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S. Scherneck - One of the best experts on this subject based on the ideXlab platform.
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Hamster Polyomavirus-derived virus-like particles are able to transfer in vitro encapsidated plasmid DNA to mammalian cells
Virus Genes, 2007Co-Authors: Tatyana Voronkova, S. Scherneck, Muhsin Özel, Andris Kazaks, Velta Ose, Paul Pumpens, Rainer UlrichAbstract:The authentic major capsid protein 1 (VP1) of Hamster Polyomavirus (HaPyV) consists of 384 amino acid (aa) residues (42 kDa). Expression from an additional in-frame initiation codon located upstream from the authentic VP1 open reading frame (at position −4) might result in the synthesis of a 388 aa-long, amino-terminally extended VP1 (aa −4 to aa 384; VP1^ext). In a plasmid-mediated Drosophila Schneider (S2) cell expression system, both VP1 derivatives as well as a VP1^ext variant with an amino acid exchange of the authentic Met1Gly (VP1^ext-M1) were expressed to a similar high level. Although all three proteins were detected in nuclear as well as cytoplasmic fractions, formation of virus-like particles (VLPs) was observed exclusively in the nucleus as confirmed by negative staining electron microscopy. The use of a tryptophan promoter-driven Escherichia coli expression system resulted in the efficient synthesis of VP1 and VP1^ext and formation of VLPs. In addition, establishment of an in vitro disassembly/reassembly system allowed the encapsidation of plasmid DNA into VLPs. Encapsidated DNA was found to be protected against the action of DNase I. Mammalian COS-7 and CHO cells were transfected with HaPyV-VP1-VLPs carrying a plasmid encoding enhanced green fluorescent protein (eGFP). In both cell lines eGFP expression was detected indicating successful transfer of the plasmid into the cells, though at a still low level. Cesium chloride gradient centrifugation allowed the separation of VLPs with encapsidated DNA from “empty” VLPs, which might be useful for further optimization of transfection. Therefore, heterologously expressed HaPyV-VP1 may represent a promising alternative carrier for foreign DNA in gene transfer applications.
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chimeric bacteriophage fr virus like particles harboring the immunodominant c terminal region of Hamster Polyomavirus vp1 induce a strong vp1 specific antibody response in rabbits and mice
Viral Immunology, 2002Co-Authors: Tatyana Voronkova, S. Scherneck, Wolfgang Arnold, Burkhard Jandrig, Kestutis Sasnauskas, Andris Kazaks, Velta Ose, Adrian Grosch, Dace Skrastina, Paul PumpensAbstract:The late region of the Hamster Polyomavirus (HaPyV, former HaPV) genome encodes three structural proteins VP1, VP2, and VP3, where VP1 represents the major capsid protein of 384 amino acids. Screening of sera from HaPyV-infected papilloma-bearing and papilloma-free Hamsters demonstrated the immunodominant features of all three capsid proteins. For both groups of Hamsters in the C-terminal region of VP1 immunodominant B-cell epitopes were identified in the regions between amino acids 305 and 351 and amino acids 351 and 384. The high flexibility of the C-terminal region of VP1 was confirmed by the formation of chimeric virus-like particles based on the coat protein of the RNA bacteriophage fr which was previously found to tolerate only very short-sized foreign insertions. Phage fr coat protein-derived virus-like particles tolerated the N-terminal fusion of amino acids 333-384, 351-384, 351-374, and 364-384, respectively, of VP1. The induction of VP1-specific antibodies in rabbits and mice by immunization with chimeric virus-like particles harboring amino acids 333-384, 351-384, and 364-384, respectively, of VP1 suggested the immunodominant nature of the C-terminal region of VP1.
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the Hamster Polyomavirus a brief review of recent knowledge
Virus Genes, 2001Co-Authors: S. Scherneck, Rainer Ulrich, J FeunteunAbstract:The Hamster Polyomavirus (HaPV) was first described in 1967 as a virus associated with skin epithelioma of the Syrian Hamster. The tumors appear spontaneously in a Hamster colony bred in Berlin-Buch (HaB). Virus particles isolated from skin epitheliomas cause lymphoma and leukemia when injected into newborn Hamsters from a distinct colony bred in Potsdam, Germany (HaP). The viral genome has been totally sequenced and the overall genetic organization establishes HaPV as a member of the Polyomaviruses. HaPV is a second example of an middle T (MT) antigen encoding Polyomavirus and nucleotide sequence homologies designates the mouse Polyomavirus (Py) as the closest relative. Lymphomas induced by HaPV in HaP Hamsters do not contain virus particles but instead accumulate different amounts of nonrandomly deleted free and/or integrated viral genomes. Transgenic mice produced by microinjection of HaPV DNA into the pronucleus of fertilized eggs of Gat: NMRI mice developed both, epitheliomas and lymphomas. Both tumor types contain extrachromosomal DNA. HaPV DNA was found to replicate in Hamster lymphoid and fibroblast cell lines. Fully reproductive cycles could be detected only in GD36 lymphoblastic leukemia cells. HaPV carries the full transforming properties of a Polyomavirus in vitro. Immortalization of primary rat cells is essentially carried out by the HaPV large T (LT) antigen and coexpression of HaPV MT and HaPV small T (ST) antigen is required for full transformation of rat fibroblasts. The preferential binding of HaPV MT to c-Fyn, a Src family kinase, has been proposed as a mechanism leading to lymphoid malignancies. Heterologous expression of HaPV-VP1 allowed the formation of virus like particles (VLPs) resembling HaPV particles. The high flexibility of HaPV-VP1 for insertion of foreign peptides offers a broad range of potential applications, especially in vaccine development.
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Formation of Immunogenic Virus-like Particles by Inserting Epitopes into Surface-Exposed Regions of Hamster Polyomavirus Major Capsid Protein
Virology, 2000Co-Authors: Alma Gedvilaite, S. Scherneck, Cornelius Frommel, Burkhard Jandrig, Kestutis Sasnauskas, Burkhard Micheel, Muhsin Özel, Olaf Behrsing, Juozas Staniulis, Rainer UlrichAbstract:Abstract We generated highly immunogenic virus-like particles that are based on the capsid protein VP1 of the Hamster Polyomavirus (HaPV-VP1) and harbor inserted foreign epitopes. The HaPV-VP1 regions spanning amino acids 81–88 (position 1), 222/223 (2), 244–246 (3), and 289–294 (4) were predicted to be surface exposed. An epitope of the pre-S1 region of the hepatitis B virus (designated S1; amino acid sequence DPAFR) was introduced into the predicted positions of VP1. All VP1/S1 fusion proteins were expressed in yeast and generated virus-like particles. Immunoassays using the S1-specific monoclonal antibody MA18/7 and immunization of C57Bl6 mice with different VP1/S1 constructs showed a pronounced reactivity and a strong S1-specific antibody response for particles carrying the insert in position 1, 2, 1+2, and 1+3. Our results suggest that HaPV-VP1 represents a highly flexible carrier moiety for the insertion of foreign sequences offering a broad range of potential uses, especially in vaccine development.
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an immunodominant cross reactive b cell epitope region is located at the c terminal part of the Hamster Polyomavirus major capsid protein vp1
Viral Immunology, 2000Co-Authors: Hassen Siray, S. Scherneck, Cornelius Frommel, Tatyana Voronkova, Stefanie Hahn, Wolfgang Arnold, Jens Schneidermergener, Rainer G UlrichAbstract:ABSTRACT The VP1 represents the major capsid protein of the Hamster Polyomavirus (HaPV). Here we describe the mapping of epitopes along the VP1 using Escherichia coli-expressed VP1-dihydrofolate re...
J Feunteun - One of the best experts on this subject based on the ideXlab platform.
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the Hamster Polyomavirus a brief review of recent knowledge
Virus Genes, 2001Co-Authors: S. Scherneck, Rainer Ulrich, J FeunteunAbstract:The Hamster Polyomavirus (HaPV) was first described in 1967 as a virus associated with skin epithelioma of the Syrian Hamster. The tumors appear spontaneously in a Hamster colony bred in Berlin-Buch (HaB). Virus particles isolated from skin epitheliomas cause lymphoma and leukemia when injected into newborn Hamsters from a distinct colony bred in Potsdam, Germany (HaP). The viral genome has been totally sequenced and the overall genetic organization establishes HaPV as a member of the Polyomaviruses. HaPV is a second example of an middle T (MT) antigen encoding Polyomavirus and nucleotide sequence homologies designates the mouse Polyomavirus (Py) as the closest relative. Lymphomas induced by HaPV in HaP Hamsters do not contain virus particles but instead accumulate different amounts of nonrandomly deleted free and/or integrated viral genomes. Transgenic mice produced by microinjection of HaPV DNA into the pronucleus of fertilized eggs of Gat: NMRI mice developed both, epitheliomas and lymphomas. Both tumor types contain extrachromosomal DNA. HaPV DNA was found to replicate in Hamster lymphoid and fibroblast cell lines. Fully reproductive cycles could be detected only in GD36 lymphoblastic leukemia cells. HaPV carries the full transforming properties of a Polyomavirus in vitro. Immortalization of primary rat cells is essentially carried out by the HaPV large T (LT) antigen and coexpression of HaPV MT and HaPV small T (ST) antigen is required for full transformation of rat fibroblasts. The preferential binding of HaPV MT to c-Fyn, a Src family kinase, has been proposed as a mechanism leading to lymphoid malignancies. Heterologous expression of HaPV-VP1 allowed the formation of virus like particles (VLPs) resembling HaPV particles. The high flexibility of HaPV-VP1 for insertion of foreign peptides offers a broad range of potential applications, especially in vaccine development.
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THE N TERMINUS OF Hamster Polyomavirus MIDDLE T ANTIGEN CARRIES A DETERMINANT FOR SPECIFIC ACTIVATION OF P59C-FYN
Journal of virology, 1997Co-Authors: Laurence Goutebroze, N Dunant, K Ballmer-hofer, J FeunteunAbstract:Transformation by rodent Polyomaviruses is mediated primarily by middle T antigen, a membrane-bound protein that does not carry an intrinsic enzymatic activity but interacts and subverts the activity of cellular regulators of proliferation. The multiple protein partners of murine Polyomavirus (Py) middle T antigen include the tyrosine kinases c-Src and, to a lesser extent, c-Fyn and c-Yes. By contrast, the Hamster Polyomavirus (HaPV) middle T antigen selectively activates the c-Fyn gene product. This difference may account for the contrasting tumor patterns induced by the two viruses. The sequences of the respective N-terminal and C-terminal functional domains of murine Py and HaPV middle T antigens are highly conserved whereas the intervening stretches are clearly divergent, leading to the speculation that this divergence may direct the specificity for tyrosine kinase activation. We have addressed this issue by constructing a chimera middle T antigen molecule carrying the N-terminal domain from HaPV (exon 1) in phase with the other two domains from murine Py (exon 2). The biological properties of this chimera molecule are indistinguishable from those of HaPV middle T antigen; it specifically activates p59c-Fyn and carries the transforming phenotype of the HaPV middle T antigen on rat fibroblasts.
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The Hamster Polyomavirus
Infectious Agents and Pathogenesis, 1995Co-Authors: S. Scherneck, J FeunteunAbstract:The Hamster Polyomavirus (HaPV) was originally described in 1967 by Graffi et al. as a virus associated with skin epithelioma of the Syrian Hamster.(1–4) The tumors appear spontaneously in animals at about 3 months to more than 1 year of age in a laboratory colony bred in Berlin Buch, Germany (HaB). Virus-particles identified in cell extracts prepared from skin epitheliomas cause lymphoma and leukemia when injected into newborn Hamsters from a distinct and practically tumor-free colony bred in Potsdam, Germany (HaP). In contrast to the skin epithelioma, the hematopoietic tumors are virus-free but accumulate large numbers of nonran-domly deleted extrachromosomal viral DNA. Although HaPV interaction with keratinized cells may be reminiscent of the papillomavirus life cycle, the recent characterization of the viral genome classifies it as a Polyomavirus. However, the HaPV tumor spectrum, which reflects the capacity of the virus to infect both undifferentiated keratinocytes and lymphocytes, is unique within the papovavirus family and raises interesting questions concerning the expression and interaction of viral oncogenes in different cellular contexts (Fig. 1). It should be emphasized that the HaPV described in the review may not be a singular isolate: a closely related virus has been described as the etiological agent of Syrian Hamster skin epithelioma in Alabama.(5)
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mutations within the Hamster Polyomavirus large t antigen domain involved in prb binding impair virus productive cycle and immortalization capacity
Oncogene, 1993Co-Authors: Laurence Goutebroze, S. Scherneck, J FeunteunAbstract:Hamster Polyomavirus (HaPV) causes lymphoma and leukemia when injected into newborn Syrian Hamsters and achieves full transformation of rodent fibroblasts in vitro. It offers a comprehensive model to study at a molecular level the contributions of the viral oncogenes to neoplastic transformation in vitro and in the animal. We have investigated the ability of HaPV large T antigen to form a complex with the product of the retinoblastoma gene (pRb) in vitro. In this report, we demonstrate that HaPV large T antigen can indeed complex the pRb polypeptide. In order to investigate to what extent this interaction might contribute to tumor induction by the virus, we have introduced two different point mutations within the putative pRb-binding sequence of large T antigen, and as a preliminary to in vivo experiments we have studied their effects in vitro on some biological activities relevant to tumor induction. We show that the substitution (Glu-134-->Lys) obliterates pRb binding, suggesting that Glu-134 participates in the interaction between pRb and large T antigen, whereas the substitution (Glu-135-->Lys) has no effect. The Lys-134 mutation is strongly deleterious to the immortalization capacity of the viral genome, whereas the Lys-135 mutation has no effect. Neither of the two mutations affects the capacity of the viral genome to induce foci formation in the rat established cell line F111. These results indicate that the interaction between large T and pRb is required in the immortalization process but irrelevant to transformation. Both mutants show at least partial impairment of replication and productive cycle.
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distinct segments of the Hamster Polyomavirus regulatory region have differential effects on dna replication
Journal of General Virology, 1993Co-Authors: J FeunteunAbstract:The replication of plasmids containing various fragments of the Hamster Polyomavirus (HaPV) DNA non-coding region was tested in a permissive Hamster cell line. We first investigated the importance of some methodological parameters including the time course and the amount of transfecting plasmid DNA and have shown that these factors can greatly influence the relative amount of newly replicated DNA accumulated within the transfected cells. Taking these into account, quantitative comparisons could be made showing the effect of various parts of the regulatory sequence on the HaPV DNA replication.
J Feunteun - One of the best experts on this subject based on the ideXlab platform.
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episomal amplification or chromosomal integration of the viral genome alternative pathways in Hamster Polyomavirus induced lymphomas
Journal of Virology, 1995Co-Authors: S Mazur, J FeunteunAbstract:The state and expression of the Hamster Polyomavirus genome in a large panel of virus-induced lymphomas have been investigated. The viral genome is present within tumor cells either as abundant nonrandomly deleted extrachromosomal copies or as a single copy integrated into cellular DNA. We show that these two physical states are likely to be functionally equivalent: first, deletion and integration of the viral genome both inactivate the late coding region; second, the amount of viral early RNAs yielded by a single integrated copy appears to be very similar to that associated with several thousands of extrachromosomal copies of the viral genome. These data underline two essential requisites for Hamster Polyomavirus to become lymphomagenous: suppression of the late coding functions of the viral genome and expression of the viral oncogenes above a threshold level.
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in vivo replication of the Hamster Polyomavirus genome and generation of specific deletions in the process of lymphomagenesis
Journal of Virology, 1994Co-Authors: S Mazur, M Goodhardt, J FeunteunAbstract:Hamster Polyomavirus (HaPV) causes lymphomas when injected into newborn Hamsters. These tumors are virus-free but accumulate large amounts of deleted extrachromosomal viral genomes. In order to identify the major sites of virus replication in animals, we have monitored the HaPV DNA present in different organs at various times after injection. The data demonstrate that viral replication preferentially occurs in lymphoid organs. Lymphoma-associated viral genomes display specific deletions. PCR analysis shows that such viral genomes are the only variants detectable in infected animals, suggesting that they are generated by a specific cellular mechanism. We have tested the possible role of the lymphoid cell-specific V(D)J recombination activity in the generation of these specific variants. Our results indicate that this mechanism is not solely responsible for the viral genome rearrangement, if involved at all.
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viral genomes maintained extrachromosomally in Hamster Polyomavirus induced lymphomas display a cell specific replication in vitro
Journal of Virology, 1993Co-Authors: S Mazur, J FeunteunAbstract:Hamster Polyomavirus causes lymphomas when injected into newborn Syrian Hamsters. Large amounts of extrachromosomal viral genomes are accumulated in the lymphoma cells. These genomes are characterized by deletions affecting the late coding region as well as a specific part of the noncoding regulatory region. By contrast with wild-type genomes, lymphoma-associated genomes replicate in a lymphoblastoid cell line but not in a fibroblastic cell line. The deletion acts in a cis-dominant manner and is the primary determinant of this host-range effect on replication. The boundaries of the regulatory region necessary for viral DNA replication in the two cell contexts have been defined. The regulatory region can be functionally divided in two domains: one domain (distal from the origin of replication) is necessary for viral genome replication in fibroblasts, whereas the other domain (proximal to the origin of replication) is functional only in the lymphoblastoid cell context and contains the sequence specifically conserved in the lymphoma-associated genomes. This sequence harbors a motif recognized by a lymphoblastoid cell-specific trans-acting factor.
S Mazur - One of the best experts on this subject based on the ideXlab platform.
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episomal amplification or chromosomal integration of the viral genome alternative pathways in Hamster Polyomavirus induced lymphomas
Journal of Virology, 1995Co-Authors: S Mazur, J FeunteunAbstract:The state and expression of the Hamster Polyomavirus genome in a large panel of virus-induced lymphomas have been investigated. The viral genome is present within tumor cells either as abundant nonrandomly deleted extrachromosomal copies or as a single copy integrated into cellular DNA. We show that these two physical states are likely to be functionally equivalent: first, deletion and integration of the viral genome both inactivate the late coding region; second, the amount of viral early RNAs yielded by a single integrated copy appears to be very similar to that associated with several thousands of extrachromosomal copies of the viral genome. These data underline two essential requisites for Hamster Polyomavirus to become lymphomagenous: suppression of the late coding functions of the viral genome and expression of the viral oncogenes above a threshold level.
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in vivo replication of the Hamster Polyomavirus genome and generation of specific deletions in the process of lymphomagenesis
Journal of Virology, 1994Co-Authors: S Mazur, M Goodhardt, J FeunteunAbstract:Hamster Polyomavirus (HaPV) causes lymphomas when injected into newborn Hamsters. These tumors are virus-free but accumulate large amounts of deleted extrachromosomal viral genomes. In order to identify the major sites of virus replication in animals, we have monitored the HaPV DNA present in different organs at various times after injection. The data demonstrate that viral replication preferentially occurs in lymphoid organs. Lymphoma-associated viral genomes display specific deletions. PCR analysis shows that such viral genomes are the only variants detectable in infected animals, suggesting that they are generated by a specific cellular mechanism. We have tested the possible role of the lymphoid cell-specific V(D)J recombination activity in the generation of these specific variants. Our results indicate that this mechanism is not solely responsible for the viral genome rearrangement, if involved at all.
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viral genomes maintained extrachromosomally in Hamster Polyomavirus induced lymphomas display a cell specific replication in vitro
Journal of Virology, 1993Co-Authors: S Mazur, J FeunteunAbstract:Hamster Polyomavirus causes lymphomas when injected into newborn Syrian Hamsters. Large amounts of extrachromosomal viral genomes are accumulated in the lymphoma cells. These genomes are characterized by deletions affecting the late coding region as well as a specific part of the noncoding regulatory region. By contrast with wild-type genomes, lymphoma-associated genomes replicate in a lymphoblastoid cell line but not in a fibroblastic cell line. The deletion acts in a cis-dominant manner and is the primary determinant of this host-range effect on replication. The boundaries of the regulatory region necessary for viral DNA replication in the two cell contexts have been defined. The regulatory region can be functionally divided in two domains: one domain (distal from the origin of replication) is necessary for viral genome replication in fibroblasts, whereas the other domain (proximal to the origin of replication) is functional only in the lymphoblastoid cell context and contains the sequence specifically conserved in the lymphoma-associated genomes. This sequence harbors a motif recognized by a lymphoblastoid cell-specific trans-acting factor.
Rainer G Ulrich - One of the best experts on this subject based on the ideXlab platform.
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Hamster Polyomavirus research past present and future
Viruses, 2021Co-Authors: Burkhard Jandrig, Alma Gedvilaite, Hans Krause, Wolfgang Zimmermann, Emilija Vasiliunaite, Rainer G UlrichAbstract:Hamster Polyomavirus (Mesocricetus auratus Polyomavirus 1, HaPyV) was discovered as one of the first rodent Polyomaviruses at the end of the 1960s in a colony of Syrian Hamsters (Mesocricetus auratus) affected by skin tumors. Natural HaPyV infections have been recorded in Syrian Hamster colonies due to the occurrence of skin tumors and lymphomas. HaPyV infections of Syrian Hamsters represent an important and pioneering tumor model. Experimental infections of Syrian Hamsters of different colonies are still serving as model systems (e.g., mesothelioma). The observed phylogenetic relationship of HaPyV to murine Polyomaviruses within the genus AlphaPolyomavirus, and the exclusive detection of other cricetid Polyomaviruses, i.e., common vole (Microtus arvalis Polyomavirus 1) and bank vole (Myodes glareolus Polyomavirus 1) Polyomaviruses, in the genus BetaPolyomavirus, must be considered with caution, as knowledge of rodent-associated Polyomaviruses is still limited. The genome of HaPyV shows the typical organization of Polyomaviruses with an early and a late transcriptional region. The early region encodes three tumor (T) antigens including a middle T antigen; the late region encodes three capsid proteins. The major capsid protein VP1 of HaPyV was established as a carrier for the generation of autologous, chimeric, and mosaic virus-like particles (VLPs) with a broad range of applications, e.g., for the production of epitope-specific antibodies. Autologous VLPs have been applied for entry and maturation studies of dendritic cells. The generation of chimeric and mosaic VLPs indicated the high flexibility of the VP1 carrier protein for the insertion of foreign sequences. The generation of pseudotype VLPs of original VP1 and VP2–foreign protein fusion can further enhance the applicability of this system. Future investigations should evaluate the evolutionary origin of HaPyV, monitor its occurrence in wildlife and Syrian Hamster breeding, and prove its value for the generation of potential vaccine candidates and as a gene therapy vehicle.
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Genome Sequences of a Rat Polyomavirus Related to Murine Polyomavirus, Rattus norvegicus Polyomavirus 1
Genome Announcements, 2015Co-Authors: Bernhard Ehlers, Dania Richter, Franz-rainer Matuschka, Rainer G UlrichAbstract:We amplified and sequenced six complete genomes of a Polyomavirus from feral Norway rats (Rattus norvegicus) and from a long-term breeding colony derived from Norway rats. This virus, which is closely related to Hamster Polyomavirus and murine Polyomavirus, may contribute to understanding the evolutionary history of rodent Polyomaviruses.
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cellular and humoral immunogenicity of Hamster Polyomavirus derived virus like particles harboring a mucin 1 cytotoxic t cell epitope
Viral Immunology, 2008Co-Authors: David C Dorn, Kestutis Sasnauskas, Muhsin Özel, Robert Lawatscheck, Aurelija Zvirbliene, Egle Aleksaite, Gabriele Pecher, Martin Raftery, Gunther Schonrich, Rainer G UlrichAbstract:In this study, we examined Hamster Polyomavirus (HaPyV) major capsid protein VP1-derived virus-like particles (VLPs) as a carrier for a human tumor-associated cytotoxic T lymphocyte (CTL) epitope. The VP1 tolerated the insertion of an HLA-*A2-restricted CTL epitope from human mucin 1 (MUC1) into two sites independently and simultaneously, without interfering with assembly of chimeric VLPs. Chimeric VLPs did not differ in the entry pathway or maturation potential of human dendritic cells (hDCs) compared to unmodified VLPs. Recently we demonstrated that immunization of BALB/c mice with chimeric VLPs harboring two MUC1 insertions resulted in the generation of MUC1-specific monoclonal antibodies. Here we demonstrate that the monoclonal antibodies generated react specifically with human tumor cells. Co-cultivation of chimeric VLP-primed hDCs with autologous peripheral blood leukocytes resulted in the activation of MUC1 epitope–specific CD8+ T cells. This was evidenced by IFN-γ secretion of an expanded MUC1-spe...
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an immunodominant cross reactive b cell epitope region is located at the c terminal part of the Hamster Polyomavirus major capsid protein vp1
Viral Immunology, 2000Co-Authors: Hassen Siray, S. Scherneck, Cornelius Frommel, Tatyana Voronkova, Stefanie Hahn, Wolfgang Arnold, Jens Schneidermergener, Rainer G UlrichAbstract:ABSTRACT The VP1 represents the major capsid protein of the Hamster Polyomavirus (HaPV). Here we describe the mapping of epitopes along the VP1 using Escherichia coli-expressed VP1-dihydrofolate re...
