bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effect of Dung and Dispersal on Postdispersal Seed Predation of Attalea phalerata (Arecaceae) by Bruchid Beetles1
Authors: Rios Rodrigo S. , Pacheco Luis F. 
Published: August 2006

ABSTRACTLow postdispersal mortality of palm seeds in tapir dung is hypothesized to result from the mechanical barrier provided by dung against bruchid infestation and/or from the distance to adult palms at which seeds are dispersed. We tested these hypotheses by distributing endocarps of Attalea phalerata Mart. ex Spreng. in experimental dung piles in Beni, Bolivia. Predation rates were significantly lower for seeds covered by dung than for exposed or partially covered seeds, but did not differ between seeds placed below and 50 m away from palms. Thus, dung, not short‐distance dispersal, protects seeds against bruchid beetles, and may ultimately promote survival of palm seeds.
SDSS J2125−0813: the evidence for the origination of optical Fe ii emission lines from an accretion disc near a central black hole
Authors: Zhang Xue-Guang , Dultzin-Hacyan D. , Wang Ting-Gui 
Published: August 2006

Abstract
We report on the radio-quiet quasar SDSS J2125−0813 which obviously emits optical Fe ii emission lines and double-peaked broad Balmer emission lines. Using the accretion disc model for double-peaked, broad, low-ionization emission lines, we reproduce the composite line spectra at the optical band between 4100 and 5600 Å. Broad Fe ii emission lines can be fitted simultaneously with the broad Hβ and Mg i lines, such that all broad lines have an elliptical disc profile with the same disc parameters. This result indicates that the optical Fe ii emission lines originate from the accretion disc near the central black hole which produces the double-peaked broad Balmer emission lines. Furthermore, we find that the object has a dimensionless accretion rate , which is much larger than the accretion rate for the advection-dominated accretion flow (ADAF) mode, and that the energy budget of the accretion disc is enough to power the double-peaked broad Balmer emission lines.
Blood and AIDS: an international political history
Authors: Schmidt P. 
Published: August 2006

The politics of health was never tested more in the Western democracies than when the acquired immunodeficiency syndrome (AIDS) surfaced at the beginning of the 1980s. In those countries it became the most important medical event of the last half of the 20th century. The significance of AIDS was not only as a disease that took away lives, but also as a disease that had great effects on social and political life. The involvement of the blood community in their national problems when AIDS appeared in the industrialized countries persists to this day in unresolved questions in other parts of the world. An analysis is presented on those blood politics in the USA, France, Japan and Canada. Those events had different roots and effects depending on the various national blood programmes and policies, on donor and patient populations and, not incidentally, on decisions made and secrets kept. The events that related blood to AIDS in the industrialized nations in the 1980s and 1990s are still in progress in other parts of the world. The mistakes made in the West and the resultant effects on social and economic progress offer a modern history lesson for the rest of the world.
Cross Talk between PML and p53 during Poliovirus Infection: Implications for Antiviral Defense
Authors: Pampin Mathieu , Simonin Yannick , Blondel Bruno , Percherancier Yann , Chelbi-Alix Mounira K. 
Published: August 2006

ABSTRACT
PML nuclear bodies (NBs) are dynamic intranuclear structures harboring numerous transiently or permanently localized proteins. PML, the NBs' organizer, is directly induced by interferon, and its expression is critical for antiviral host defense. We describe herein the molecular events following poliovirus infection that lead to PML-dependent p53 activation and protection against virus infection. Poliovirus infection induces PML phosphorylation through the extracellular signal-regulated kinase pathway, increases PML SUMOylation, and induces its transfer from the nucleoplasm to the nuclear matrix. These events result in the recruitment of p53 to PML NBs, p53 phosphorylation on Ser15, and activation of p53 target genes leading to the induction of apoptosis. Moreover, the knock-down of p53 by small interfering RNA results in higher poliovirus replication, suggesting that p53 participates in antiviral defense. This effect, which requires the presence of PML, is transient since poliovirus targets p53 by inducing its degradation in a proteasome- and MDM2-dependent manner. Our results provide evidence of how poliovirus counteracts p53 antiviral activity by regulating PML and NBs, thus leading to p53 degradation.
The E6 Protein of the Cutaneous Human Papillomavirus Type 8 Can Stimulate the Viral Early and Late Promoters by Distinct Mechanisms
Authors: Müller-Schiffmann Andreas , Beckmann Julia , Steger Gertrud 
Published: August 2006

ABSTRACT
The expression of the proteins encoded by human papillomaviruses (HPVs) is tightly linked to the differentiation program of the infected keratinocytes. The late promoter, expressing the structural proteins, becomes activated in the differentiated keratinocytes, while the early promoter is also active in the basal layers. We have shown previously that the viral transcriptional regulator E2 and the cellular coactivator p300 cooperate in activation of gene expression of HPV8, which infects the skin and is associated with epidermodysplasia verruciformis. Here we demonstrate that this activation is further stimulated after overexpression of the E6 oncoprotein of HPV8 (8E6). RNase protection experiments revealed that 8E6 efficiently cooperates with 8E2 and p300 in activation of the late promoter. In addition, the early promoter, which did not respond to 8E2 and/or p300, was stimulated more than fourfold by 8E6. Our data suggest that both promoters are activated via distinct mechanisms, since the activation of the early promoter was achieved by the N-terminal moiety of 8E6; in contrast, its C-terminal half was sufficient for late promoter activation. This was markedly reduced by the deletion of amino acids 132 to 136 of 8E6, which also abolished the binding to p300, indicating that a direct interaction between 8E6 and p300 is involved. Moreover, a 45-amino-acid segment within the C/H3 region of p300 is required for 8E6 to stimulate the coactivator function of p300. Our results demonstrate for the first time that an E6 oncoprotein of HPV directly contributes to the regulation of HPV gene expression.
Mutational Pathways, Resistance Profile, and Side Effects of Cyanovirin Relative to Human Immunodeficiency Virus Type 1 Strains with N-Glycan Deletions in Their gp120 Envelopes
Authors: Balzarini Jan , Van Laethem Kristel , Peumans Willy J. , Van Damme Els J. M. , Bolmstedt Anders , Gago Federico , Schols Dominique 
Published: August 2006

ABSTRACT

Limited data are available on the genotypic and phenotypic resistance profile of the α-(1-2)mannose oligomer-specific prokaryotic lectin cyanovirin (CV-N). Therefore, a more systematic investigation was carried out to obtain a better view of the interaction between CV-N and human immunodeficiency virus type 1 (HIV-1) gp120. When HIV-1-infected CEM cell cultures were exposed to CV-N in a dose-escalating manner, a total of eight different amino acid mutations exclusively located at N-glycosylation sites in the envelope surface gp120 were observed. Six of the eight mutations resulted in the deletion of high-mannose type N-glycans (i.e., at amino acid positions 230, 332, 339, 386, 392, and 448). Two mutations (i.e., at position 136 and 160) deleted a complex type N-glycan in the variable V1/V2 domain of gp120. The level of phenotypic resistance of the mutated virus strains against CV-N generally correlated with the number of glycan deletions in gp120, although deletion of the glycans at N-230, N-392, and N-448 generally afforded a more pronounced CV-N resistance than other N-glycan deletions. However, the extent of the decrease of antiviral activity of CV-N against the mutated virus strains was markedly less pronounced than observed for α(1-3)- and α(1-6)-mannose-specific plant lectins
Hippeastrum
hybrid agglutinin (HHA) and
Galanthus nivalis
agglutinin (GNA), which points to the existence of a higher genetic barrier for CV-N. This is in agreement with a more consistent suppression of a wider variety of HIV-1 clades by CV-N than by HHA and GNA. Whereas the antiviral and in vitro antiproliferative activity of CV-N can be efficiently reversed by mannan, the pronounced mitogenic activity of CV-N on peripheral blood mononuclear cells was unaffected by mannan, indicating that some of the observed side effects of CV-N are unrelated to its carbohydrate specificity/activity.
Rational Design of Genetically Stable, Live-Attenuated Poliovirus Vaccines of All Three Serotypes: Relevance to Poliomyelitis Eradication
Authors: Macadam Andrew J. , Ferguson Geraldine , Stone David M. , Meredith Janet , Knowlson Sarah , Auda Ghazi , Almond Jeffrey W. , Minor Philip D. 
Published: August 2006

ABSTRACT
The global eradication of poliomyelitis caused by wild-type virus is likely to be completed within the next few years, despite immense logistic and political difficulties, and may ultimately be followed by the cessation of vaccination. However, the existing live-attenuated vaccines have the potential to revert to virulence, causing occasional disease, and viruses can be shed by immunocompromised individuals for prolonged periods of time. Moreover, several outbreaks of poliomyelitis have been shown to be caused by viruses derived from the Sabin vaccine strains. The appearance of such strains depends on the prevailing circumstances but poses a severe obstacle to strategies for stopping vaccination. Vaccine strains that are incapable of reversion at a measurable rate would provide a possible solution. Here, we describe the constructions of strains of type 3 poliovirus that are stabilized by the introduction of four mutations in the 5′ noncoding region compared to the present vaccine. The strains are genetically and phenotypically stable under conditions where the present vaccine loses the attenuating mutation in the 5′ noncoding region completely. Type 1 and type 2 strains in which the entire 5′ noncoding regions of Sabin 1 and Sabin 2 were replaced exactly with that of one of the type 3 strains were also constructed. The genetic stability of 5′ noncoding regions of these viruses matched that of the type 3 strains, but significant phenotypic reversion occurred, illustrating the potential limitations of a rational approach to the genetic stabilization of live RNA virus vaccines.
Abrogation of Viral Interleukin-6 (vIL-6)-Induced Signaling by Intracellular Retention and Neutralization of vIL-6 with an Anti-vIL-6 Single-Chain Antibody Selected by Phage Display
Authors: Kovaleva Marina , Bussmeyer Ingo , Rabe Björn , Grötzinger Joachim , Sudarman Enge , Eichler Jutta , Conrad Udo , Rose-John Stefan , Scheller Jürgen 
Published: August 2006

ABSTRACTHuman herpesvirus 8 (HHV-8) encodes several putative oncogenes, which are homologues to cellular host genes known to function in cell cycle regulation, control of apoptosis, and cytokine signaling. Viral interleukin (vIL-6) is believed to play an important role in the pathogenesis of Kaposi's sarcoma as well as primary effusion lymphoma and multicentric Castleman's disease. Therefore, vIL-6 is a promising target for novel therapies directed against HHV-8-associated diseases. By phage display screening of human synthetic antibody libraries, we have selected a specific recombinant antibody, called monoclonal anti-vIL-6 (MAV), binding to vIL-6. The epitope recognized by MAV was localized on the top of the D helix of the vIL-6 protein, which is a part of receptor binding site III. Consequently, MAV specifically inhibits vIL-6-mediated growth of the primary effusion lymphoma-derived cell line BCBL-1 and blocks STAT3 phosphorylation in the human hepatoma cell line HepG2. Since it was previously found that vIL-6 can also induce signals from within the cell, presumably within the endoplasmic reticulum, we fused the recombinant antibody MAV with the endoplasmic retention sequence KDEL (MAV-KDEL). As a result, COS-7 cells expressing MAV-KDEL and synthesizing vIL-6 ceased to secrete the cytokine. Moreover, we observed that vIL-6 that was bound to MAV-KDEL and retained in the endoplasmic reticulum did not induce STAT3 phosphorylation in HepG2 cells. We conclude that the activity of the intracellularly retained vIL-6 protein is neutralized by MAV-KDEL. Our results might represent a novel therapeutic strategy to neutralize virally encoded growth factors or oncogenes.
All Three Variable Regions of the TRIM5α B30.2 Domain Can Contribute to the Specificity of Retrovirus Restriction
Authors: Ohkura Sadayuki , Yap Melvyn W. , Sheldon Tom , Stoye Jonathan P. 
Published: August 2006

ABSTRACTRecent studies have revealed the contribution of TRIM5α to retrovirus restriction in cells from a variety of primate species. TRIM5α consists of a tripartite motif (the RBCC domain) followed by a B30.2 domain. The B30.2 domain is thought to be involved in determination of restriction specificity and contains three variable regions. To investigate the relationship between the phylogeny of primate TRIM5α and retrovirus restriction specificity, a series of chimeric TRIM5α consisting of the human RBCC domain followed by the B30.2 domain from various primates was constructed. These constructs showed restriction profiles largely consistent with the origin of the B30.2 domain. Restriction specificity was further investigated with a variety of TRIM5αs containing mixed or mutated B30.2 domains. This study revealed the importance of all three variable regions for determining restriction specificity. Based on the molecular structures of other PRYSPRY domains solved recently, a model for the molecular structure of the B30.2 domain of TRIM5α was developed. The model revealed that the variable regions of the B30.2 domain are present as loops located on one side of the B30.2 core structure. It is hypothesized that these three loops form a binding surface for virus and that evolutionary changes in any one of the loops can alter restriction specificity.
Murine Polyomavirus Requires the Endoplasmic Reticulum Protein Derlin-2 To Initiate Infection
Authors: Lilley Brendan N. , Gilbert Joanna M. , Ploegh Hidde L. , Benjamin Thomas L. 
Published: August 2006

ABSTRACT
The pathways by which viruses enter cells are diverse, but in all cases, infection necessitates the transfer of the viral genome across a cellular membrane. Polyomavirus (Py) particles, after binding to glycolipid and glycoprotein receptors at the cell surface, are delivered to the lumen of the endoplasmic reticulum (ER). The nature and extent of virus disassembly in the ER, how the viral genome is transported to the cytosol and subsequently to the nucleus, and whether any cellular proteins are involved are not known. Here, we identify an ER-resident protein, Derlin-2, a factor implicated in the removal of misfolded proteins from the ER for cytosolic degradation, as a component of the machinery required for mouse Py to establish an infection. Inhibition of Derlin-2 function by expression of either a dominant-negative form of Derlin-2 or a short hairpin RNA that reduces Derlin-2 levels blocks Py infection by 50 to 75%. The block imposed by Derlin-2 inhibition occurs after the virus reaches the ER and can be bypassed by the introduction of Py DNA into the cytosol. These findings suggest a mode of Py entry that involves cytosolic access via the quality control machinery in the ER.
Endoplasmic Reticulum Stress and Neurodegeneration in Rats Neonatally Infected with Borna Disease Virus
Authors: Williams B. L. , Lipkin W. I. 
Published: August 2006

ABSTRACTBorna disease virus infection of neonatal rats results in a characteristic behavioral syndrome and apoptosis of subsets of neurons in the hippocampus and cerebellum (neonatal Borna disease [NBD]). The cellular mechanisms leading to neurodevelopmental damage in NBD have not been fully elucidated. Insights into this model may have general implications for understanding the pathogenesis of virus-associated neurodevelopmental damage. Here we report the presence of endoplasmic reticulum (ER) stress markers and activation of the unfolded protein response in the NBD hippocampus and cerebellum. Specific findings included enhanced PERK-mediated phosphorylation of eif2α and concomitant regulation of ATF4 translation; IRE1-mediated splicing of XBP1 mRNA; and cleavage of the ATF6 protein in NBD rat brains. We found evidence for regional and cell type-specific divergence in the expression of ER stress-induced proapoptotic and quality control signals. Our results demonstrate that ER stress induction in death-susceptible Purkinje neurons in NBD is associated with the expression of the proapoptotic molecule CHOP in the absence of compensatory expression of the ER quality control molecules Bip and protein disulfide isomerase. In contrast, ER stress in death-resistant astrocytes is associated with complementary expression of CHOP and ER quality control signals. These results implicate an imbalance between ER stress-mediated apoptosis and survival signaling as a critical determinant of neural cell fate in NBD.
Antibody Responses Elicited in Macaques Immunized with Human Immunodeficiency Virus Type 1 (HIV-1) SF162-Derived gp140 Envelope Immunogens: Comparison with Those Elicited during Homologous Simian/Human Immunodeficiency Virus SHIVSF162P4and Heterologous HIV-1 Infection
Authors: Derby Nina R. , Kraft Zane , Kan Elaine , Crooks Emma T. , Barnett Susan W. , Srivastava Indresh K. , Binley James M. , Stamatatos Leonidas 
Published: August 2006

ABSTRACTThe antibody responses elicited in rhesus macaques immunized with soluble human immunodeficiency virus (HIV) Env gp140 proteins derived from the R5-tropic HIV-1 SF162 virus were analyzed and compared to the broadly reactive neutralizing antibody responses elicited during chronic infection of a macaque with a simian/human immunodeficiency virus (SHIV) expressing the HIV-1 SF162 Env, SHIVSF162P4, and humans infected with heterologous HIV-1 isolates. Four gp140 immunogens were evaluated: SF162gp140, ΔV2gp140 (lacking the crown of the V2 loop), ΔV3gp140 (lacking the crown of the V3 loop), and ΔV2ΔV3gp140 (lacking both the V2 and V3 loop crowns). SF162gp140 and ΔV2gp140 have been previously evaluated by our group in a pilot study, but here, a more comprehensive analysis of their immunogenic properties was performed. All four gp140 immunogens elicited stronger anti-gp120 than anti-gp41 antibodies and potent homologous neutralizing antibodies (NAbs) that primarily targeted the first hypervariable region (V1 loop) of gp120, although SF162gp140 also elicited anti-V3 NAbs. Heterologous NAbs were elicited by SF162gp140 and ΔV2gp140 but were weak in potency and narrow in specificity. No heterologous NAbs were elicited by ΔV3gp140 or ΔV2ΔV3gp140. In contrast, the SHIVSF162P4-infected macaque and HIV-infected humans generated similar titers of anti-gp120 and anti-gp41 antibodies and NAbs of significant breadth against primary HIV-1 isolates, which did not target the V1 loop. The difference in V1 loop immunogenicity between soluble gp140 and virion-associated gp160 Env proteins derived from SF162 may be the basis for the observed difference in the breadth of neutralization in sera from the immunized and infected animals studied here.
Effect of lactoferrin on EnteroaggregativeE. coli(EAEC)This paper is one of a selection of papers published in this Special Issue, entitled 7th International Conference on Lactoferrin: Structure, Function, and Applications, and has undergone the Journal’s usual peer review process.
Authors: Ochoa Theresa J. , Brown Eric L. , Guion Chase E. , Chen Jane Z. , McMahon Robert J. , Cleary Thomas G. 
Published: August 2006

We previously demonstrated that lactoferrin inhibits adherence of enteropathogenic Escherichia coli to HEp-2 cells and decreases invasiveness of Shigella flexneri in HeLa cells by disruption of the type III secretory system (TTSS) of both enteropathogens. To determine whether these effects were specific to the TTSS, we assessed the activity of bovine lactoferrin on enteroaggregative E. coli (EAEC), enteropathogens whose virulence is not TTSS dependent. Bovine lactoferrin at a concentration of 1.0 and 0.1 mg/mL inhibited EAEC growth. Saturation with iron reversed the bacteriostatic effect. Lactoferrin under nonbacteriostatic conditions decreased EAEC adherence to HEp-2 cells as evaluated by microscopy and CFUs; this effect was not iron dependent. Lactoferrin inhibited EAEC biofilm formation and increased autoagglutination. Lactoferrin blocks EAEC adherence by inducing release and degradation of aggregative adherence fimbria, a key element of EAEC pathogenesis. We hypothesized that lactoferrin binding to lipid A of lipopolysaccharide disrupts the virulence proteins anchored to the bacterial outermembrane. These data suggest that the effect of lactoferrin on surface proteins is not restricted to organisms having a TTSS.
Influences of orally administered lactoferrin on IFN-γ and IL-10 production by intestinal intraepithelial lymphocytes and mesenteric lymph-node cellsThis paper is one of a selection of papers published in this Special Issue, entitled 7th International Conference on Lactoferrin: Structure, Function, and Applications, and has undergone the Journal's usual peer review process.
Authors: Takakura Natsuko , Wakabayashi Hiroyuki , Yamauchi Koji , Takase Mitsunori 
Published: August 2006

Intestinal mucosal immunity plays an important role in mucosal and systemic immune responses. We investigated the influences of orally administered bovine lactoferrin (LF) on cytokine production by intestinal intraepithelial lymphocytes (IEL) and mesenteric lymph-node (MLN) cells, especially T cells. Bovine LF or bovine serum albumin (control) was administered to mice once daily for 3 d. After 24 h from the last administration, IEL of the jejunum and ileum and MLN cells were isolated. These cells were cultured with and without the anti-T-cell-receptor antibody, and then the culture supernatants were assayed for cytokines with ELISA. Oral LF did not affect the ratio of T-cell subpopulations in IEL and MLN; however, LF enhanced both interferon (IFN)-γ and interleukin (IL)-10 production by unstimulated IEL and by IEL stimulated with the αβ T-cell receptor but not with the γδ T-cell receptor. LF also enhanced both IFN-γ and IL-10 production by stimulated and unstimulated MLN cells. The production level of IFN-γ by MLN cells was correlated with that of IL-10. These results suggest that oral LF enhances the production of both Th1-type and Th2/Tr-type cytokines in the small intestine of healthy animals.