3 and 6 months post-op to evaluate regeneration of the bone defects. After a healing period of 6 months, whole mandibles were removed for micro-CT and histological analyses. The post-op CT images showed that more bone had formed at all experimental sites than at control sites. At 3 months post-op, the volume of bone at defect sites covered with PLGC membrane plus 250 µg of bFGF was significantly greater than it was at defect sites covered with PLGC membrane plus 50 µg of bFGF. At 6 months post-op, however, this difference was smaller and not statistically significant. Micro-CT measurement showed that the volume of new bone regenerated at bone-defect sites, covered with PLGC membrane plus bFGF, was significantly greater than that of control sites. However, the presence or absence of bFGF in the collagen sponge did not significantly affect the bone density of new bone. These results suggest that the macroporous bioresorbable PLGC membrane plus collagen sponge containing bFGF effectively facilitates healing in GBR procedures.
NF-Y is necessary for hematopoietic stem cell proliferation and survival
Authors: Bungartz Gerd , Land Hannah , Scadden David T. , Emerson Stephen G. 
Published: November 2011

Abstract
HSC function depends on the tight control of proliferation and the balance between self-renewal and differentiation. Here, we report that the trimeric transcription factor NF-Y is critical for the survival of cycling, but not quiescent HSCs. With the use of a conditional knockout mouse model, we demonstrate that NF-Ya deletion creates an accumulation of HSCs in G2/M and prompts apoptosis, causing hematopoietic failure and death of the animal. These defects are accompanied by the dysregulation of multiple genes that influence cell cycle control (cyclin b1 and p21), apoptosis (Bcl-2), and self-renewal (HoxB4, Notch1, Bmi-1) and are independent of p53. Our results identify NF-Y as a pivotal upstream participant in a regu-latory network necessary for the pre-servation of cycling HSCs.