The Experts below are selected from a list of 7914 Experts worldwide ranked by ideXlab platform
Christopher Coleclough - One of the best experts on this subject based on the ideXlab platform.
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safety and immunogenicity of an intranasal Sendai Virus based vaccine for human parainfluenza Virus type i and respiratory syncytial Virus sevrsv in adults
Human Vaccines & Immunotherapeutics, 2021Co-Authors: Felicia Scaggs Huang, Karen S. Slobod, Allen Portner, Charles J Russell, Robert E Sealy, David I Bernstein, Toru Takimoto, Michael M Meagher, Bart G Jones, Christopher ColecloughAbstract:SeVRSV is a replication-competent Sendai Virus (SeV)-based vaccine carrying the respiratory syncytial Virus (RSV) fusion protein (F) gene. Unmanipulated, non-recombinant SeV is a murine parainfluen...
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intranasal Sendai Virus vaccine protects african green monkeys from infection with human parainfluenza Virus type one
Vaccine, 1997Co-Authors: Julia L Hurwitz, Mark Y Sangster, Christopher Coleclough, Allen Portner, Kenneth F Soike, Robert E Sealy, Dawn H DawsonAbstract:Human parainfluenza Virus-type I (hPIV-1) infections are a common cause of "group" and hospitalizations among young children. Here we address the possibility of using the xenotropic Sendai Virus [a mouse parainfluenza Virus (PIV)] as a vaccine for hPIV-1. Sendai Virus was administered to six African green monkeys (Cercopithecus aethiops) by the intranasal (i.n.) route. A long lasting Virus-specific antibody response was elicited, both in the serum and nasal cavity. Sendai Virus caused no apparent clinical symptoms in the primates, but live Virus was detected in the nasal cavity for several days after inoculation. No Virus was detected after a second dose of Sendai Virus was administered on day 126 after the initial priming. Animals were challenged with hPIV-1 i.n. on day 154. All six vaccinated animals were fully protected from infection while six of six control animals were infected with hPIV-1. The antibody responses induced by Sendai Virus immunizations proved to be greater than those induced by hPIV-1. These results demonstrate that unmanipulated Sendai Virus is an effective vaccine against hPIV-1 in a primate model and may constitute a practical vaccine for human use.
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human parainfluenza Virus type 1 immunization of infant mice protects from subsequent Sendai Virus infection
Virology, 1995Co-Authors: Mark Y Sangster, Christopher Coleclough, F S Smith, Julia L HurwitzAbstract:Human parainfluenza Virus type 1 (hPIV-1) infections are a common cause of "croup" and hospitalizations among young children, yet no vaccine is yet available. Sendai Virus (mouse PIV-1) is the closest known homologue of hPIV-1. Here we address the possibility of using a xenotropic, nonpathogenic PIV as a vaccine in infants, by assessing the efficacy of hPIV-1 vaccination of infant mice against a subsequent challenge with Sendai Virus. hPIV-1 was administered intranasally to mice age 3-6 days and shown by serum antibody ELISA and elispot analysis to elicit Virus-specific IgM and isotype-switched antibody-forming cells (AFC). The response was completely cross-reactive between hPIV-1 and Sendai Virus. Mice were challenged with Sendai Virus 6-8 weeks later and generated AFC and serum antibody responses composed of IgM, as well as IgG and IgA, unlike challenged, age-matched controls. The high IgM response among AFC was not seen in mice primed as adults with hPIV-1 and challenged with Sendai Virus. The hPIV-1 priming of infant mice afforded protection, as the majority of these mice survived the lethal Sendai Virus challenge, as did all adult primed animals. These data support the notion that the unmodified xenotropic Sendai Virus might function effectively in human infants as a vaccine against hPIV-1.
Allen Portner - One of the best experts on this subject based on the ideXlab platform.
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safety and immunogenicity of an intranasal Sendai Virus based vaccine for human parainfluenza Virus type i and respiratory syncytial Virus sevrsv in adults
Human Vaccines & Immunotherapeutics, 2021Co-Authors: Felicia Scaggs Huang, Karen S. Slobod, Allen Portner, Charles J Russell, Robert E Sealy, David I Bernstein, Toru Takimoto, Michael M Meagher, Bart G Jones, Christopher ColecloughAbstract:SeVRSV is a replication-competent Sendai Virus (SeV)-based vaccine carrying the respiratory syncytial Virus (RSV) fusion protein (F) gene. Unmanipulated, non-recombinant SeV is a murine parainfluen...
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safety and immunogenicity of intranasal murine parainfluenza Virus type 1 Sendai Virus in healthy human adults
Vaccine, 2004Co-Authors: Karen S. Slobod, Jerry L Shenep, Jorge Lujanzilbermann, Kim J Allison, Brita Brown, Ruth Ann Scroggs, Allen Portner, Chris ColecloughAbstract:Abstract Human parainfluenza Virus-type 1 (hPIV-1) is the most common cause of pediatric laryngotracheobronchitis (croup) and results in close to 30,000 US hospitalizations each year [Ped. Inf. Dis. J. 20 (2001) 646]. No effective vaccine is available. We examined murine PIV-1 (Sendai Virus, SeV) as a live, xenotropic vaccine for the closely related human PIV-1 in a phase I, dose escalation study in healthy adults. Intranasal Sendai Virus was uniformly well-tolerated and showed evidence of immunogenicity in three of nine vaccinees despite pre-existing, cross-reactive immunity presumably induced by previous exposure to human PIV-1. Results encourage future trials to evaluate the efficacy of Sendai Virus in preventing human PIV-1 infection in infants and children.
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intranasal Sendai Virus vaccine protects african green monkeys from infection with human parainfluenza Virus type one
Vaccine, 1997Co-Authors: Julia L Hurwitz, Mark Y Sangster, Christopher Coleclough, Allen Portner, Kenneth F Soike, Robert E Sealy, Dawn H DawsonAbstract:Human parainfluenza Virus-type I (hPIV-1) infections are a common cause of "group" and hospitalizations among young children. Here we address the possibility of using the xenotropic Sendai Virus [a mouse parainfluenza Virus (PIV)] as a vaccine for hPIV-1. Sendai Virus was administered to six African green monkeys (Cercopithecus aethiops) by the intranasal (i.n.) route. A long lasting Virus-specific antibody response was elicited, both in the serum and nasal cavity. Sendai Virus caused no apparent clinical symptoms in the primates, but live Virus was detected in the nasal cavity for several days after inoculation. No Virus was detected after a second dose of Sendai Virus was administered on day 126 after the initial priming. Animals were challenged with hPIV-1 i.n. on day 154. All six vaccinated animals were fully protected from infection while six of six control animals were infected with hPIV-1. The antibody responses induced by Sendai Virus immunizations proved to be greater than those induced by hPIV-1. These results demonstrate that unmanipulated Sendai Virus is an effective vaccine against hPIV-1 in a primate model and may constitute a practical vaccine for human use.
David L Woodland - One of the best experts on this subject based on the ideXlab platform.
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functionally heterogeneous cd8 t cell memory is induced by Sendai Virus infection of mice
Journal of Virology, 1999Co-Authors: Edward J Usherwood, Robert J Hogan, David L Woodland, Twala L Hogg, Graham Crowther, Sherri L Surman, John D AltmanAbstract:It has recently been established that memory CD8(+) T cells induced by viral infection are maintained at unexpectedly high frequencies in the spleen. While it has been established that these memory cells are phenotypically heterogeneous, relatively little is known about the functional status of these cells. Here we investigated the proliferative potential of CD8(+) memory T cells induced by Sendai Virus infection. High frequencies of CD8(+) T cells specific for both dominant and subdominant Sendai Virus epitopes persisted for many weeks after primary infection, and these cells were heterogeneous with respect to CD62L expression (approximately 20% CD62L(hi) and 80% CD62L(lo)). Reactivation of these cells with the antigenic peptide in vitro induced strong proliferation of antigen-specific CD8(+) T cells. However, approximately 20% of the cells failed to proliferate in vitro in response to a cognate peptide but nevertheless differentiated into effector cells and acquired full cytotoxic potential. These cells also expressed high levels of CD62L (in marked contrast to the CD62L(lo) status of the proliferating cells in the culture). Direct isolation of CD62L(hi) and CD62L(lo) CD8(+) T cells from memory mice confirmed the correlation of this marker with proliferative potential. Taken together, these data demonstrate that Sendai Virus infection induces high frequencies of memory CD8(+) T cells that are highly heterogeneous in terms of both their phenotype and their proliferative potential.
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induction of cd8 t cell responses to dominant and subdominant epitopes and protective immunity to Sendai Virus infection by dna vaccination
Journal of Immunology, 1998Co-Authors: Yongjin Chen, Robert G Webster, David L WoodlandAbstract:While recent studies have demonstrated that DNA vaccination induces potent CD8 + T cell memory in vivo, it is unclear whether this memory is qualitatively and quantitatively comparable with that induced by natural viral infection. In the current studies, we have investigated the induction of CD8 + memory CTL responses to Sendai Virus nucleoprotein (NP) in C57BL/6 mice following gene gun vaccination. The data demonstrate that this mode of vaccination induces potent long-lived memory CTL precursors (CTLp) specific for both the dominant (NP 324–332 /K b ) and the subdominant (NP 324–332 /D b ) epitopes of NP. The frequencies of T cells specific for each of these epitopes in the spleen is about 1:2000 CD8 + T cells, similar to those induced by intranasal infection with Sendai Virus. Moreover, the induction of memory CTLp by DNA vaccination is independent of MHC class II molecules or Ab, as is the case for memory CTLp induction by live Sendai Virus infection. CTLp specific for both epitopes are capable of migrating to the lung following Sendai Virus infection and express potent cytotoxic activity at the site of infection. Consistent with this activity, DNA vaccination with Sendai Virus NP induced a substantial degree of Ab-independent protection from a challenge with a lethal dose of Sendai Virus. Taken together, these data demonstrate that for the parameters tested, DNA vaccination is indistinguishable from live Virus infection in terms of priming functional memory CTLp with broad specificity for both dominant and subdominant T cell epitopes.
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efficient priming of cd8 memory t cells specific for a subdominant epitope following Sendai Virus infection
Journal of Immunology, 1997Co-Authors: G A Cole, Twala L Hogg, M A Coppola, David L WoodlandAbstract:The relationship between the primary effector CTL response to viral infection and the subsequent pool of memory CTL precursors (CTLp) is poorly understood. Here, we have analyzed the induction of both effector CTL and memory CTLp to dominant and subdominant epitopes following Sendai Virus infection of C57BL/6 mice. A single peptide derived from the Sendai Virus nucleoprotein (NP(324-332)) binds to both H-2 Kb and Db MHC class I molecules, generating both immunodominant (NP(324-332)/Kb) and subdominant (NP(324-332)/Db) epitopes. Following intranasal Sendai Virus infection, NP(324-332)/Kb-specific CTL dominated the primary effector CTL response in the lung and were present at high frequency in the memory CTLp pool. In contrast, NP(324-332)/Db-specific CTL were not a detectable component of the effector response to primary Sendai Virus infection. However, memory CTLp specific for this subdominant epitope were induced at frequencies approaching those of CTLp specific for the immunodominant epitope. These data indicate that memory CTLp specific for subdominant epitopes can be primed by Sendai Virus infection in the absence of a detectable effector response. To determine whether CTLp memory to subdominant epitopes is functional in the context of Sendai Virus infection, memory CTLp specific for a subdominant epitope were selectively primed by vaccination. These cells dominated the subsequent effector CTL response to Sendai Virus infection, demonstrating that memory CTLp primed against subdominant epitopes can participate in an immune response and effectively compete with T cells specific for immunodominant epitopes. These data have implications for the development of vaccines designed to emphasize cellular immunity.
Julia L Hurwitz - One of the best experts on this subject based on the ideXlab platform.
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intranasal Sendai Virus vaccine protects african green monkeys from infection with human parainfluenza Virus type one
Vaccine, 1997Co-Authors: Julia L Hurwitz, Mark Y Sangster, Christopher Coleclough, Allen Portner, Kenneth F Soike, Robert E Sealy, Dawn H DawsonAbstract:Human parainfluenza Virus-type I (hPIV-1) infections are a common cause of "group" and hospitalizations among young children. Here we address the possibility of using the xenotropic Sendai Virus [a mouse parainfluenza Virus (PIV)] as a vaccine for hPIV-1. Sendai Virus was administered to six African green monkeys (Cercopithecus aethiops) by the intranasal (i.n.) route. A long lasting Virus-specific antibody response was elicited, both in the serum and nasal cavity. Sendai Virus caused no apparent clinical symptoms in the primates, but live Virus was detected in the nasal cavity for several days after inoculation. No Virus was detected after a second dose of Sendai Virus was administered on day 126 after the initial priming. Animals were challenged with hPIV-1 i.n. on day 154. All six vaccinated animals were fully protected from infection while six of six control animals were infected with hPIV-1. The antibody responses induced by Sendai Virus immunizations proved to be greater than those induced by hPIV-1. These results demonstrate that unmanipulated Sendai Virus is an effective vaccine against hPIV-1 in a primate model and may constitute a practical vaccine for human use.
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human parainfluenza Virus type 1 immunization of infant mice protects from subsequent Sendai Virus infection
Virology, 1995Co-Authors: Mark Y Sangster, Christopher Coleclough, F S Smith, Julia L HurwitzAbstract:Human parainfluenza Virus type 1 (hPIV-1) infections are a common cause of "croup" and hospitalizations among young children, yet no vaccine is yet available. Sendai Virus (mouse PIV-1) is the closest known homologue of hPIV-1. Here we address the possibility of using a xenotropic, nonpathogenic PIV as a vaccine in infants, by assessing the efficacy of hPIV-1 vaccination of infant mice against a subsequent challenge with Sendai Virus. hPIV-1 was administered intranasally to mice age 3-6 days and shown by serum antibody ELISA and elispot analysis to elicit Virus-specific IgM and isotype-switched antibody-forming cells (AFC). The response was completely cross-reactive between hPIV-1 and Sendai Virus. Mice were challenged with Sendai Virus 6-8 weeks later and generated AFC and serum antibody responses composed of IgM, as well as IgG and IgA, unlike challenged, age-matched controls. The high IgM response among AFC was not seen in mice primed as adults with hPIV-1 and challenged with Sendai Virus. The hPIV-1 priming of infant mice afforded protection, as the majority of these mice survived the lethal Sendai Virus challenge, as did all adult primed animals. These data support the notion that the unmodified xenotropic Sendai Virus might function effectively in human infants as a vaccine against hPIV-1.
Wolfgang J Neubert - One of the best experts on this subject based on the ideXlab platform.
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Sendai Virus vectors as an emerging negative strand rna viral vector system
Journal of Gene Medicine, 2003Co-Authors: Michael Bitzer, S. Armeanu, Ulrich M Lauer, Wolfgang J NeubertAbstract:The power to manipulate the genome of negative-strand RNA Viruses, including the insertion of additional non-viral genes, has led to the development of a new class of viral vectors for gene transfer approaches. The murine parainfluenza Virus type I, or Sendai Virus (SeV), has emerged as a prototype Virus of this vector group, being employed in numerous in vitro as well as animal studies over the last few years. Extraordinary features of SeV are the remarkably brief contact time that is necessary for cellular uptake, a strong but adjustable expression of foreign genes, efficient infection in the respiratory tract despite a mucus layer, transduction of target cells being independent of the cell cycle, and an exclusively cytoplasmic replication cycle without any risk of chromosomal integration. In this review we describe the current knowledge of Sendai Virus vector (SeVV) development as well as the results of first-generation vector applications under both in vitro and in vivo conditions. So far, Sendai Virus vectors have been identified to be a highly efficient transduction tool for a broad range of different tissues and applications. Future directions in vector design and development are discussed.
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Caspase-8 and Apaf-1-independent Caspase-9 Activation in Sendai Virus-infected Cells
The Journal of biological chemistry, 2002Co-Authors: Michael Bitzer, S. Armeanu, Florian Prinz, Guy Ungerechts, Wolfgang A. Wybranietz, Martin Spiegel, Christian Bernlöhr, Francesco Cecconi, Michael Gregor, Wolfgang J NeubertAbstract:Apoptotic cell death is of central importance in the pathogenesis of viral infections. Activation of a cascade of cysteine proteases, i.e. caspases, plays a key role in the effector phase of Virus-induced apoptosis. However, little is known about pathways leading to the activation of initiator caspases in Virus-infected host cells. Recently, we have shown that Sendai Virus (SeV) infection triggers apoptotic cell death by activation of the effector caspase-3 and initiator caspase-8. We now investigated mechanisms leading to the activation of another initiator caspase, caspase-9. Unexpectedly we found that caspase-9 cleavage is not dependent on the presence of active caspases-3 or -8. Furthermore, the presence of caspase-9 in mouse embryonic fibroblast (MEF) cells was a prerequisite for Sendai Virus-induced apoptotic cell death. Caspase-9 activation occurred without the release of cytochrome c from mitochondria and was not dependent on the presence of Apaf-1 or reactive oxygen intermediates. Our results therefore suggest an alternative mechanism for caspase-9 activation in virally infected cells beside the well characterized pathways via death receptors or mitochondrial cytochrome c release.
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long term replication of Sendai Virus defective interfering particle nucleocapsids in stable helper cell lines
Journal of Virology, 1994Co-Authors: W Willenbrink, Wolfgang J NeubertAbstract:An essential prerequisite for generating a stable helper cell line, which constitutively expresses functional Sendai Virus RNA-dependent RNA polymerase, is the expression of all three Sendai Virus nucleocapsid (NC) proteins, NP, P, and L, simulataneously. Generating a stable helper cell line was accomplished by cotransfecting cell line 293 with all three corresponding viral genes under the control of cytomegaloVirus promoter-enhancer elements. Cotransfection with a dominant selectable marker enabled selection for stably transfected cells. The levels of the expressed P and NP proteins reached up to 1/10th and 1/20th of the protein levels in Sendai Virus-infected cells, respectively. The Sendai Virus polymerase activity of the coexpressed proteins was demonstrated by an in vivo polymerase assay. The cell clone H29 gave the strongest signal and produced DI genomes continuously for at least 3 months. This result demonstrates that it is possible to stably express adequate levels of all three viral NC proteins to form Sendai Virus polymerase activity, thereby performing the replication and encapsidation of viral RNA, essential prerequisites for a helper cell line to be competent in producing recombinant Viruses.
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rapid sequencing of the Sendai Virus 6 8 kb large l gene through primer walking with an automated dna sequencer
Journal of Virological Methods, 1992Co-Authors: H Giesecke, B Obermaier, H Domdey, Wolfgang J NeubertAbstract:The determination of the complete DNA sequence of the large (L) polymerase gene of Sendai Virus strain Fushimi was used to explore the potential and feasibility of primer walking with fluorescent dye-labelled dideoxynucleotide terminators on an automated ABI DNA sequencer. The rapid identification of the complete sequence demonstrated that this approach is a time- and cost-saving alternative to classical sequencing techniques. Analysis of the data revealed that the L gene of Sendai Virus strain Fushimi consists of exactly 6800 nucleotides and that the deduced amino acid sequence identifies a single open reading frame encoding a protein of 252.876 kDa. In contrast to Sendai Virus strain Enders, the L mRNA of strain Fushimi is monocistronic. The comparison of the deduced amino acid sequences of the L genes of three different Sendai Virus strains confirmed the existence of conserved as well as variable regions in the L protein and revealed a high grade of conservation in the carboxyterminal third. Furthermore, functional amino acid sequence motifs, like elements of RNA-dependent RNA polymerases and ATP-binding sites as postulated previously, were identified.
