The Experts below are selected from a list of 237 Experts worldwide ranked by ideXlab platform
Weiquan Liu - One of the best experts on this subject based on the ideXlab platform.
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The 5' Untranslated Region of the Capsid Protein 2 Gene of Mink Enteritis Virus Is Essential for Its Expression.
Journal of virology, 2018Co-Authors: Shuang-shuang Yang, Jigui Wang, Shangjin Cui, Weiquan LiuAbstract:Mink Enteritis Virus (MEV), as a parvoVirus, is among the smallest of the animal DNA Viruses. The limited genome leads to multifunctional sequences and complex gene expression regulation. Here, we show that the expression of viral capsid protein 2 (VP2) of MEV requires its 5' untranslated regions (5' UTR) which promote VP2 gene expression at both transcriptional and translational levels. The expression of VP2 was inhibited in several common eukaryotic expression vectors. Our data showed that the 5' UTR of VP2 enhanced capsid gene transcription but not increased stability or promotes nucleocytoplasmic export of VP2 mRNA. Analysis of the functions of 5' UTR fragments showed that the proximal region (nucleotides [nt] 1 to 270; that is, positions +1 to +270 relative to the transcription initiation site, nt 2048 to 2317 of MEV-L) of 5' UTR of VP2 was necessary for VP2 transcription and also promoted the activity of P38 promoter. Unexpectedly, further analysis showed that deletion of the distal region (nt 271 to 653) of the 5' UTR of VP2 almost completely abolished VP2 translation in the presence of P38, whereas the transcription was still induced significantly. Furthermore, using a luciferase reporter bicistronic system, we identified that the 5' UTR had an internal ribosome entry site-like function which could be enhanced by NS1 via the site at nt 382 to 447. Mutation of the 5' UTR in the MEV full-length clones further showed that the 5' UTR was required for VP2 gene expression. Together, our data reveal an undiscovered function of 5' UTR of MEV VP2 in regulating viral gene expression.IMPORTANCE MEV, a parvoVirus, causes acute Enteritis in Mink. In the present report, we describe an untranslated sequence-dependent mechanism by which MEV regulates capsid gene expression. Our results highlight the roles of untranslated sequences in regulating the transcriptional activity of P38 promoter and translation of capsid genes. These data also reveal the possibility of an unusual translation mechanism in capsid protein expression and the multiple functions of nonstructural protein. A better understanding of the gene expression regulation mechanism of this Virus will help in the design of new vaccines and targets for antiviral agents against MEV.
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Induction and suppression of type I interferon responses by Mink Enteritis Virus in CRFK cells
Veterinary microbiology, 2016Co-Authors: Xiaomei Zhang, Jigui Wang, Yaping Mao, Weiquan LiuAbstract:Mink Enteritis Virus (MEV) is one of the most important viral pathogens causing serious disease in Mink. Type I interferon (IFN) plays a critical role in antiviral innate immunity and, for successful infection, many Viruses have evolved evasive strategies against it. Here, we show that MEV infection does not evoke IFN or interferon-stimulated genes (ISGs) responses in feline kidney (CRFK) cells, and that MEV suppresses IFN production in both poly I:C-stimulated and untreated cells. In CRFK cells pre-exposure to IFN, show that infection with, and replication of, MEV remain unaffected. This inhibition appears to be mediated by the MEV nonstructural protein (NS1) with its ORI-binding domain playing a major role.
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The phosphorylation of Ser221 in VP2 of Mink Enteritis Virus and its roles in Virus amplification
Virus research, 2016Co-Authors: Qiang Hou, Jigui Wang, Yaping Mao, Shuang Wang, Weiquan LiuAbstract:Recent reports have indicated that phosphorylation of capsid proteins plays an important role in virion assemblage. Autonomous parvoViruses are among the smallest known Viruses with an ssDNA genome enclosed within an icosahedral capsid. Here, we demonstrate that a structural protein (VP2) of one member, Mink Enteritis Virus (MEV), is phosphorylated at serine-221 (Ser221) in vivo. Mutant Viruses containing an S221A non-phosphorylatable alanine substitution, or an S221E glutamic acid substitution to mimic serine phosphorylation, were able to express VP2 but had either limited ability or were unable to propagate in feline F81 cells. We propose a new mechanism whereby VP2 phosphorylation plays an essential role in amplification during MEV infection.
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MicroRNA miR-320a and miR-140 inhibit Mink Enteritis Virus infection by repression of its receptor, feline transferrin receptor.
Virology journal, 2014Co-Authors: Jia-zeng Sun, Jigui Wang, Yaping Mao, Shuang Wang, Qiang Hou, Daoli Yuan, Weiquan LiuAbstract:Mink Enteritis Virus (MEV) is one of the most important pathogens in the Mink industry. Recent studies have shed light into the role of microRNAs (miRNAs), small noncoding RNAs of length ranging from 18–23 nucleotides (nt), as critical modulators in the host-pathogen interaction networks. We previously showed that miRNA miR-181b can inhibit MEV replication by repression of viral non-structural protein 1 expression. Here, we report that two other miRNAs (miR-320a and miR-140) inhibit MEV entry into feline kidney (F81) cells by downregulating its receptor, transferrin receptor (TfR), by targeting the 3′ untranslated region (UTR) of TfR mRNA, while being themselves upregulated.
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MicroRNA profile analysis of a feline kidney cell line before and after infection with Mink Enteritis Virus.
Gene, 2014Co-Authors: Jia-zeng Sun, Jigui Wang, Shuang Wang, Daoli Yuan, Basse Mame Birame, Weiquan LiuAbstract:MicroRNAs (miRNAs) are small regulatory RNAs that play a significant role in eukaryotes by targeting mRNAs for cleavage or translational repression. Recent studies have also shown them to be associated with cellular changes following viral infection. Mink Enteritis Virus (MEV) is one of the most important viral pathogens in the Mink industry. To study the involvement of miRNAs in the MEV infection process, we used Illumina's ultrahigh throughput approach to sequencing miRNA libraries from the feline kidney (F81) cell line before and after infection with MEV. Using this bioinformatics approach we identified 196 known mammalian miRNA orthologs belonging to 152 miRNA families in F81 cells. Additionally, 97 miRNA*s of these miRNAs were detected. As well as known miRNAs, 384 and 398 novel miRNA precursor candidates were identified in uninfected and MEV-infected F81 cells respectively that have not been reported in other mammals. In MEV-infected cells 3 miRNAs were significantly down-regulated and 4 up-regulated including 3 significantly. The majority (12 of 16) of randomly selected miRNA expression profiles by qRT-PCR were consistent with those identified by deep sequencing. A total of 88 miRNAs were predicted to target interferon-associated genes; 6 appear to target the 3'UTR of MEV-specific receptor transferring receptor mRNAs; and 8 to target the MEV mRNA coding region. No miRNAs coded by MEV itself were detected.
Jigui Wang - One of the best experts on this subject based on the ideXlab platform.
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The 5' Untranslated Region of the Capsid Protein 2 Gene of Mink Enteritis Virus Is Essential for Its Expression.
Journal of virology, 2018Co-Authors: Shuang-shuang Yang, Jigui Wang, Shangjin Cui, Weiquan LiuAbstract:Mink Enteritis Virus (MEV), as a parvoVirus, is among the smallest of the animal DNA Viruses. The limited genome leads to multifunctional sequences and complex gene expression regulation. Here, we show that the expression of viral capsid protein 2 (VP2) of MEV requires its 5' untranslated regions (5' UTR) which promote VP2 gene expression at both transcriptional and translational levels. The expression of VP2 was inhibited in several common eukaryotic expression vectors. Our data showed that the 5' UTR of VP2 enhanced capsid gene transcription but not increased stability or promotes nucleocytoplasmic export of VP2 mRNA. Analysis of the functions of 5' UTR fragments showed that the proximal region (nucleotides [nt] 1 to 270; that is, positions +1 to +270 relative to the transcription initiation site, nt 2048 to 2317 of MEV-L) of 5' UTR of VP2 was necessary for VP2 transcription and also promoted the activity of P38 promoter. Unexpectedly, further analysis showed that deletion of the distal region (nt 271 to 653) of the 5' UTR of VP2 almost completely abolished VP2 translation in the presence of P38, whereas the transcription was still induced significantly. Furthermore, using a luciferase reporter bicistronic system, we identified that the 5' UTR had an internal ribosome entry site-like function which could be enhanced by NS1 via the site at nt 382 to 447. Mutation of the 5' UTR in the MEV full-length clones further showed that the 5' UTR was required for VP2 gene expression. Together, our data reveal an undiscovered function of 5' UTR of MEV VP2 in regulating viral gene expression.IMPORTANCE MEV, a parvoVirus, causes acute Enteritis in Mink. In the present report, we describe an untranslated sequence-dependent mechanism by which MEV regulates capsid gene expression. Our results highlight the roles of untranslated sequences in regulating the transcriptional activity of P38 promoter and translation of capsid genes. These data also reveal the possibility of an unusual translation mechanism in capsid protein expression and the multiple functions of nonstructural protein. A better understanding of the gene expression regulation mechanism of this Virus will help in the design of new vaccines and targets for antiviral agents against MEV.
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Induction and suppression of type I interferon responses by Mink Enteritis Virus in CRFK cells
Veterinary microbiology, 2016Co-Authors: Xiaomei Zhang, Jigui Wang, Yaping Mao, Weiquan LiuAbstract:Mink Enteritis Virus (MEV) is one of the most important viral pathogens causing serious disease in Mink. Type I interferon (IFN) plays a critical role in antiviral innate immunity and, for successful infection, many Viruses have evolved evasive strategies against it. Here, we show that MEV infection does not evoke IFN or interferon-stimulated genes (ISGs) responses in feline kidney (CRFK) cells, and that MEV suppresses IFN production in both poly I:C-stimulated and untreated cells. In CRFK cells pre-exposure to IFN, show that infection with, and replication of, MEV remain unaffected. This inhibition appears to be mediated by the MEV nonstructural protein (NS1) with its ORI-binding domain playing a major role.
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The phosphorylation of Ser221 in VP2 of Mink Enteritis Virus and its roles in Virus amplification
Virus research, 2016Co-Authors: Qiang Hou, Jigui Wang, Yaping Mao, Shuang Wang, Weiquan LiuAbstract:Recent reports have indicated that phosphorylation of capsid proteins plays an important role in virion assemblage. Autonomous parvoViruses are among the smallest known Viruses with an ssDNA genome enclosed within an icosahedral capsid. Here, we demonstrate that a structural protein (VP2) of one member, Mink Enteritis Virus (MEV), is phosphorylated at serine-221 (Ser221) in vivo. Mutant Viruses containing an S221A non-phosphorylatable alanine substitution, or an S221E glutamic acid substitution to mimic serine phosphorylation, were able to express VP2 but had either limited ability or were unable to propagate in feline F81 cells. We propose a new mechanism whereby VP2 phosphorylation plays an essential role in amplification during MEV infection.
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MicroRNA miR-320a and miR-140 inhibit Mink Enteritis Virus infection by repression of its receptor, feline transferrin receptor.
Virology journal, 2014Co-Authors: Jia-zeng Sun, Jigui Wang, Yaping Mao, Shuang Wang, Qiang Hou, Daoli Yuan, Weiquan LiuAbstract:Mink Enteritis Virus (MEV) is one of the most important pathogens in the Mink industry. Recent studies have shed light into the role of microRNAs (miRNAs), small noncoding RNAs of length ranging from 18–23 nucleotides (nt), as critical modulators in the host-pathogen interaction networks. We previously showed that miRNA miR-181b can inhibit MEV replication by repression of viral non-structural protein 1 expression. Here, we report that two other miRNAs (miR-320a and miR-140) inhibit MEV entry into feline kidney (F81) cells by downregulating its receptor, transferrin receptor (TfR), by targeting the 3′ untranslated region (UTR) of TfR mRNA, while being themselves upregulated.
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establishment of a rescue system for an autonomous parvoVirus Mink Enteritis Virus
Virus Research, 2014Co-Authors: Daoli Yua, Jigui Wang, Yaping Mao, Shuang Wang, Qiang Hou, Weiqua LiuAbstract:Abstract Construction and characterization of a full-length infectious clone (pMEV) of Mink Enteritis Virus are described. Feline kidney cells (F81) were transfected with pMEV containing an engineered BamHI site that served as a genetic marker. The rescued Virus was indistinguishable from its parental Virus. The availability of a MEV infectious clone will facilitate studies of viral replication and pathogenicity and will permit the elucidation of determinants of the host range of the parvoVirus.
Kristian Dalsgaard - One of the best experts on this subject based on the ideXlab platform.
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plant derived vaccine protects target animals against a viral disease
Nature Biotechnology, 1997Co-Authors: Kristian Dalsgaard, Åse Uttenthal, Søren Kamstrup, Tim D. Jones, Andrew Merryweather, William D.o. Hamilton, Ronald S. Boshuizen, George P. Lomonossoff, Joannes Pieter Maria Langeveld, C PortaAbstract:The successful expression of animal or human Virus epitopes on the surface of plant Viruses has recently been demonstrated. These chimeric Virus particles (CVPs) could represent a cost-effective and safe alternative to conventional animal cell-based vaccines. We report the insertion of oligonucleotides coding for a short linear epitope from the VP2 capsid protein of Mink Enteritis Virus (MEV) into an infectious cDNA clone of cowpea mosaic Virus and the successful expression of the epitope on the surface of CVPs when propagated in the black-eyed bean, Vigna unguiculata. The efficacy of the CVPs was established by the demonstration that one subcutaneous injection of 1 mg of the CVPs in Mink conferred protection against clinical disease and virtually abolished shedding of Virus after challenge with virulent MEV, demonstrating the potential utility of plant CVPs as the basis for vaccine development. The epitope used occurs in three different Virus species-MEV, canine parvoVirus, and feline panleukopenia Virus- and thus the same vaccine could be used in three economically important viral hosts-Mink, dogs, and cats, respectively.
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Plant–derived vaccine protects target animals against a viral disease
Nature Biotechnology, 1997Co-Authors: Kristian Dalsgaard, Åse Uttenthal, Jan P. M. Langeveld, Søren Kamstrup, Tim D. Jones, Fan Xu, Andrew Merryweather, William D.o. Hamilton, Ronald S. Boshuizen, George P. LomonossoffAbstract:The successful expression of animal or human Virus epitopes on the surface of plant Viruses has recently been demonstrated. These chimeric Virus particles (CVPs) could represent a cost-effective and safe alternative to conventional animal cell-based vaccines. We report the insertion of oligonucleotides coding for a short linear epitope from the VP2 capsid protein of Mink Enteritis Virus (MEV) into an infectious cDNA clone of cowpea mosaic Virus and the successful expression of the epitope on the surface of CVPs when propagated in the black-eyed bean, Vigna unguiculata . The efficacy of the CVPs was established by the demonstration that one subcutaneous injection of 1 mg of the CVPs in Mink conferred protection against clinical disease and virtually abolished shedding of Virus after challenge with virulent MEV, demonstrating the potential utility of plant CVPs as the basis for vaccine development. The epitope used occurs in three different Virus species—MEV, canine parvoVirus, and feline panleukopenia Virus—and thus the same vaccine could be used in three economically important viral hosts—Mink, dogs, and cats, respectively.
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Full protection in Mink against Mink Enteritis Virus with new generation canine parvoVirus vaccines based on synthetic peptide or recombinant protein.
Vaccine, 1995Co-Authors: Jan P. M. Langeveld, Åse Uttenthal, Søren Kamstrup, Bertel Strandbygaard, C. Vela, Kristian Dalsgaard, N. J. C. M. Beekman, Rob H. Meloen, J I CasalAbstract:Abstract Two recently developed vaccines—one based on synthetic peptide and one based on recombinant capsid protein—fully protected dogs against heavy experimental canine parvoVirus (CPV) infection. The high sequence homology (>98%) and antigenic similarity between CPV and Mink Enteritis Virus (MEV), feline panleukopenia Virus, and raccoon parvoVirus, suggest that both vaccines could protect Mink, cats and raccoons against these respective host range variants. This was tested in Mink and turned out to be the case. The two vaccines were fully protective and as effective as a conventional commercial vaccine based on inactivated Virus. Surprisingly, this protection was obtained after only a single injection. Furthermore, the vaccinal dose of 150 μg of conjugated peptide or 3 μg of recombinant VP2 particles per animal, are sufficiently low to be cost-effective and applicable on a large scale.
Masami Mochizuki - One of the best experts on this subject based on the ideXlab platform.
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successive deaths of a captive snow leopard uncia uncia and a serval leptailurus serval by infection with feline panleukopenia Virus at sapporo maruyama zoo
Journal of Veterinary Medical Science, 2011Co-Authors: Hideaki Yamamoto, Naotaka Ishiguro, Motohiro Horiuchi, Masami Mochizuki, Yukiko Sassa, Takashi Umemura, Takayuki MiyazawaAbstract:Feline parvoViruses were isolated from frozen samples of intestines taken from a snow leopard (Uncia uncia) and a serval (Leptailurus serval) that died successively at Sapporo Maruyama Zoo in Hokkaido, Japan. Isolates possessed an antigenic epitope for both the feline panleukopenia Virus (FPLV) and Mink Enteritis Virus, identified with a hemagglutination inhibition test. Sequencing analyses of the VP2 region of the isolates revealed that the two isolates were identical and of the FPLV-type. These results suggested that FPLV was introduced from a feral cat which entered the zoo and transmitted the Virus inside the zoo.
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feline host range of canine parvoVirus recent emergence of new antigenic types in cats
Emerging Infectious Diseases, 2002Co-Authors: Yasuhiro Ikeda, Takayuki Miyazawa, Kazuya Nakamura, Yukinobu Tohya, Eiji Takahashi, Masami MochizukiAbstract:Since the emergence of Canine parvoVirus (CPV-2) in the late 1970s, CPV-2 has evolved consecutively new antigenic types, CPV-2a and 2b. Although CPV-2 did not have a feline host range, CPV-2a and 2b appear to have gained the ability to replicate in cats. Recent investigations demonstrate the prevalence of CPV-2a and 2b infection in a wide range of cat populations. We illustrate the pathogenic potential of CPV in cats and assess the risk caused by CPV variants. uman health and animal welfare continue to be challenged by rapidly evolving pathogens. Although many details about specific host-parasite systems have been reported, our understanding of host range alteration and the evolution of virulence remains rudimentary. We reviewed the evolution of carnivore parvoViruses with particular reference to Canine parvoVirus (CPV) infection in cats. These parvoViruses’ molecular and phenotypic evolutionary pattern provides an exemplary system to study pathogen-host relationships and the evolution of virulence, both essential factors for understanding newly emerging infectious diseases. Emergence of Mink Enteritis Virus
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epitope mapping of a monoclonal antibody specific to feline panleukopenia Virus and Mink Enteritis Virus
Journal of Veterinary Medical Science, 1997Co-Authors: Motohiro Horiuchi, Naotaka Ishiguro, Masami Mochizuki, Hideyuki Nagasawa, Morikazu ShinagawaAbstract:To obtain monoclonal antibodies (MAbs) specific to feline panleukopenia Virus (FPLV) and Mink Enteritis Virus (MEV), 15 hybridomas secreting MAbs against MEV-Abashiri were established and the properties of the MAbs were analyzed. The cross-reactivity of MAbs revealed that one MAb, P2-215 was specific for FPLV and MEV, whereas the remaining fourteen MAbs reacted with canine parvoVirus (CPV), FPLV, and MEV. Epitope analyses using various CPV/MEV chimeric Viruses revealed that the MAb P2-215 recognized the epitope comprised of amino acid 93-Lys in VP2, which is known to be FPLV and MEV-specific.
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isolation of canine parvoVirus from a cat manifesting clinical signs of feline panleukopenia
Journal of Clinical Microbiology, 1996Co-Authors: Masami Mochizuki, H Hiragi, M San C Gabriel, M. Horiuchi, Nobuhiro YasudaAbstract:Twenty-seven feline parvoVirus (FPV) isolates were recovered from cats clinically diagnosed with feline panleukopenia (FPL) for assessing antigenic and genomic properties of FPL Viruses (FPLV) recently prevalent among cats in Japan. All isolates, with the exception of one novel isolate, FPV-314, possessed homologous properties, and their subgroups in FPVs were identified as FPLV. The FPV-314 isolate, which was from a 1.5-year-old cat which manifested clinical signs of FPL and died on the 13th day after the first medical examination, was finally identified as canine parvoVirus (CPV) because it lacked a specific antigenic epitope commonly detected in FPLV and Mink Enteritis Virus and because the nucleotide sequence of the capsid protein gene was almost identical to those of CPV-2a and -2b antigenic type strains recently prevalent among dogs in Japan. The present result together with our previous findings (M. Mochizuki, R. Harasawa, and H. Nakatani. Vet. Microbiol. 38:1-10, 1993) indicates the possibility that CPV and FPLV undergo mutual interspecies transmission between dogs and cats, and it is postulated that they may cause disease in some adventitious hosts.
Åse Uttenthal - One of the best experts on this subject based on the ideXlab platform.
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plant derived vaccine protects target animals against a viral disease
Nature Biotechnology, 1997Co-Authors: Kristian Dalsgaard, Åse Uttenthal, Søren Kamstrup, Tim D. Jones, Andrew Merryweather, William D.o. Hamilton, Ronald S. Boshuizen, George P. Lomonossoff, Joannes Pieter Maria Langeveld, C PortaAbstract:The successful expression of animal or human Virus epitopes on the surface of plant Viruses has recently been demonstrated. These chimeric Virus particles (CVPs) could represent a cost-effective and safe alternative to conventional animal cell-based vaccines. We report the insertion of oligonucleotides coding for a short linear epitope from the VP2 capsid protein of Mink Enteritis Virus (MEV) into an infectious cDNA clone of cowpea mosaic Virus and the successful expression of the epitope on the surface of CVPs when propagated in the black-eyed bean, Vigna unguiculata. The efficacy of the CVPs was established by the demonstration that one subcutaneous injection of 1 mg of the CVPs in Mink conferred protection against clinical disease and virtually abolished shedding of Virus after challenge with virulent MEV, demonstrating the potential utility of plant CVPs as the basis for vaccine development. The epitope used occurs in three different Virus species-MEV, canine parvoVirus, and feline panleukopenia Virus- and thus the same vaccine could be used in three economically important viral hosts-Mink, dogs, and cats, respectively.
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Plant–derived vaccine protects target animals against a viral disease
Nature Biotechnology, 1997Co-Authors: Kristian Dalsgaard, Åse Uttenthal, Jan P. M. Langeveld, Søren Kamstrup, Tim D. Jones, Fan Xu, Andrew Merryweather, William D.o. Hamilton, Ronald S. Boshuizen, George P. LomonossoffAbstract:The successful expression of animal or human Virus epitopes on the surface of plant Viruses has recently been demonstrated. These chimeric Virus particles (CVPs) could represent a cost-effective and safe alternative to conventional animal cell-based vaccines. We report the insertion of oligonucleotides coding for a short linear epitope from the VP2 capsid protein of Mink Enteritis Virus (MEV) into an infectious cDNA clone of cowpea mosaic Virus and the successful expression of the epitope on the surface of CVPs when propagated in the black-eyed bean, Vigna unguiculata . The efficacy of the CVPs was established by the demonstration that one subcutaneous injection of 1 mg of the CVPs in Mink conferred protection against clinical disease and virtually abolished shedding of Virus after challenge with virulent MEV, demonstrating the potential utility of plant CVPs as the basis for vaccine development. The epitope used occurs in three different Virus species—MEV, canine parvoVirus, and feline panleukopenia Virus—and thus the same vaccine could be used in three economically important viral hosts—Mink, dogs, and cats, respectively.
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Full protection in Mink against Mink Enteritis Virus with new generation canine parvoVirus vaccines based on synthetic peptide or recombinant protein.
Vaccine, 1995Co-Authors: Jan P. M. Langeveld, Åse Uttenthal, Søren Kamstrup, Bertel Strandbygaard, C. Vela, Kristian Dalsgaard, N. J. C. M. Beekman, Rob H. Meloen, J I CasalAbstract:Abstract Two recently developed vaccines—one based on synthetic peptide and one based on recombinant capsid protein—fully protected dogs against heavy experimental canine parvoVirus (CPV) infection. The high sequence homology (>98%) and antigenic similarity between CPV and Mink Enteritis Virus (MEV), feline panleukopenia Virus, and raccoon parvoVirus, suggest that both vaccines could protect Mink, cats and raccoons against these respective host range variants. This was tested in Mink and turned out to be the case. The two vaccines were fully protective and as effective as a conventional commercial vaccine based on inactivated Virus. Surprisingly, this protection was obtained after only a single injection. Furthermore, the vaccinal dose of 150 μg of conjugated peptide or 3 μg of recombinant VP2 particles per animal, are sufficiently low to be cost-effective and applicable on a large scale.
