bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Promiscuous CC Chemokine Receptor D6 Is a Functional Coreceptor for Primary Isolates of Human Immunodeficiency Virus Type 1 (HIV-1) and HIV-2 on Astrocytes
Authors: Neil Stuart J. D. , Aasa-Chapman Marlen M. I. , Clapham Paul R. , Nibbs Robert J. , McKnight Áine , Weiss Robin A. 
Published: July 2005

ABSTRACT
The role of coreceptors other than CCR5 and CXCR4 in the pathogenesis of human immunodeficiency virus (HIV) disease is controversial. Here we show that a promiscuous CC chemokine receptor, D6, can function as a coreceptor for various primary dual-tropic isolates of HIV type 1 (HIV-1) and HIV-2. Furthermore, D6 usage is common among chimeric HIV-1 constructs bearing the gp120 proteins of isolates from early seroconverting patients. D6 mRNA and immunoreactivity were demonstrated to be expressed in HIV-1 target cells such as macrophages, peripheral blood mononuclear cells, and primary astrocytes. In primary astrocytes, an RNA interference-mediated knockdown of D6 expression inhibited D6-tropic isolate infection. D6 usage may account for some previous observations of alternative receptor tropism for primary human cells. Thus, D6 may be an important receptor for HIV pathogenesis in the brain and for the early dissemination of virus in the host.
Inhibition, Escape, and Attenuated Growth of Severe Acute Respiratory Syndrome Coronavirus Treated with Antisense Morpholino Oligomers
Authors: Neuman Benjamin W. , Stein David A. , Kroeker Andrew D. , Churchill Michael J. , Kim Alice M. , Kuhn Peter , Dawson Philip , Moulton Hong M. , Bestwick Richard K. , Iversen Patrick L. , Buchmeier Michael J. 
Published: July 2005

ABSTRACT
The recently emerged severe acute respiratory syndrome coronavirus (SARS-CoV) is a potent pathogen of humans and is capable of rapid global spread. Peptide-conjugated antisense morpholino oligomers (P-PMO) were designed to bind by base pairing to specific sequences in the SARS-CoV (Tor2 strain) genome. The P-PMO were tested for their capacity to inhibit production of infectious virus as well as to probe the function of conserved viral RNA motifs and secondary structures. Several virus-targeted P-PMO and a random-sequence control P-PMO showed low inhibitory activity against SARS coronavirus. Certain other virus-targeted P-PMO reduced virus-induced cytopathology and cell-to-cell spread as a consequence of decreasing viral amplification. Active P-PMO were effective when administered at any time prior to peak viral synthesis and exerted sustained antiviral effects while present in culture medium. P-PMO showed low nonspecific inhibitory activity against translation of nontargeted RNA or growth of the arenavirus lymphocytic choriomeningitis virus. Two P-PMO targeting the viral transcription-regulatory sequence (TRS) region in the 5′ untranslated region were the most effective inhibitors tested. After several viral passages in the presence of a TRS-targeted P-PMO, partially drug-resistant SARS-CoV mutants arose which contained three contiguous base point mutations at the binding site of a TRS-targeted P-PMO. Those partially resistant viruses grew more slowly and formed smaller plaques than wild-type SARS-CoV. These results suggest PMO compounds have powerful therapeutic and investigative potential toward coronavirus infection.
Rmcf2
, a Xenotropic Provirus in the Asian Mouse Species
Mus castaneus
, Blocks Infection by Polytropic Mouse Gammaretroviruses
Authors: Wu Tiyun , Yan Yuhe , Kozak Christine A. 
Published: July 2005

ABSTRACT

Cells from the Asian wild mouse species
Mus castaneus
are resistant to infection by the polytropic host range group of mouse gammaretroviruses. Two factors are responsible for this resistance: a defective XPR1 cell surface receptor for polytropic murine leukemia viruses (P-MLVs), and a resistance factor detectable only in interspecies hybrids between
M. castaneus
and mice with an XPR1 variant that permits infection by xenotropic MLVs (X-MLVs) as well as P-MLVs. This second novel virus resistance phenotype has been associated with expression of viral Env glycoprotein; Northern blotting with specific hybridization probes identified a spliced X-MLV
env
message unique to virus-resistant mice. These observations suggest that resistance is due to expression of one or more endogenous X-MLV envelope genes that interfere with infection by exogenous P-MLVs.
M. castaneus
contains multiple X-MLV proviruses, but serial backcrosses reduced this proviral content and permitted identification of a single proviral
env
sequence inherited with resistance. The resistance phenotype and the provirus were mapped to the same site on distal chromosome 18. The provirus was shown to be a full-length provirus highly homologous to previously described X-MLVs. Use of viral pseudotypes confirmed that this resistance gene, termed
Rmcf2
, prevents entry of P-MLVs.
Rmcf2
resembles the virus resistance genes
Fv4
and
Rmcf
in that it produces Env glycoprotein but fails to produce infectious virus; the proviruses associated with all three resistance genes have fatal defects. This type of provirus Env-mediated resistance represents an important defense mechanism in wild mouse populations exposed to endemic infections.
Shutoff of RNA Polymerase II Transcription by Poliovirus Involves 3C Protease-Mediated Cleavage of the TATA-Binding Protein at an Alternative Site: Incomplete Shutoff of Transcription Interferes with Efficient Viral Replication
Authors: Kundu Pallob , Raychaudhuri Santanu , Tsai Weimin , Dasgupta Asim 
Published: July 2005

ABSTRACT

The TATA-binding protein (TBP) plays a crucial role in cellular transcription catalyzed by all three DNA-dependent RNA polymerases. Previous studies have shown that TBP is targeted by the poliovirus (PV)-encoded protease 3C
pro
to bring about shutoff of cellular RNA polymerase II-mediated transcription in PV-infected cells. The processing of the majority of viral precursor proteins by 3C
pro
involves cleavages at glutamine-glycine (Q-G) sites. We present evidence that suggests that the transcriptional inactivation of TBP by 3C
pro
involves cleavage at the glutamine 104-serine 105 (Q104-S105) site of TBP and not at the Q18-G19 site as previously thought. The TBP Q104-S105 cleavage by 3C
pro
is greatly influenced by the presence of an aliphatic amino acid at the P4 position, a hallmark of 3C
pro
-mediated proteolysis. To examine the importance of host cell transcription shutoff in the PV life cycle, stable HeLa cell lines were created that express recombinant TBP resistant to cleavage by the viral proteases, called GG rTBP. Transcription shutoff was significantly impaired and delayed in GG rTBP cells upon infection with poliovirus compared with the cells that express wild-type recombinant TBP (wt rTBP). Infection of GG rTBP cells with poliovirus resulted in small plaques, significantly reduced viral RNA synthesis, and lower viral yields compared to the wt rTBP cell line. These results suggest that a defect in transcription shutoff can lead to inefficient replication of poliovirus in cultured cells.
Deletion of the Herpes Simplex Virus VP22-Encoding Gene (UL49) Alters the Expression, Localization, and Virion Incorporation of ICP0
Authors: Elliott Gillian , Hafezi Wali , Whiteley Alison , Bernard Emmanuelle 
Published: July 2005

ABSTRACT
The role of the herpes simplex virus tegument protein VP22 is not yet known. Here we describe the characterization of a virus in which the entire VP22 open reading frame has been deleted. We show that VP22 is not essential for virus growth but that virus lacking VP22 (Δ22) displays a cell-specific replication defect in epithelial MDBK cells. Virus particles assembled in the absence of VP22 show few obvious differences to wild-type (WT) particles, except for a moderate reduction in glycoproteins gD and gB. In addition, the Δ22 virus exhibits a general delay in the initiation of virus protein synthesis, but this is not due to a glycoprotein-related defect in virus entry. Intriguingly, however, the absence of VP22 has an obvious effect on the intracellular level of the immediate-early (IE) protein ICP0. Moreover, following translocation from the nucleus to the cytoplasm, ICP0 is unable to localize to the characteristic cytoplasmic sites observed in a WT infection. We demonstrate that, in WT-infected cells, VP22 and ICP0 are concentrated in the same cytoplasmic sites. Furthermore, we show that, while ICP0 and ICP4 are components of WT extracellular virions, the altered localization of ICP0 in the cytoplasm of Δ22-infected cells correlates with an absence of both ICP0 and ICP4 from Δ22 virions. Hence, while a role has not yet been defined for virion IE proteins in virus infection, our results suggest that their incorporation is a specific event requiring the tegument protein VP22. This report provides the first direct evidence that VP22 influences virus assembly.
The Capsid Protein of Satellite Panicum Mosaic Virus Contributes to Systemic Invasion and Interacts with Its Helper Virus
Authors: Omarov Rustem T. , Qi Dong , Karen-Beth Scholthof G. 
Published: July 2005

ABSTRACTSatellite panicum mosaic virus (SPMV) depends on its helper Panicum mosaic virus (PMV) for replication and spread in host plants. The SPMV RNA encodes a 17-kDa capsid protein (CP) that is essential for formation of its 16-nm virions. The results of this study indicate that in addition to the expression of the full-length SPMV CP from the 5′-proximal AUG start codon, SPMV RNA also expresses a 9.4-kDa C-terminal protein from the third in-frame start codon. Differences in solubility between the full-length protein and its C-terminal product were observed. Subcellular fractionation of infected plant tissues showed that SPMV CP accumulates in the cytosol, cell wall-, and membrane-enriched fractions. However, the 9.4-kDa protein exclusively cofractionated with cell wall- and membrane-enriched fractions. Earlier studies revealed that the 5′-untranslated region (5′-UTR) from nucleotides 63 to 104 was associated with systemic infection in a host-specific manner in millet plants. This study shows that nucleotide deletions and insertions in the 5′-UTR plus simultaneous truncation of the N-terminal part of the CP impaired SPMV spread in foxtail millet, but not in proso millet plants. In contrast, the expression of the full-length version of SPMV CP efficiently compensated the negative effect of the 5′-UTR deletions in foxtail millet. Finally, immunoprecipitation assays revealed the presence of a specific interaction between the capsid proteins of SPMV and its helper virus (PMV). Our findings show that the SPMV CP has several biological functions, including facilitating efficient satellite virus infection and movement in millet plants.
A Virus Essential for Insect Host-Parasite Interactions Encodes Cystatins
Authors: Espagne E. , Douris V. , Lalmanach G. , Provost B. , Cattolico L. , Lesobre J. , Kurata S. , Iatrou K. , Drezen J.-M. , Huguet E. 
Published: July 2005

ABSTRACT

Cotesia congregata
is a parasitoid wasp that injects its eggs in the host caterpillar
Manduca sexta
. In this host-parasite interaction, successful parasitism is ensured by a third partner: a bracovirus. The relationship between parasitic wasps and bracoviruses constitutes one of the few known mutualisms between viruses and eukaryotes. The
C. congregata
bracovirus (CcBV) is injected at the same time as the wasp eggs in the host hemolymph. Expression of viral genes alters the caterpillar's immune defense responses and developmental program, resulting in the creation of a favorable environment for the survival and emergence of adult parasitoid wasps. Here, we describe the characterization of a CcBV multigene family which is highly expressed during parasitism and which encodes three proteins with homology to members of the cystatin superfamily. Cystatins are tightly binding, reversible inhibitors of cysteine proteases. Other cysteine protease inhibitors have been described for lepidopteran viruses; however, this is the first description of the presence of cystatins in a viral genome. The expression and purification of a recombinant form of one of the CcBV cystatins, cystatin 1, revealed that this viral cystatin is functional having potent inhibitory activity towards the cysteine proteases papain, human cathepsins L and B and
Sarcophaga
cathepsin B in assays in vitro. CcBV cystatins are, therefore, likely to play a role in host caterpillar physiological deregulation by inhibiting host target proteases in the course of the host-parasite interaction.
Mapping of the Hepatitis B Virus Pre-S1 Domain Involved in Receptor Recognition
Authors: Barrera Azeneth , Guerra Bernadette , Notvall Lena , Lanford Robert E. 
Published: July 2005

ABSTRACTHepatitis B virus (HBV) and woolly monkey hepatitis B virus (WMHBV) are primate hepadnaviruses that display restricted tissue and host tropisms. Hepatitis D virus (HDV) particles pseudotyped with HBV and WMHBV envelopes (HBV-HDV and WM-HDV) preferentially infect human and spider monkey hepatocytes, respectively, thereby confirming host range bias in vitro. The analysis of chimeric HBV and WMHBV large (L) envelope proteins suggests that the pre-S1 domain may comprise two regions that affect infectivity: one within the amino-terminal 40 amino acids of pre-S1 and one downstream of this region. In the present study, we further characterized the role of the amino terminus of pre-S1 in infectivity by examining the ability of synthetic peptides to competitively block HDV infection of primary human and spider monkey hepatocytes. A synthetic peptide representing the first 45 residues of the pre-S1 domain of the HBV L protein blocked infectivity of HBV-HDV and WM-HDV, with a requirement for myristylation of the amino terminal residue. Competition studies with truncated peptides suggested that pre-S1 residues 5 to 20 represent the minimal domain for inhibition of HDV infection and, thus, presumably represent the residues involved in virus-host receptor interaction. Recombinant pre-S1 proteins expressed in insect cells blocked infection with HBV-HDV and WM-HDV at a concentration of 1 nanomolar. The ability of short pre-S1 peptides to efficiently inhibit HDV infection suggests that they represent suitable ligands for identification of the HBV receptor and that a pre-S1 mimetic may represent a rational therapy for the treatment of HBV infection.
Age-Dependent Role for CCR5 in Antiviral Host Defense against Herpes Simplex Virus Type 2
Authors: Ank Nina , Petersen Klavs , Malmgaard Lene , Mogensen Søren C. , Paludan Søren R. 
Published: July 2005

ABSTRACTElimination of viral infections is dependent on rapid recruitment and activation of leukocytes with antiviral activities to infected areas. Chemokines constitute a class of cytokines that have regulatory effects on leukocyte migration and activity. In this study we have studied the role of CC chemokine receptor 1 (CCR1) and CCR5 in host defense during a generalized herpes simplex virus type 2 (HSV-2) infection. Whereas both 4- and 8-week-old CCR1−/−mice resembled wild-type mice (C57BL/6) with respect to defense against the infection, significantly higher virus titers were seen in the livers and brains of 4-week-old CCR5−/−mice. At the age of 8 weeks, CCR5−/−were indistinguishable from wild-type mice and cleared the infection from liver and spleen. Although 4-week-old CCR5−/−mice were able to recruit natural killer (NK) cells to the site of infection, these cells had reduced cytotoxic activity compared to NK cells from wild-type mice. This was not due to lower production of alpha/beta interferon or interleukin-12, two well-described activators of cytotoxic activity in NK cells. We also noted that the spleens of young CCR5−/−mice did not increase in size during infection as did the spleens of wild-type and CCR1−/−mice. This observation was accompanied by impaired proliferation of CCR5−/−splenocytes (SCs) ex vivo. Moreover, migration of CD8+T cells to the liver in response to infection was impaired in CCR5−/−mice, and adoptive transfer of SCs from CCR5−/−mice infected for 6 days into newly infected wild-type mice did not improve antiviral activity in the liver, in contrast to what was seen in mice receiving immune SCs from wild-type mice. Altogether, this study shows that CCR5 plays an age-dependent role in host defense against HSV-2 by supporting both the innate and adaptive immune response.
Murine Coronavirus Requires Lipid Rafts for Virus Entry and Cell-Cell Fusion but Not for Virus Release
Authors: Choi Keum S. , Aizaki Hideki , Lai Michael M. C. 
Published: July 2005

ABSTRACT

Thorp and Gallagher first reported that depletion of cholesterol inhibited virus entry and cell-cell fusion of mouse hepatitis virus (MHV), suggesting the importance of lipid rafts in MHV replication (E. B. Thorp and T. M. Gallagher, J. Virol.
78:
2682-2692, 2004). However, the MHV receptor is not present in lipid rafts, and anchoring of the MHV receptor to lipid rafts did not enhance MHV infection; thus, the mechanism of lipid rafts involvement is not clear. In this study, we defined the mechanism and extent of lipid raft involvement in MHV replication. We showed that cholesterol depletion by methyl β-cyclodextrin or filipin did not affect virus binding but reduced virus entry. Furthermore, MHV spike protein bound to nonraftraft membrane at 4°C but shifted to lipid rafts at 37°C, indicating a redistribution of membrane following virus binding. Thus, the lipid raft involvement in MHV entry occurs at a step following virus binding. We also found that the viral spike protein in the plasma membrane of the infected cells was associated with lipid rafts, whereas that in the Golgi membrane, where MHV matures, was not. Moreover, the buoyant density of the virion was not changed when MHV was produced from the cholesterol-depleted cells, suggesting that MHV does not incorporate lipid rafts into the virion. These results indicate that MHV release does not involve lipid rafts. However, MHV spike protein has an inherent ability to associate with lipid rafts. Correspondingly, cell-cell fusion induced by MHV was retarded by cholesterol depletion, consistent with the association of the spike protein with lipid rafts in the plasma membrane. These findings suggest that MHV entry requires specific interactions between the spike protein and lipid rafts, probably during the virus internalization step.
Genetic Analysis of the Polyomavirus DnaJ Domain
Authors: Whalen Kerry A. , de Jesus Rowena , Kean Jennifer A. , Schaffhausen Brian S. 
Published: July 2005

ABSTRACT

Polyomavirus T antigens share a common N-terminal sequence that comprises a DnaJ domain. DnaJ domains activate DnaK molecular chaperones. The functions of J domains have primarily been tested by mutation of their conserved HPD residues. Here, we report detailed mutagenesis of the polyomavirus J domain in both large T (63 mutants) and middle T (51 mutants) backgrounds. As expected, some J mutants were defective in binding DnaK (Hsc70); other mutants retained the ability to bind Hsc70 but were defective in stimulating its ATPase activity. Moreover, the J domain behaves differently in large T and middle T. A given mutation was twice as likely to render large T unstable as it was to affect middle T stability. This apparently arose from middle T's ability to bind stabilizing proteins such as protein phosphatase 2A (PP2A), since introduction of a second mutation preventing PP2A binding rendered some middle T J-domain mutants unstable. In large T, the HPD residues are critical for Rb-dependent effects on the host cell. Residues Q32, A33, Y34, H49, M52, and N56 within helix 2 and helix 3 of the large T J domain were also found to be required for Rb-dependent transactivation. Cyclin A promoter assays showed that J domain function also contributes to large T transactivation that is independent of Rb. Single point mutations in middle T were generally without effect. However, residue Q37 is critical for middle T's ability to form active signaling complexes. The Q37A middle T mutant was defective in association with pp60
c-src
and in transformation.
Dialectics and Crisis Theory: A Response to Tony Smith
Authors: Fine Ben , Milonakis Dimitris , Lapavitsas Costas 
Published: July 2005

AbstractBrenner's ‘The Economics of Global Turbulence’ has induced a flood of responses, the vast majority of them critical, especially on grounds of (divergence from Marx's) method and theory. Tony Smith1 is an exception in seeking to defend Brenner, mostly by pushing his arguments further and by attacking his critics, including ourselves. In part, Smith interprets Brenner and credits him with positions that he can either defend for himself or, as we suspect, reject. Our concern in this reply is not to address issues through the prism of Brenner but to assess Smith's own contribution critically on its own terms and merits.
Vygotsky on Language and Social Consciousness: Underpinning the Use of Voloshinov in the Study of Popular Protest
Authors: Collins Chik 
Published: July 2005

AbstractThe term ‘Bakhtin Circle’ is used to refer to a group of Russian thinkers centred around Mikhail Bakhtin in the years following the 1917 Revolution. The group's prime concern was with the importance of questions of language-use in social life, and with the way in which language-use registered conflicts between social groups and classes. Prominent members, as well as Bakhtin himself, included P.N. Medvedev and V.N. Voloshinov. Between 1929, when a number of members were arrested, and his death in 1975, Bakhtin continued to work on the issues which had occupied the group.
The Concept of Money
Authors:   Vakhitov,   Vakhitov
Published: July 2005

AbstractThe authors of this article—a lawyer and economist—describe modern developments in the forms and functions of money and examine the question of whether the current legal regulation (in the Russian Federation) adequately reflects such developments. The authors suggest that the rule applicable to non-cash money be applied to cash money since the distinction in legal regulation is based more on traditions than it is on actual differences in substance.
Russia's "Dictatorship of Law" and the European Court of Human Rights
Authors:   Kahn
Published: July 2005

AbstractThis article is an adaptation of a lecture given at St. Antony's College, Oxford on 5 July 2003 in honor of the fiftieth anniversary of the Centre for Russian and East European Studies at Oxford University. The author evaluates the effect of the European Convention on Human Rights on Russian law and politics. Russia has been a signatory to the Convention for five years. The author argues that the full power of the Convention as a force for reform in Russia was unanticipated at the time of Russia's accession. Nevertheless, the Convention has been the catalyst for substantial reforms, especially in the criminal justice system. The author examines these reforms as well as the increasing number of cases in which Russia is a respondent before the European Court of Human Rights in Strasbourg. Drawing on interviews, the Court's statistics and his own experience training Russian human rights lawyers, the author charts the rapid growth in Russia of interest in the Strasbourg process.