bluuebunny/crossref_metadata_2025_split huggingface dataset:
Species Recognition and Clinical Relevance of the Zygomycetous GenusLichtheimia(syn.Absidia Pro Parte,Mycocladus)
Authors: Alastruey-Izquierdo Ana , Hoffmann Kerstin , de Hoog G. Sybren , Rodriguez-Tudela Juan Luis , Voigt Kerstin , Bibashi Evangelia , Walther Grit 
Published: April 2010

ABSTRACTThe zygomycete genusLichtheimia(syn.Absidia pro parte,Mycocladus) consists of saprotrophic fungi inhabiting soil or dead plant material.Lichtheimia corymbifera(syn.Absidia corymbifera,Mycocladus corymbifer) andLichtheimia ramosa(syn.Absidia ramosa,Mycocladus ramosus) may cause fulminant infections in patients with impaired immunity. The present study investigated the species boundaries inLichtheimiausing genealogical concordance phylogenetic species recognition (by comparison of the genealogies of the internal transcribed spacer [ITS] sequence, the D1/D2 region of the large subunit [LSU], and actin), biological species recognition by mating tests, as well as morphological and physiological characteristics. The three molecular markers used were selected by evaluating the polymorphisms and paralogies of several loci, including those for β-tubulin, translation elongation factor 1α, the two largest subunits of the RNA polymerase II (RPB1 and RPB2), the mitochondrial cytochromecoxidase subunit I (COI), and the mitochondrial small-subunit (mtSSU) rDNA, among four strains belonging to different putative species. Comparing the genealogies of the ITS, LSU, and actin genes, we recognized seven phylogenetic species. However, mating tests did not show intrinsic reproductive barriers for two pairs of the phylogenetic species. Therefore, we regard five species inLichtheimato be confirmed:Lichtheimia corymbifera,L. ornatacomb. nov.,L. ramosa,L. hyalospora, andL. sphaerocystissp. nov. Only the first three species seem to have clinical relevance.Lichtheimia blakesleeanais reduced to a synonym ofLichtheimia hyalospora. We provide a detailed description ofLichtheimia sphaerocystissp. nov. and a key for the identification of all accepted species identified in the present study on the basis of their morphological traits and growth at different temperatures.
Comparison of the Luminex Respiratory Virus Panel Fast Assay with In-House Real-Time PCR for Respiratory Viral Infection Diagnosis
Authors: Gadsby Naomi J. , Hardie Alison , Claas Eric C. J. , Templeton Kate E. 
Published: April 2010

ABSTRACT
The Luminex xTAG Respiratory Virus Panel (RVP) assay has been shown to offer improved diagnostic sensitivity over traditional viral culture methods and to have a sensitivity comparable to those of individual real-time nucleic acid tests for respiratory viruses. The objective of this retrospective study was to test a new, streamlined version of this assay, the RVP Fast assay, which requires considerably less run time and operator involvement. The study compared the performance of the RVP Fast assay with those of viral culture, a direct fluorescent assay (DFA), and a panel of single and multiplex real-time PCRs in the testing of 286 respiratory specimens submitted to the Edinburgh Specialist Virology Centre for routine diagnosis of viral infection between December 2007 and February 2009. At least one respiratory viral infection was detected in 13.6% of specimens by culture and DFA combined, in 49.7% by real-time PCR, and in 46.2% by the RVP Fast assay. The sensitivity and specificity of the RVP Fast assay compared to the results of real-time PCR as the gold standard were 78.8% and 99.6%, respectively. Real-time PCR-positive specimens missed by the RVP Fast assay generally had low viral loads or were positive for adenovirus. Additionally, a small number of specimens were positive by the RVP Fast assay but were not detected by real-time PCR. For some viral targets, only a small number of positive results were found in our sample set using either method; therefore, the sensitivity of detection of the RVP Fast assay for individual targets could be investigated further with a greater number of virus-positive specimens.
Identification of a Domain of the Baculovirus
Autographa californica
Multiple Nucleopolyhedrovirus Single-Strand DNA-Binding Protein LEF-3 Essential for Viral DNA Replication
Authors: Yu Mei , Carstens Eric B. 
Published: April 2010

ABSTRACT

Autographa californica
multiple nucleopolyhedrovirus (AcMNPV)
lef-3
is one of nine genes required for viral DNA replication in transient assays. LEF-3 is predicted to contain several domains related to its functions, including nuclear localization, single-strand DNA binding, oligomerization, interaction with P143 helicase, and interaction with a viral alkaline nuclease. To investigate the essential nature of LEF-3 and the roles it may play during baculovirus DNA replication, a
lef-3
null bacmid (bKO-lef3) was constructed in
Escherichia coli
and characterized in Sf21 cells. The results showed that AcMNPV
lef-3
is essential for DNA replication, budded virus production, and late gene expression
in vivo
. Cells transfected with the
lef-3
knockout bacmid produced low levels of early proteins (P143, DNA polymerase, and early GP64) and no late proteins (P47, VP39, or late GP64). To investigate the functional role of domains within the LEF-3 open reading frame in the presence of the whole viral genome, plasmids expressing various LEF-3 truncations were transfected into Sf21 cells together with bKO-lef3 DNA. The results showed that expression of AcMNPV LEF-3 amino acids 1 to 125 was sufficient to stimulate viral DNA replication and to support late gene expression. Expression of
Choristoneura fumiferana
MNPV
lef-3
did not rescue any LEF-3 functions. The construction of a LEF-3 amino acid 1 to 125 rescue bacmid revealed that this region of LEF-3, when expressed in the presence of the rest of the viral genome, stimulated viral DNA replication and late and very late protein expression, as well as budded virus production.
Combinatorial Latency Reactivation for HIV-1 Subtypes and Variants
Authors: Burnett John C. , Lim Kwang-il , Calafi Arash , Rossi John J. , Schaffer David V. , Arkin Adam P. 
Published: April 2010

ABSTRACTThe eradication of HIV-1 will likely require novel clinical approaches to purge the reservoir of latently infected cells from a patient. We hypothesize that this therapy should target a wide range of latent integration sites, act effectively against viral variants that have acquired mutations in their promoter regions, and function across multiple HIV-1 subtypes. By using primary CD4+and Jurkat cell-basedin vitroHIV-1 latency models, we observe that single-agent latency reactivation therapy is ineffective against most HIV-1 subtypes. However, we demonstrate that the combination of two clinically promising drugs—namely, prostratin and suberoylanilide hydroxamic acid (SAHA)—overcomes the limitations of single-agent approaches and can act synergistically for many HIV-1 subtypes, including A, B, C, D, and F. Finally, by identifying the proviral integration position of latent Jurkat cell clones, we demonstrate that this drug combination does not significantly enhance the expression of endogenous genes nearest to the proviral integration site, indicating that its effects may be selective.
The Rab11 Pathway Is Required for Influenza A Virus Budding and Filament Formation
Authors: Bruce Emily A. , Digard Paul , Stuart Amanda D. 
Published: April 2010

ABSTRACT
Influenza A virus buds through the apical plasma membrane, forming enveloped virus particles that can take the shape of pleomorphic spheres or vastly elongated filaments. For either type of virion, the factors responsible for separation of viral and cell membranes are not known. We find that cellular Rab11 (a small GTP-binding protein involved in endocytic recycling) and Rab11-family interacting protein 3 ([FIP3] which plays a role in membrane trafficking and regulation of actin dynamics) are both required to support the formation of filamentous virions, while Rab11 is additionally involved in the final budding step of spherical particles. Cells transfected with Rab11 GTP-cycling mutants or depleted of Rab11 or FIP3 content by small interfering RNA treatment lost the ability to form virus filaments. Depletion of Rab11 resulted in up to a 100-fold decrease in titer of spherical virus released from cells. Scanning electron microscopy of Rab11-depleted cells showed high densities of virus particles apparently stalled in the process of budding. Transmission electron microscopy of thin sections confirmed that Rab11 depletion resulted in significant numbers of abnormally formed virus particles that had failed to pinch off from the plasma membrane. Based on these findings, we see a clear role for a Rab11-mediated pathway in influenza virus morphogenesis and budding.
Evidence for Translational Regulation by the Herpes Simplex Virus Virion Host Shutoff Protein
Authors: Saffran Holly A. , Read G. Sullivan , Smiley James R. 
Published: April 2010

ABSTRACT

The herpes simplex virus (HSV) virion host shutoff protein (vhs) encoded by gene UL41 is an mRNA-specific RNase that triggers accelerated degradation of host and viral mRNAs in infected cells. We report here that vhs is also able to modulate reporter gene expression without greatly altering the levels of the target mRNA in transient-transfection assays conducted in HeLa cells. We monitored the effects of vhs on a panel of bicistronic reporter constructs bearing a variety of internal ribosome entry sites (IRESs) located between two test cistrons. As expected, vhs inhibited the expression of the 5′ cistrons of all of these constructs; however, the response of the 3′ cistron varied with the IRES: expression driven from the wild-type EMCV IRES was strongly suppressed, while expression controlled by a mutant EMCV IRES and the cellular ApaF1, BiP, and DAP5 IRES elements was strongly activated. In addition, several HSV type 1 (HSV-1) 5′ untranslated region (5′ UTR) sequences also served as positive vhs response elements in this assay. IRES activation was also observed in 293 and HepG2 cells, but no such response was observed in Vero cells. Mutational analysis has yet to uncouple the ability of vhs to activate 3′ cistron expression from its shutoff activity. Remarkably, repression of 5′ cistron expression could be observed under conditions where the levels of the reporter RNA were not correspondingly reduced. These data provide strong evidence that vhs can modulate gene expression at the level of translation and that it is able to activate cap-independent translation through specific
cis
-acting elements.
Hepatitis C Virus Hypervariable Region 1 Modulates Receptor Interactions, Conceals the CD81 Binding Site, and Protects Conserved Neutralizing Epitopes
Authors: Bankwitz Dorothea , Steinmann Eike , Bitzegeio Julia , Ciesek Sandra , Friesland Martina , Herrmann Eva , Zeisel Mirjam B. , Baumert Thomas F. , Keck Zhen-yong , Foung Steven K. H. , Pécheur Eve-Isabelle , Pietschmann Thomas 
Published: April 2010

ABSTRACTThe variability of the hepatitis C virus (HCV), which likely contributes to immune escape, is most pronounced in hypervariable region 1 (HVR1) of viral envelope protein 2. This domain is the target for neutralizing antibodies, and its deletion attenuates replicationin vivo. Here we characterized the relevance of HVR1 for virus replicationin vitrousing cell culture-derived HCV. We show that HVR1 is dispensable for RNA replication. However, viruses lacking HVR1 (ΔHVR1) are less infectious, and separation by density gradients revealed that the population of ΔHVR1 virions comprises fewer particles with low density. Strikingly, ΔHVR1 particles with intermediate density (1.12 g/ml) are as infectious as wild-type virions, while those with low density (1.02 to 1.08 g/ml) are poorly infectious, despite quantities of RNA and core similar to those in wild-type particles. Moreover, ΔHVR1 particles exhibited impaired fusion, a defect that was partially restored by an E1 mutation (I347L), which also rescues infectivity and which was selected during long-term culture. Finally, ΔHVR1 particles were no longer neutralized by SR-B1-specific immunoglobulins but were more prone to neutralization and precipitation by soluble CD81, E2-specific monoclonal antibodies, and patient sera. These results suggest that HVR1 influences the biophysical properties of released viruses and that this domain is particularly important for infectivity of low-density particles. Moreover, they indicate that HVR1 obstructs the viral CD81 binding site and conserved neutralizing epitopes. These functions likely optimize virus replication, facilitate immune escape, and thus foster establishment and maintenance of a chronic infection.
p62/Sequestosome-1 Associates with and Sustains the Expression of Retroviral Restriction Factor TRIM5α
Authors: O'Connor Christopher , Pertel Thomas , Gray Seth , Robia Seth L. , Bakowska Joanna C. , Luban Jeremy , Campbell Edward M. 
Published: April 2010

ABSTRACT
TRIM5 proteins mediate a potent block to the cross-species transmission of retroviruses, the most well known being the TRIM5α protein from rhesus macaques, which potently inhibits human immunodeficiency virus type 1 (HIV-1) infection. This restriction occurs at an early stage in the replication cycle and is mediated by the binding of TRIM5 proteins to determinants present in the retroviral capsid. TRIM5α, as well as other TRIM family proteins, has been shown to be regulated by interferons (IFN). Here we show that TRIM5α associates with another IFN-induced gene, sequestosome-1/p62 (p62). p62 plays a role in several signal transduction cascades that are important for maintaining the antiviral state of cells. Here we demonstrate that p62 localizes to both human and rhesus macaque TRIM5α cytoplasmic bodies, and fluorescence resonance energy transfer (FRET) analysis demonstrates that these proteins closely associate in these structures. When p62 expression was knocked down via small interfering RNA (siRNA), the number of TRIM5α cytoplasmic bodies and the level of TRIM5α protein expression were reduced in cell lines stably expressing epitope-tagged versions of TRIM5α. In accordance with these data, p62 knockdown resulted in reduced TRIM5α-mediated retroviral restriction in cells expressing epitope-tagged TRIM5α or expressing endogenously expressed human TRIM5α. p62 may therefore operate to enhance TRIM5α-mediated retroviral restriction, contributing to the antiviral state of cells following IFN treatment.
Route of Adenovirus-Based HIV-1 Vaccine Delivery Impacts the Phenotype and Trafficking of Vaccine-Elicited CD8
+
T Lymphocytes
Authors: Kaufman David R. , Bivas-Benita Maytal , Simmons Nathaniel L. , Miller Darby , Barouch Dan H. 
Published: April 2010

ABSTRACT

Candidate HIV-1 vaccine regimens utilizing intramuscularly (i.m.) administered recombinant adenovirus (rAd)-based vectors can induce potent mucosal cellular immunity. However, the degree to which mucosal rAd vaccine routing might alter the quality and anatomic distribution of vaccine-elicited CD8
+
T lymphocytes remains unclear. We show that the route of vaccination critically impacts not only the magnitude but also the phenotype and trafficking of antigen-specific CD8
+
T lymphocytes in mice. I.m. rAd immunization induced robust local transgene expression and elicited high-frequency, polyfunctional CD8
+
T lymphocytes that trafficked broadly to both systemic and mucosal compartments. In contrast, intranasal (i.n.) rAd immunization led to similarly robust local transgene expression but generated low-frequency, monofunctional CD8
+
T lymphocytes with restricted anatomic trafficking patterns. Respiratory rAd immunization elicited systemic and mucosal CD8
+
T lymphocytes with phenotypes and trafficking properties distinct from those elicited by i.m. or i.n. rAd immunization. Our findings indicate that the anatomic microenvironment of antigen expression critically impacts the phenotype and trafficking of antigen-specific CD8
+
T lymphocytes.
Coinfection of Hepatic Cell Lines with Human Immunodeficiency Virus and Hepatitis B Virus Leads to an Increase in Intracellular Hepatitis B Surface Antigen
Authors: Iser David M. , Warner Nadia , Revill Peter A. , Solomon Ajantha , Wightman Fiona , Saleh Suha , Crane Megan , Cameron Paul U. , Bowden Scott , Nguyen Tin , Pereira Cândida F. , Desmond Paul V. , Locarnini Stephen A. , Lewin Sharon R. 
Published: April 2010

ABSTRACT
Liver-related mortality is increased in the setting of HIV-hepatitis B virus (HBV) coinfection. However, interactions between HIV and HBV to explain this observation have not been described. We hypothesized that HIV infection of hepatocytes directly affects the life cycle of HBV. We infected human hepatic cell lines expressing HBV (Hep3B and AD38 cells) or not expressing HBV (Huh7, HepG2, and AD43 cells) with laboratory strains of HIV (NL4-3 and AD8), as well as a vesicular stomatitis virus (VSV)-pseudotyped HIV expressing enhanced green fluorescent protein (EGFP). Following HIV infection with NL4-3 or AD8 in hepatic cell lines, we observed a significant increase in HIV reverse transcriptase activity which was infectious. Despite no detection of surface CD4, CCR5, and CXCR4 by flow cytometry, AD8 infection of AD38 cells was inhibited by maraviroc and NL4-3 was inhibited by AMD3100, demonstrating that HIV enters AD38 hepatic cell lines via CCR5 or CXCR4. High-level infection of AD38 cells (50%) was achieved using VSV-pseudotyped HIV. Coinfection of the AD38 cell line with HIV did not alter the HBV DNA amount or species as determined by Southern blotting or nucleic acid signal amplification. However, coinfection with HIV was associated with a significant increase in intracellular HBsAg when measured by Western blotting, quantitative HBsAg, and fluorescence microscopy. We conclude that HIV infection of HBV-infected hepatic cell lines significantly increased intracellular HBsAg but not HBV DNA synthesis and that increased intrahepatic HBsAg secondary to direct infection by HIV may contribute to accelerated liver disease in HIV-HBV-coinfected individuals.
Autologous Neutralizing Antibodies to the Transmitted/Founder Viruses Emerge Late after Simian Immunodeficiency Virus SIVmac251 Infection of Rhesus Monkeys
Authors: Yeh Wendy W. , Rahman Ishita , Hraber Peter , Coffey Rory T. , Nevidomskyte Daiva , Giri Ayush , Asmal Mohammed , Miljkovic Svetlana , Daniels Marcus , Whitney James B. , Keele Brandon F. , Hahn Beatrice H. , Korber Bette T. , Shaw George M. , Seaman Michael S. , Letvin Norman L. 
Published: April 2010

ABSTRACT

While the simian immunodeficiency virus (SIV)-infected rhesus monkey is an important animal model for human immunodeficiency virus type 1 (HIV-1) infection of humans, much remains to be learned about the evolution of the humoral immune response in this model. In HIV-1 infection, autologous neutralizing antibodies emerge 2 to 3 months after infection. However, the ontogeny of the SIV-specific neutralizing antibody response in mucosally infected animals has not been defined. We characterized the kinetics of the autologous neutralizing antibody response to the transmitted/founder SIVmac251 using a pseudovirion-based TZM-bl cell assay and monitored
env
sequence evolution using single-genome amplification in four rhesus animals that were infected via intrarectal inoculations. We show that the SIVmac251 founder viruses induced neutralizing antibodies at 5 to 8 months after infection. Despite their slow emergence and low titers, these neutralizing antibodies selected for escape mutants that harbored substitutions and deletions in variable region 1 (V1), V2, and V4 of Env. The neutralizing antibody response was initially focused on V4 at 5 to 8 months after infection and then targeted V1/V2 and V4 by 16 months. These findings reveal a striking delay in the development of neutralizing antibodies in SIVmac-infected animals, thus raising questions concerning the suitability of SIVmac251 as a challenge strain to screen AIDS vaccines that elicit neutralizing antibodies as a means to prevent virus acquisition. They also illustrate the capacity of the SIVmac quasispecies to modify antigenic determinants in response to very modest titers of neutralizing antibodies.
Postmenopausal breast cancer and occupational exposures
Authors: Labrèche France , Goldberg Mark S , Valois Marie-France , Nadon Louise 
Published: April 2010

ObjectiveTo determine whether exposures in the workplace to organic solvents and to other agents, such as polycyclic aromatic hydrocarbons, are associated with increased risks of developing postmenopausal breast cancer.MethodsBetween 1996 and 1997 a case–control study was conducted in Montreal, Quebec. Cases comprised 556 women, aged 50–75 years, with incident malignant breast cancer, and their controls were 613 women with other cancers, frequency matched for age, date of diagnosis and hospital. An expert team of chemists and industrial hygienists translated their job histories into exposure to about 300 agents.ResultsOdds ratios (ORs) were increased for the usual risk factors for breast cancer and, adjusting for these, risks increased with occupational exposure to several agents, and were highest for exposures occurring before age 36 years. Increased ORs were found for each 10-year increment in duration of exposure, before age 36 years (OR<36), to acrylic fibres (OR<36=7.69) and to nylon fibres (OR<36=1.99). For oestrogen-positive and progesterone-negative tumours, the OR doubled or more for each 10-year increase in exposure to monoaromatic hydrocarbons, and to acrylic and rayon fibres. The OR<36also doubled for exposure to organic solvents that metabolise into reactive oxygen species, and to acrylic fibres. A threefold increase was found for oestrogen- and progesterone-positive tumours, with exposure to polycyclic aromatic hydrocarbons from petroleum sources.ConclusionCertain occupational exposures appear to increase the risk of developing postmenopausal breast cancer, although some findings might be due to chance or to undetected bias. Our findings are consistent with the hypothesis that breast tissue is more sensitive to adverse effects if exposure occurs when breast cells are still proliferating. More refined analyses, adjusting for hormonal receptor subtypes and studies focusing on certain chemical exposures are required to further our understanding of the role of chemicals in the development of breast cancer.
Regional stratigraphic architecture and reservoir types of the Oligo-Miocene deposits in the Dezful Embayment (Asmari and Pabdeh Formations) SW Iran
Authors: van Buchem F. S. P. , Allan T. L. , Laursen G. V. , Lotfpour M. , Moallemi A. , Monibi S. , Motiei H. , Pickard N. A. H. , Tahmasbi A. R. , Vedrenne V. , Vincent B. 
Published: April 2010

Abstract
A regional sequence stratigraphic model is proposed for the Oligo-Miocene Asmari and Pabdeh Formations in the Dezful Embayment of SW Iran. The model is based on both new detailed sedimentological observations in outcrops, core and well logs, and an improved high-resolution chronostratigraphic framework constrained by Sr isotope stratigraphy and biostratigraphy. A better understanding of the stratigraphic architecture distinguishes four, geographically separated types of Asmari reservoirs.
Three Oligocene sequences (of Rupelian, early Chattian and late Chattian age) and three Miocene sequences (of early Aquitanian, late Aquitanian and early Burdigalian age) have been distinguished, representing a period of 15.4 Ma. The stratigraphic architecture of these sequences is primarily controlled by glacio-eustatic sea-level fluctuations, which determined the distribution of carbonates, sandstones and anhydrites in this sedimentary system. Tectonic control became important in the Burdigalian with a regional tilt down towards the NE. The lithological heterogeneity, the complex geometries, and both early and late diagenetic alterations are the basis for a classification of four main stratigraphic reference types for the Asmari Reservoirs: Type 1, sandstone dominated; Type 2, mixed carbonate-siliciclastic; Type 3, mixed carbonate-anhydrite; and Type 4, carbonate dominated. The sequence stratigraphic model predicts how and when these types change laterally from one to another.