bluuebunny/crossref_metadata_2025_split huggingface dataset:
Meaning of health for Japanese elders who have had a stroke
Authors: TAKAHASHI Ryutaro , LIEHR Patricia , NISHIMURA Chie , ITO Mio , SUMMERS Linda C. 
Published: May 2005

AbstractAim:  This study was conducted to explore the meaning of health for Japanese elders who have had a stroke.Methods:  A secondary analysis of existing data was conducted by using phenomenological methods. Twenty‐four male and female stroke patients, whose average age was 76 ± 7.2 years, described the meaning of health with one researcher. Researchers from Japan and the USA analysed the data through email communication and scheduled visits. The five‐step analysis method began from the English transcriptions of descriptions to finally identify a structural definition of health for Japanese elders who have had a stroke.Results:  The structural definition identifies health as a fundamentally valuable gift recognized by stroke patients as they try to adjust to their present circumstance, defined by their past experience, and as they consider dimensions of everyday living from a new perspective. Judgments about how they are doing are created through the eyes and expressions of others who interact with them and through everyday markers of usual life, like a good appetite, easy breathing and smooth thinking and moving.Conclusions:  Comparable with other studies, elderly Japanese stroke survivors seek a revised but familiar, stable ‘self’ based on a new frame of reference incorporating their past with the person they are now. Unlike other stroke survivors of previous studies, these Japanese elders considered fundamental human patterns such as breathing and eating as markers for good health, and they used the assessments of others to judge their progress. There is a need for health‐care providers to thoughtfully engage with stroke survivors to determine the most meaningful approaches to care and engagement demands and understand that their interactions are intricately woven into the patient's health experience.
Effects of aided and unaided support of the neck while sitting (with back support), on autonomic nervous system activities
Authors: OKUBO Nobuko , HISHINUMA Michiko 
Published: May 2005

AbstractAim:  To compare the effects of neck support and no neck support while sitting (with back support), on the autonomic nervous system for the purpose of developing effective consciousness disturbance nursing techniques based on patient posture.Methods:  Seven healthy women followed two patterns in a cross‐over design study: (i) sitting in a position with back support but no neck support, sitting with both back and neck support; and (ii) sitting in a position with both back and neck support, sitting with back support but no neck support. The intervention involved unaided support of the subject's neck with each subject supporting their own neck. Coarse Graining Spectral Analysis was used to measure the effect of the two positions on the autonomic nervous system.Results:  Sitting in a position with back support but no neck support increased the function of the sympathetic nervous system and decreased the function of the parasympathetic nervous system more than sitting in a position with both back and neck support.Conclusion:  Unaided support of the neck stimulated the autonomic nervous system. We infer from this, therefore, that consciousness disturbance patients may benefit in terms of preventing disuse syndrome and improving their consciousness levels by developing a nursing technique involving unaided support of the neck.
Proteolytic Processing of Sapovirus ORF1 Polyprotein
Authors: Oka Tomoichiro , Katayama Kazuhiko , Ogawa Satoko , Hansman Grant S. , Kageyama Tsutomu , Ushijima Hiroshi , Miyamura Tatsuo , Takeda Naokazu 
Published: May 2005

ABSTRACT

The genome of
Sapovirus
(SaV), a causative agent of gastroenteritis in humans and swine, contains either two or three open reading frames (ORFs). Functional motifs characteristic to the 2C-like NTPase (NTPase), VPg, 3C-like protease (Pro), 3D-like RNA-dependent RNA polymerase (Pol), and capsid protein (VP1) are encoded in the ORF1 polyprotein, which is afterwards cleaved into the nonstructural and structural proteins. We recently determined the complete genome sequence of a novel human SaV strain, Mc10, which has two ORFs. To investigate the proteolytic cleavage of SaV ORF1 and the function of protease on the cleavage, both full-length and truncated forms of the ORF1 polyprotein either with or without mutation in
1171
Cys to Ala of the GDCG motif were expressed in an in vitro coupled transcription-translation system. The translation products were analyzed directly by sodium dodecyl sulfate-polyacrylamide gel electrophoresis or by immunoprecipitation with region-specific antibodies. The ORF1 polyprotein was processed into at least 10 major proteins: p11, p28, p35, p32, p14, p70, p60, p66, p46, and p120. Seven of these products were arranged in the following order: NH
2
-p11-p28-p35(NTPase)-p32-p14(VPg)-p70(Pro-Pol)-p60(VP1)-COOH. p66, p46 and p120 were precursors of p28-p35 (NTPase), p32-p14 (VPg), and p32-p14 (VPg)-p70 (Pro-Pol), respectively. Mutagenesis in the 3C-like protease motif fully abolished the proteolytic activity. The cleavage map of SaV ORF1 is similar to those of other heretofore known members of the family
Caliciviridae
, especially to rabbit hemorrhagic disease virus, a member of the genus
Lagovirus
.
Dendritic Cell Precursors Are Permissive to Dengue Virus and Human Immunodeficiency Virus Infection
Authors: Kwan Wing-Hong , Helt Anna-Marija , Marañón Concepción , Barbaroux Jean-Baptiste , Hosmalin Anne , Harris Eva , Fridman Wolf H. , Mueller Chris G. F. 
Published: May 2005

ABSTRACTCD14+interstitial cells reside beneath the epidermis of skin and mucosal tissue and may therefore play an important role in viral infections and the shaping of an antiviral immune response. However, in contrast to dendritic cells (DC) or blood monocytes, these antigen-presenting cells (APC) have not been well studied. We have previously described long-lived CD14+cells generated from CD34+hematopoietic progenitors, which may represent model cells for interstitial CD14+APC. Here, we show that these cells carry DC-SIGN and differentiate into immature DC in the presence of granulocyte-macrophage colony-stimulating factor. We have compared the CD14+cells and the DC derived from these cells with respect to dengue virus and human immunodeficiency virus type 1 (HIV-1) infection. Both cell types are permissive to dengue virus infection, but the CD14+cells secrete the anti-inflammatory cytokine interleukin 10 and no tumor necrosis factor alpha. Regarding HIV, the CD14+cells are permissive to HIV-1, release higher p24 levels than the derived DC, and more efficiently activate HIV Pol-specific CD8+memory T cells. The CD14+DC precursors infected with either virus retain their DC differentiation potential. The results suggest that interstitial CD14+APC may contribute to HIV-1 and dengue virus infection and the shaping of an antiviral immune response.
Chimeric Dengue 2 PDK-53/West Nile NY99 Viruses Retain the Phenotypic Attenuation Markers of the Candidate PDK-53 Vaccine Virus and Protect Mice against Lethal Challenge with West Nile Virus
Authors: Huang Claire Y.-H. , Silengo Shawn J. , Whiteman Melissa C. , Kinney Richard M. 
Published: May 2005

ABSTRACT

Chimeric dengue serotype 2/West Nile (D2/WN) viruses expressing prM-E of WN NY99 virus in the genetic background of wild-type D2 16681 virus and two candidate D2 PDK-53 vaccine variants (PDK53-E and PDK53-V) were engineered. The viability of the D2/WN viruses required incorporation of the WN virus-specific signal sequence for prM. Introduction of two mutations at M-58 and E-191 in the chimeric cDNA clones further improved the viability of the chimeras constructed in all three D2 carriers. Two D2/WN chimeras (D2/WN-E2 and -V2) engineered in the backbone of the PDK53-E and -V viruses retained all of the PDK-53 vaccine characteristic phenotypic markers of attenuation and were immunogenic in mice and protected mice from a high-dose 10
7
PFU challenge with wild-type WN NY99 virus. This report further supports application of the genetic background of the D2 PDK-53 virus as a carrier for development of live-attenuated, chimeric flavivirus vaccines in general and the development of a chimeric D2/WN vaccine virus against WN disease in particular.
Double-Stranded RNA Binding by Human Cytomegalovirus pTRS1
Authors: Hakki Morgan , Geballe Adam P. 
Published: May 2005

ABSTRACT
The human cytomegalovirus (HCMV) TRS1 and IRS1 genes rescue replication of vaccinia virus (VV) that has a deletion of the double-stranded RNA binding protein gene E3L (VVΔE3L). Like E3L, these HCMV genes block the activation of key interferon-induced, double-stranded RNA (dsRNA)-activated antiviral pathways. We investigated the hypothesis that the products of these HCMV genes act by binding to dsRNA. pTRS1 expressed by cell-free translation or by infection of mammalian cells with HCMV or recombinant VV bound to dsRNA. Competition experiments revealed that pTRS1 preferentially bound to dsRNA compared to double-stranded DNA or single-stranded RNA. 5′- and 3′-end deletion analyses mapped the TRS1 dsRNA-binding domain to amino acids 74 through 248, a region of identity to pIRS1 that contains no homology to known dsRNA-binding proteins. Deletion of the majority of this region (Δ86-246) completely abrogated dsRNA binding. To determine the role of the dsRNA-binding domain in the rescue of VVΔE3L replication, wild-type or deletion mutants of TRS1 were transfected into HeLa cells, which were then infected with VVΔE3L. While full-length TRS1 rescued VVΔE3L replication, deletion mutants affecting a carboxy-terminal region of TRS1 that is not required for dsRNA binding failed to rescue VVΔE3L. Analyses of stable cell lines revealed that the carboxy-terminal domain is necessary to prevent the shutoff of protein synthesis and the phosphorylation of eIF2α after VVΔE3L infection. Thus, pTRS1 contains an unconventional dsRNA-binding domain at its amino terminus, but a second function involving the carboxy terminus is also required for countering host cell antiviral responses.
BZLF1 Activation of the Methylated Form of the
BRLF1
Immediate-Early Promoter Is Regulated by BZLF1 Residue 186
Authors: Bhende Prasanna M. , Seaman William T. , Delecluse Henri-Jacques , Kenney Shannon C. 
Published: May 2005

ABSTRACT

The Epstein-Barr virus (EBV) genome is highly methylated in latently infected cells. We recently reported that the EBV immediate-early (IE) protein BZLF1 (Z) preferentially binds to and activates transcription from the methylated form of the
BRLF1
IE gene promoter (Rp). We now report that serine residue 186 in the Z DNA-binding domain plays an important role in the ability of Z to bind to and activate methylated Rp. A Z mutant containing an alanine residue at position 186 [Z(S186A)] was significantly defective in binding to methylated, as well as unmethylated, ZREs (Z-responsive elements) in Rp and was unable to activate lytic EBV gene transcription from the methylated or demethylated form of the viral genome. A Z mutant containing threonine at residue 186 [Z(S186T)] bound only to the methylated form of the ZRE-2 site in Rp and induced lytic EBV gene transcription from the methylated, but not demethylated, form of the viral genome. The defect in both of these mutants was primarily due to an inability to activate the Rp in the context of the viral genome. Finally, a Z mutant containing an aspartic acid at position 186 [Z(S186D)] did not bind to either the consensus AP-1 site or to the methylated or unmethylated Rp ZRE-2 site and did not induce lytic gene transcription. These results indicate that replacement of serine with threonine at residue 186 in the Z DNA-binding domain differentially affects its ability to reactivate the unmethylated, versus methylated, viral genome.
Suppression of Virus Load by Highly Active Antiretroviral Therapy in Rhesus Macaques Infected with a Recombinant Simian Immunodeficiency Virus Containing Reverse Transcriptase from Human Immunodeficiency Virus Type 1
Authors: North Thomas W. , Van Rompay Koen K. A. , Higgins Joanne , Matthews Timothy B. , Wadford Debra A. , Pedersen Niels C. , Schinazi Raymond F. 
Published: May 2005

ABSTRACT
We have modeled highly active antiretroviral therapy (HAART) for AIDS in rhesus macaques infected with a chimera (RT-SHIV) of simian immunodeficiency virus containing reverse transcriptase from human immunodeficiency virus type-1 (HIV-1). Seven RT-SHIV-infected macaques were treated with a combination of efavirenz (200 mg orally once daily), lamivudine (8 mg/kg subcutaneously once daily), and tenofovir (30 mg/kg subcutaneously once daily). Plasma viral RNA levels in all animals were reduced by more than 1,000-fold after 4 weeks and, in six of the seven animals, were reduced to undetectable levels after 10 weeks. Virus loads increased slightly between 12 and 16 weeks of treatment, associated with problems with the administration of efavirenz. After a change in the method of efavirenz administration, virus loads declined again and remained undetectable in the majority of animals for the duration of therapy. Treatment was stopped for three animals after 36 weeks of therapy, and virus loads increased rapidly. Posttreatment RT-SHIV isolates had no mutations associated with resistance to any of the three drugs. Efavirenz treatment was stopped, but lamivudine and tenofovir treatment for two other macaques was continued. The virus load in one of these two animals rebounded; virus from this animal was initially free of drug-resistance mutations but acquired the K65R mutation in reverse transcriptase at 11 weeks after efavirenz treatment was withdrawn. These results mimic HAART of HIV-1-infected humans. The RT-SHIV/rhesus macaque model should be useful for studies of tissue reservoirs and sites of residual replication that are not possible or practical with humans.
Epstein-Barr Virus LMP2A Alters In Vivo and In Vitro Models of B-Cell Anergy, but Not Deletion, in Response to Autoantigen
Authors: Swanson-Mungerson Michelle A. , Caldwell Robert G. , Bultema Rebecca , Longnecker Richard 
Published: May 2005

ABSTRACT
A significant percentage of the population latently harbors Epstein-Barr virus (EBV) in B cells. One EBV-encoded protein, latent membrane protein 2A (LMP2A), is expressed in tissue culture models of EBV latent infection, in human infections, and in many of the EBV-associated proliferative disorders. LMP2A constitutively activates proteins involved in the B-cell receptor (BCR) signal transduction cascade and inhibits the antigen-induced activation of these proteins. In the present study, we investigated whether LMP2A alters B-cell receptor signaling in primary B cells in vivo and in vitro. LMP2A does not inhibit antigen-induced tolerance in response to strong stimuli in an in vivo tolerance model in which B cells are reactive to self-antigen. In contrast, LMP2A bypasses anergy induction in response to low levels of soluble hen egg lysozyme (HEL) both in vivo and in vitro as determined by the ability of LMP2A-expressing HEL-specific B cells to proliferate and induce NF-κB nuclear translocation after exposure to low levels of antigen. Furthermore, LMP2A induces NF-κB nuclear translocation independent of BCR cross-linking. Since NF-κB is required to bypass tolerance induction, this LMP2A-dependent NF-κB activation may complete the tolerogenic signal induced by low levels of soluble HEL. Overall, the findings suggest that LMP2A may not inhibit BCR-induced signals under all conditions as previously suggested by studies with EBV immortalized B cells.
Vaccinia Virus Induces Strong Immunoregulatory Cytokine Production in Healthy Human Epidermal Keratinocytes: a Novel Strategy for Immune Evasion
Authors: Liu Luzheng , Xu Zhan , Fuhlbrigge Robert C. , Peña-Cruz Victor , Lieberman Judy , Kupper Thomas S. 
Published: May 2005

ABSTRACTIatrogenic cutaneous infection with vaccinia virus (VV) and naturally occurring systemic infection with variola virus both lead to the characteristic skin “pox” lesions. Despite significant medical experience with both viruses, surprisingly little is understood about the interactions between these poxviruses and healthy resident skin cells. In recent years, it has become clear that skin plays an essential role in modulating both innate and adaptive immune responses, in part by producing and responding to a variety of cytokines and chemokines upon stimulation. Antagonists of many of these compounds are encoded in poxvirus genomes. Infection of skin cells with poxvirus may lead to a unique pattern of cytokine and chemokine production that might alter the cutaneous immune surveillance function. In this study, we infected primary cultures of human skin cells with VV and monitored antigen expression, virus replication, and cytokine production from the infected cells. While T cells, Langerhans cells, and dermal dendritic cells were infected abortively, keratinocytes, dermal fibroblasts, and dermal microvascular endothelial cells (HMVEC-d) all supported the complete virus life cycle. In contrast to the robust viral replication in fibroblasts and HMVEC-d, only limited viral replication was observed in keratinocytes. Importantly, VV infection of keratinocytes led to up-regulation of immunoregulatory and Th2 cytokines, including transforming growth factor β, interleukin-10 (IL-10), and IL-13. We propose that the rapid induction of keratinocyte Th2 and immunoregulatory cytokines represents a poxvirus strategy to evade immune surveillance, and the limited viral multiplication in keratinocytes may be a protective mechanism to help the immune system “win the race.”
A Virus-Encoded Inhibitor That Blocks RNA Interference in Mammalian Cells
Authors: Sullivan Christopher S. , Ganem Don 
Published: May 2005

ABSTRACT
Nodamura virus (NoV) is a small RNA virus that is infectious for insect and mammalian hosts. We have developed a highly sensitive assay of RNA interference (RNAi) in mammalian cells that shows that the NoV B2 protein functions as an inhibitor of RNAi triggered by either short hairpin RNAs or small interfering RNAs. In the cell, NoV B2 binds to pre-Dicer substrate RNA and RNA-induced silencing complex (RISC)-processed RNAs and inhibits the Dicer cleavage reaction and, potentially, one or more post-Dicer activities. In vitro, NoV B2 inhibits Dicer-mediated RNA cleavage in the absence of any other host factors and specifically binds double-stranded RNAs corresponding in structure to Dicer substrates and products. Its abilities to bind to Dicer precursor and post-Dicer RISC-processed RNAs suggest a mechanism of inhibition that is unique among known viral inhibitors of RNAi.
Universal Influenza B Vaccine Based on the Maturational Cleavage Site of the Hemagglutinin Precursor
Authors: Bianchi Elisabetta , Liang Xiaoping , Ingallinella Paolo , Finotto Marco , Chastain Michael A. , Fan Jiang , Fu Tong-Ming , Song Hong Chang , Horton Melanie S. , Freed Daniel C. , Manger Walter , Wen Emily , Shi Li , Ionescu Roxana , Price Colleen , Wenger Marc , Emini Emilio A. , Cortese Riccardo , Ciliberto Gennaro , Shiver John W. , Pessi Antonello 
Published: May 2005

ABSTRACTConventional influenza vaccines can prevent infection, but their efficacy depends on the degree of antigenic “match” between the strains used for vaccine preparation and those circulating in the population. A universal influenza vaccine based on invariant regions of the virus, able to provide broadly cross-reactive protection, without requiring continuous manufacturing update, would solve a major medical need. Since the temporal and geographical dominance of the influenza virus type and/or subtype (A/H3, A/H1, or B) cannot yet be predicted, a universal vaccine, like the vaccines currently in use, should include both type A and type B influenza virus components. However, while encouraging preclinical data are available for influenza A virus, no candidate universal vaccine is available for influenza B virus. We show here that a peptide conjugate vaccine, based on the highly conserved maturational cleavage site of the HA0precursor of the influenza B virus hemagglutinin, can elicit a protective immune response against lethal challenge with viruses belonging to either one of the representative, non-antigenically cross-reactive influenza B virus lineages. We demonstrate that protection by the HA0vaccine is mediated by antibodies, probably through effector mechanisms, and that a major part of the protective response targets the most conserved region of HA0, the P1 residue of the scissile bond and the fusion peptide domain. In addition, we present preliminary evidence that the approach can be extended to influenza A virus, although the equivalent HA0conjugate is not as efficacious as for influenza B virus.
The Minor Receptor Group of Human Rhinovirus (HRV) Includes HRV23 and HRV25, but the Presence of a Lysine in the VP1 HI Loop Is Not Sufficient for Receptor Binding
Authors: Vlasak Marketa , Roivainen Merja , Reithmayer Manuela , Goesler Irene , Laine Pia , Snyers Luc , Hovi Tapani , Blaas Dieter 
Published: May 2005

ABSTRACT
Like all 10 minor receptor group human rhinoviruses (HRVs), HRV23 and HRV25, previously classified as major group viruses, are neutralized by maltose binding protein (MBP)-V33333 (a soluble recombinant concatemer of five copies of repeat 3 of the very-low-density lipoprotein receptor fused to MBP), bind to low-density lipoprotein receptor in virus overlay blots, and replicate in intercellular adhesion molecule 1 (ICAM-1)-negative COS-7 cells. From phylogenetic analysis of capsid protein VP1-coding sequences, they are also known to cluster together with other minor group strains. Therefore, they belong to the minor group; there are now 12 minor group and 87 major group HRV serotypes. Sequence comparison of the VP1 capsid proteins of all HRVs revealed that the lysine in the HI loop, strictly conserved in the 12 minor group HRVs, is also present in 9 major group serotypes that are neutralized by soluble ICAM-1. Despite the presence of this lysine, they are not neutralized by MBP-V33333 and fail to replicate in COS-7 cells and in HeLa cells in the presence of an ICAM-1-blocking antibody. These nine serotypes are therefore “true” major group viruses.
The Exonuclease and Host Shutoff Functions of the SOX Protein of Kaposi's Sarcoma-Associated Herpesvirus Are Genetically Separable
Authors: Glaunsinger Britt , Chavez Leonard , Ganem Don 
Published: May 2005

ABSTRACT
The Kaposi's sarcoma-associated herpesvirus (KSHV) SOX protein, encoded by ORF37, promotes shutoff of host cell gene expression during lytic viral replication by dramatically impairing mRNA accumulation. SOX is the KSHV homolog of the alkaline exonuclease of other herpesviruses, which has been shown to function as a DNase involved in processing and packaging the viral genome. Although the exonuclease activity of these proteins is widely conserved across all herpesviruses, the host shutoff activity observed for KSHV SOX is not. We show here that SOX expression sharply reduces the half-life of target mRNAs. Extensive mutational analysis reveals that the DNase and host shutoff activities of SOX are genetically separable. Lesions affecting the DNase activity cluster in conserved regions of the protein, but residues critical for mRNA degradation are not conserved across the viral family. Additionally, we present evidence suggesting that the two different functions of SOX occur within distinct cellular compartments—DNase activity in the nucleus and host shutoff activity in the cytoplasm.