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Kevin E. Brown - One of the best experts on this subject based on the ideXlab platform.

  • comparison of the transcription profile of Simian Parvovirus with that of the human erythrovirus b19 reveals a number of unique features
    Journal of Virology, 2004
    Co-Authors: Zhengwen Liu, Kevin E. Brown, Gerard M Osullivan, Yonglie Chu, Jianming Qiu, Fang Cheng, Yuko Yoto, David J Pintel
    Abstract:

    Simian Parvovirus (SPV) is a member of the genus Erythrovirus and is closely related to the human Parvovirus B19. Natural and experimental infection of monkeys with SPV resembles B19 infection of human. We report a detailed characterization of the viral RNAs and proteins generated following transfection of cloned SPV into COS cells and SPV infection of the human erythroid progenitor line UT-7/Epo-S1. SPV and B19 are 50% identical at the nucleotide level, and although their basic transcription and protein expression profiles were generally similar, there were also significant differences. SPV pre-mRNAs contain three introns, compared to two found for B19: an additional intron was found within the capsid-coding region. RNAs in which this intron was spliced were abundant and encoded the SPV 14-kDa protein (analogous to the B19 11-kDa protein), which initiated at an AUG in the exon preceding the third intron. Unlike B19, SPV RNAs were also spliced between the donor of the first intron and the acceptor of the second intron. The third intron was additionally spliced from a portion of these molecules; these mRNAs encoded the 14-kDa protein. A portion was not spliced further and encoded VP2. Like B19, SPV has a polyadenylation signal [AAUAAA (pA)p] in the middle of the genome, which directed efficient polyadenylation of both spliced and unspliced mRNAs (encoding a putative 10-kDa protein, analogous to the B19 7.5-kDa protein, and SPV NS1, respectively). The 14-kDa protein was localized to both in the nucleus and cytoplasm.

  • Simian Parvovirus infection a potential zoonosis
    The Journal of Infectious Diseases, 2004
    Co-Authors: Kevin E. Brown, Zhengwen Liu, Giorgio A Gallinella, Ian P. Mills, Susan Wong, Gerard M Osullivan
    Abstract:

    EDITORIAL COMMENTARY Ebola Virus Ecology Joseph B. McCormick 1893MAJOR ARTICLES AND BRIEF REPORTS VIRUSES A Serological Survey of Ebola Virus Infection in Central African Nonhuman Primates E. M. Leroy, P. Telfer, B. Kumulungui, P. Yaba, P. Rouquet, P. Roques, J.-P. Gonzalez, T. G. Ksiazek, P. E. Rollin, and E. Nerrienet 1895 Simian Parvovirus Infection: A Potential Zoonosis Kevin E. Brown, Zhengwen Liu, Giorgio Gallinella, Susan Wong, Ian P. Mills, and M. Gerard O'Sullivan 1900 Antibody Maturation and Viremia after Primary Cytomegalovirus Infection, in Immunocompetent Patients and Kidney-Transplant Patients Christoph Steininger, Michael Kundi, Josef Kletzmayr, Stephan W. Aberle, and Theresia Popow-Kraupp 1908 Use of the P Gene to Genotype Human Metapneumovirus Identifies 4 Viral Subtypes Ian M. Mackay, Seweryn Bialasiewicz, Zubair Waliuzzaman, Glenys R. Chidlow, David C. Fegredo, Somprasong Laingam, Penny Adamson, Gerald B. Harnett, William Rawlinson, Michael D. Nissen, and Theo P. Sloots 1913Reduced Numbers and Impaired Ability of Myeloid and Plasmacytoid Dendritic Cells to Polarize T Helper Cells in Chronic Hepatitis C Virus Infection Tatsuya Kanto, Michiyo Inoue, Hideki Miyatake, Aki Sato, Mitsuru Sakakibara, Takayuki Yakushijin, Chika Oki, Ichiyo Itose, Naoki Hiramatsu, Tetsuo Takehara, Akinori Kasahara, and Norio Hayashi 1919 Parenteral Influenza Vaccination Influences Mucosal and Systemic T CellMediated Immunity in Healthy Adults Terry Guthrie, Christopher G. L. Hobbs, Victoria Davenport, Rachel E. Horton, Robert S. Heyderman, and Neil A. Williams 1927 AntiG Protein Antibody Responses to Respiratory Syncytial Virus Infection or Vaccination Are Associated with Inhibition of G Protein CX3C-CX3CR1 Binding and Leukocyte Chemotaxis Jennifer L. Harcourt, Ruth A. Karron, and Ralph A. Tripp 1936Variable Resistance to Palivizumab in Cotton Rats by Respiratory Syncytial Virus Mutants Xiaodong Zhao, Fu-Ping Chen, A. George Megaw, and Wayne M. Sullender 1941 HIV/AIDS Time to Virological Failure of 3 Classes of Antiretrovirals after Initiation of Highly Active Antiretroviral Therapy: Results from the 1947

  • splice junction map of Simian Parvovirus transcripts
    Journal of Virology, 2004
    Co-Authors: Kapil Vashisht, Kevin E. Brown, Kay S Faaberg, Amanda L Aber, Gerard M Osullivan
    Abstract:

    The transcription map of Simian Parvovirus (SPV), an Erythrovirus similar to Parvovirus B19, was investigated. RNA was extracted from tissues of experimentally infected cynomolgus macaques and subjected to reverse transcription-PCR with SPV-specific primers. The PCR products were cloned and sequenced to identify splice junctions. A total of 14 distinct sequences were identified as putative partial transcripts. Of these, 13 were spliced; a single unspliced transcript putatively encoded NS1. Sequence analysis revealed that spliced partial transcripts may encode portions of open reading frames for the major capsid proteins VP1 and VP2 and smaller, unknown proteins. These unspliced and spliced transcripts and putative proteins encoded by SPV were similar to those of B19. Initial splice junctions at nucleotides 279 and 333 were analogous to those at nucleotides 406 and 441, respectively, in B19. Seven of the 10 splices identified had typical GT/AG donor/acceptor junctions. The splice sites were confirmed by Northern blotting and autoradiography. In contrast to B19, which has a maximum of two splices per transcript, up to three splices were observed in SPV transcripts. A spliced transcript putatively encoding a truncated version of NS1, as seen with minute virus of mice and adeno-associated virus 2, was also observed. The findings indicate that that the splicing pattern of transcripts of SPV and B19 is similar, but SPV also has coding strategies in common with other Parvoviruses.

  • Simian Parvovirus infection: a potential zoonosis
    2004
    Co-Authors: Kevin E. Brown, Zhengwen Liu, Giorgio A Gallinella, Susan A Wong, Ian P. Mills, Gerard M. O’sullivan
    Abstract:

    Introduction. Simian Parvovirus (SPV) causes severe anemia in immunocompromised macaques. The closely related erythrovirus, Parvovirus B19, causes anemia in susceptible humans and can be grown in human bone marrow mononuclear cells in vitro. We hypothesized that SPV may infect humans and replicate in human bone marrow mononuclear cells. Methods. Serum samples from handlers of an SPV-seropositive macaque colony were tested by Western blo

  • experimental infection of cynomolgus monkeys with Simian Parvovirus
    Journal of Virology, 1997
    Co-Authors: M G Osullivan, Spencer W. Green, Neal S. Young, D K Anderson, J A Goodrich, H Tulli, Kevin E. Brown
    Abstract:

    Simian Parvovirus is a recently discovered Parvovirus that was first isolated from cynomolgus monkeys. It is similar to human B19 Parvovirus in terms of virus genome, tropism for erythroid cells, and characteristic pathology in natural infections. Cynomolgus monkeys were infected with Simian Parvovirus to investigate their potential usefulness as an animal model of human B19 Parvovirus. Six adult female cynomolgus monkeys were inoculated with purified Simian Parvovirus by the intravenous or intranasal route and monitored for evidence of clinical abnormalities; this included the preparation of complete hematological profiles. Viremia and Simian Parvovirus-specific antibody were determined in infected monkeys by dot blot and Western blot assays, respectively. Bone marrow was examined at necropsy 6, 10, or 15 days postinfection. All of the monkeys developed a smoldering, low-grade viremia that peaked approximately 10 to 12 days after inoculation. Peak viremia coincided with the appearance of specific antibody and was followed by sudden clearance of the virus and complete, but transient, absence of reticulocytes from the peripheral blood. Clinical signs were mild and involved mainly anorexia and slight weight loss. Infection was associated with a mild decrease in hemoglobin, hematocrit, and erythrocyte numbers. Bone marrow showed marked destruction of erythroid cells coincident with peak viremia. Our findings indicate that infection of healthy monkeys by Simian Parvovirus is self-limited and mild, with transient cessation of erythropoiesis. Our study has reproduced Koch's postulates and further shown that Simian Parvovirus infection of monkeys is almost identical to human B19 Parvovirus infection of humans. Accordingly, this animal model may prove valuable in the study of the pathogenesis of B19 virus infection.

Gerard M Osullivan - One of the best experts on this subject based on the ideXlab platform.

  • Simian Parvovirus infection in cynomolgus monkey heart transplant recipients causes death related to severe anemia
    Transplantation, 2006
    Co-Authors: C Schroder, Amanda L Aber, Steffen Pfeiffer, Agnes M Azimzadeh, Richard N Pierson, Gerard M Osullivan
    Abstract:

    Background. Simian Parvovirus (SPV) was first isolated from cynomolgus monkeys. Like human Parvovirus B19, this virus has a predilection for erythroid cells. During acute SPV infection, clinical signs are usually mild or inapparent, but severe anemia may occur in immunocompromised animals. We report several cases of symptomatic SPV infection in cynomolgus monkeys following heart transplantation. Methods. Twenty-three consecutive abdominal heterotopic heart transplants were studied. Viremia, measured by dot blot and/or PCR, and SPV-specific antibodies were determined retrospectively. Results. All except one animal were on an immunosuppressive protocol. In all, 48% (11/23) of transplant recipients had viremia with SPV detected at some point after transplant. An additional 22% seroconverted before or after transplant, and were asymptomatic without detectable SPV. Of the 11 acutely viremic animals, five were euthanized because of severe anemia attributed to SPV. The remaining 30% of the transplant recipients did not seroconvert and were asymptomatic. Of seven recipients of donor tissue from seropositive or viremic animals, five became viremic and three died with anemia. No immunosuppressive regimen was implicated in increased susceptibility; the one transplant recipient not treated with immunosuppressive agents died with anemia and acute viremia two weeks after explant of a rejected graft. Conclusion. SPV is an important pathogen in surgically manipulated cynomolgus monkeys, particularly with immune compromise. Once introduced into a colony, clinically silent SPV infection could be readily transmitted within the environment. Transmission and disease occur at high frequency with an organ from a PCR-negative, seropositive donor, suggesting that latent virus can be conveyed by the organ.

  • Simian Parvovirus infection a potential zoonosis
    The Journal of Infectious Diseases, 2004
    Co-Authors: Kevin E. Brown, Zhengwen Liu, Giorgio A Gallinella, Ian P. Mills, Susan Wong, Gerard M Osullivan
    Abstract:

    EDITORIAL COMMENTARY Ebola Virus Ecology Joseph B. McCormick 1893MAJOR ARTICLES AND BRIEF REPORTS VIRUSES A Serological Survey of Ebola Virus Infection in Central African Nonhuman Primates E. M. Leroy, P. Telfer, B. Kumulungui, P. Yaba, P. Rouquet, P. Roques, J.-P. Gonzalez, T. G. Ksiazek, P. E. Rollin, and E. Nerrienet 1895 Simian Parvovirus Infection: A Potential Zoonosis Kevin E. Brown, Zhengwen Liu, Giorgio Gallinella, Susan Wong, Ian P. Mills, and M. Gerard O'Sullivan 1900 Antibody Maturation and Viremia after Primary Cytomegalovirus Infection, in Immunocompetent Patients and Kidney-Transplant Patients Christoph Steininger, Michael Kundi, Josef Kletzmayr, Stephan W. Aberle, and Theresia Popow-Kraupp 1908 Use of the P Gene to Genotype Human Metapneumovirus Identifies 4 Viral Subtypes Ian M. Mackay, Seweryn Bialasiewicz, Zubair Waliuzzaman, Glenys R. Chidlow, David C. Fegredo, Somprasong Laingam, Penny Adamson, Gerald B. Harnett, William Rawlinson, Michael D. Nissen, and Theo P. Sloots 1913Reduced Numbers and Impaired Ability of Myeloid and Plasmacytoid Dendritic Cells to Polarize T Helper Cells in Chronic Hepatitis C Virus Infection Tatsuya Kanto, Michiyo Inoue, Hideki Miyatake, Aki Sato, Mitsuru Sakakibara, Takayuki Yakushijin, Chika Oki, Ichiyo Itose, Naoki Hiramatsu, Tetsuo Takehara, Akinori Kasahara, and Norio Hayashi 1919 Parenteral Influenza Vaccination Influences Mucosal and Systemic T CellMediated Immunity in Healthy Adults Terry Guthrie, Christopher G. L. Hobbs, Victoria Davenport, Rachel E. Horton, Robert S. Heyderman, and Neil A. Williams 1927 AntiG Protein Antibody Responses to Respiratory Syncytial Virus Infection or Vaccination Are Associated with Inhibition of G Protein CX3C-CX3CR1 Binding and Leukocyte Chemotaxis Jennifer L. Harcourt, Ruth A. Karron, and Ralph A. Tripp 1936Variable Resistance to Palivizumab in Cotton Rats by Respiratory Syncytial Virus Mutants Xiaodong Zhao, Fu-Ping Chen, A. George Megaw, and Wayne M. Sullender 1941 HIV/AIDS Time to Virological Failure of 3 Classes of Antiretrovirals after Initiation of Highly Active Antiretroviral Therapy: Results from the 1947

  • comparison of the transcription profile of Simian Parvovirus with that of the human erythrovirus b19 reveals a number of unique features
    Journal of Virology, 2004
    Co-Authors: Zhengwen Liu, Kevin E. Brown, Gerard M Osullivan, Yonglie Chu, Jianming Qiu, Fang Cheng, Yuko Yoto, David J Pintel
    Abstract:

    Simian Parvovirus (SPV) is a member of the genus Erythrovirus and is closely related to the human Parvovirus B19. Natural and experimental infection of monkeys with SPV resembles B19 infection of human. We report a detailed characterization of the viral RNAs and proteins generated following transfection of cloned SPV into COS cells and SPV infection of the human erythroid progenitor line UT-7/Epo-S1. SPV and B19 are 50% identical at the nucleotide level, and although their basic transcription and protein expression profiles were generally similar, there were also significant differences. SPV pre-mRNAs contain three introns, compared to two found for B19: an additional intron was found within the capsid-coding region. RNAs in which this intron was spliced were abundant and encoded the SPV 14-kDa protein (analogous to the B19 11-kDa protein), which initiated at an AUG in the exon preceding the third intron. Unlike B19, SPV RNAs were also spliced between the donor of the first intron and the acceptor of the second intron. The third intron was additionally spliced from a portion of these molecules; these mRNAs encoded the 14-kDa protein. A portion was not spliced further and encoded VP2. Like B19, SPV has a polyadenylation signal [AAUAAA (pA)p] in the middle of the genome, which directed efficient polyadenylation of both spliced and unspliced mRNAs (encoding a putative 10-kDa protein, analogous to the B19 7.5-kDa protein, and SPV NS1, respectively). The 14-kDa protein was localized to both in the nucleus and cytoplasm.

  • splice junction map of Simian Parvovirus transcripts
    Journal of Virology, 2004
    Co-Authors: Kapil Vashisht, Kevin E. Brown, Kay S Faaberg, Amanda L Aber, Gerard M Osullivan
    Abstract:

    The transcription map of Simian Parvovirus (SPV), an Erythrovirus similar to Parvovirus B19, was investigated. RNA was extracted from tissues of experimentally infected cynomolgus macaques and subjected to reverse transcription-PCR with SPV-specific primers. The PCR products were cloned and sequenced to identify splice junctions. A total of 14 distinct sequences were identified as putative partial transcripts. Of these, 13 were spliced; a single unspliced transcript putatively encoded NS1. Sequence analysis revealed that spliced partial transcripts may encode portions of open reading frames for the major capsid proteins VP1 and VP2 and smaller, unknown proteins. These unspliced and spliced transcripts and putative proteins encoded by SPV were similar to those of B19. Initial splice junctions at nucleotides 279 and 333 were analogous to those at nucleotides 406 and 441, respectively, in B19. Seven of the 10 splices identified had typical GT/AG donor/acceptor junctions. The splice sites were confirmed by Northern blotting and autoradiography. In contrast to B19, which has a maximum of two splices per transcript, up to three splices were observed in SPV transcripts. A spliced transcript putatively encoding a truncated version of NS1, as seen with minute virus of mice and adeno-associated virus 2, was also observed. The findings indicate that that the splicing pattern of transcripts of SPV and B19 is similar, but SPV also has coding strategies in common with other Parvoviruses.

Neal S. Young - One of the best experts on this subject based on the ideXlab platform.

  • experimental infection of cynomolgus monkeys with Simian Parvovirus
    Journal of Virology, 1997
    Co-Authors: M G Osullivan, Spencer W. Green, Neal S. Young, D K Anderson, J A Goodrich, H Tulli, Kevin E. Brown
    Abstract:

    Simian Parvovirus is a recently discovered Parvovirus that was first isolated from cynomolgus monkeys. It is similar to human B19 Parvovirus in terms of virus genome, tropism for erythroid cells, and characteristic pathology in natural infections. Cynomolgus monkeys were infected with Simian Parvovirus to investigate their potential usefulness as an animal model of human B19 Parvovirus. Six adult female cynomolgus monkeys were inoculated with purified Simian Parvovirus by the intravenous or intranasal route and monitored for evidence of clinical abnormalities; this included the preparation of complete hematological profiles. Viremia and Simian Parvovirus-specific antibody were determined in infected monkeys by dot blot and Western blot assays, respectively. Bone marrow was examined at necropsy 6, 10, or 15 days postinfection. All of the monkeys developed a smoldering, low-grade viremia that peaked approximately 10 to 12 days after inoculation. Peak viremia coincided with the appearance of specific antibody and was followed by sudden clearance of the virus and complete, but transient, absence of reticulocytes from the peripheral blood. Clinical signs were mild and involved mainly anorexia and slight weight loss. Infection was associated with a mild decrease in hemoglobin, hematocrit, and erythrocyte numbers. Bone marrow showed marked destruction of erythroid cells coincident with peak viremia. Our findings indicate that infection of healthy monkeys by Simian Parvovirus is self-limited and mild, with transient cessation of erythropoiesis. Our study has reproduced Koch's postulates and further shown that Simian Parvovirus infection of monkeys is almost identical to human B19 Parvovirus infection of humans. Accordingly, this animal model may prove valuable in the study of the pathogenesis of B19 virus infection.

  • clinical and epidemiological features of Simian Parvovirus infection in cynomolgus macaques with severe anemia
    Laboratory Animal Science, 1996
    Co-Authors: M G Osullivan, Spencer W. Green, Neal S. Young, D K Anderson, J E Lund, W P Brown, Kevin E. Brown
    Abstract:

    We recently identified a Simian Parvovirus (SPV) in cynomolgus monkeys with severe anemia. We describe here the clinical and epidemiological findings in the original outbreak and in a second episode of anemia involving monkeys in a drug safety study at a separate facility. The major clinical findings associated with SPV infection were a severe normocytic, normochromic anemia. In the original episode the anemia was predominantly nonregenerative, whereas in the second outbreak there was an initial strong, regenerative response. In the absence of predisposing factors, SPV infection was mild or inapparent. However, the presence of concurrent acute infection with type D Simian retrovirus in the original episode is believed to have been a major predisposing factor for the development of immunodeficiency and persistent SPV infection, culminating in severe anemia. It is unclear whether Simian retrovirus infection played a role in the second episode, but it is possible that the drug used may have been a factor, because severely anemic monkeys were in the high drug dosage group. We conclude that SPV should be considered in the differential diagnosis of severe anemia in monkeys.

  • Cloning and sequencing of the Simian Parvovirus genome.
    Virology, 1995
    Co-Authors: Kevin E. Brown, Spencer W. Green, M. Gerard O'sullivan, Neal S. Young
    Abstract:

    We recently reported the identification of a novel Simian Parvovirus in cynomolgus monkeys with severe anemia. We now describe the cloning and sequencing of 4986 nucleotides of the viral DNA. Like the human Parvovirus B19, Simian Parvovirus encapsidates both positive and negative single-stranded DNA. The positive strand contains two large open reading frames, with the left open reading frame encoding the nonstructural protein(s) and the right reading frame encoding the two capsid proteins. Simian Parvovirus has little homology with the autonomous Parvoviruses or the dependovirus AAV-2 but 50% overall homology with Parvovirus B19 DNA. At the amino acid level there was 70% homology with B19 capsid proteins and 50% homology with B19 nonstructural protein. Based on this genetic similarity and with the known tropism of the virus for cynomolgus erythroid precursors, we suggest that this new virus should be classified as a new member of the Erythrovirus genus of the Parvoviridae.

Zhengwen Liu - One of the best experts on this subject based on the ideXlab platform.

  • Simian Parvovirus infection a potential zoonosis
    The Journal of Infectious Diseases, 2004
    Co-Authors: Kevin E. Brown, Zhengwen Liu, Giorgio A Gallinella, Ian P. Mills, Susan Wong, Gerard M Osullivan
    Abstract:

    EDITORIAL COMMENTARY Ebola Virus Ecology Joseph B. McCormick 1893MAJOR ARTICLES AND BRIEF REPORTS VIRUSES A Serological Survey of Ebola Virus Infection in Central African Nonhuman Primates E. M. Leroy, P. Telfer, B. Kumulungui, P. Yaba, P. Rouquet, P. Roques, J.-P. Gonzalez, T. G. Ksiazek, P. E. Rollin, and E. Nerrienet 1895 Simian Parvovirus Infection: A Potential Zoonosis Kevin E. Brown, Zhengwen Liu, Giorgio Gallinella, Susan Wong, Ian P. Mills, and M. Gerard O'Sullivan 1900 Antibody Maturation and Viremia after Primary Cytomegalovirus Infection, in Immunocompetent Patients and Kidney-Transplant Patients Christoph Steininger, Michael Kundi, Josef Kletzmayr, Stephan W. Aberle, and Theresia Popow-Kraupp 1908 Use of the P Gene to Genotype Human Metapneumovirus Identifies 4 Viral Subtypes Ian M. Mackay, Seweryn Bialasiewicz, Zubair Waliuzzaman, Glenys R. Chidlow, David C. Fegredo, Somprasong Laingam, Penny Adamson, Gerald B. Harnett, William Rawlinson, Michael D. Nissen, and Theo P. Sloots 1913Reduced Numbers and Impaired Ability of Myeloid and Plasmacytoid Dendritic Cells to Polarize T Helper Cells in Chronic Hepatitis C Virus Infection Tatsuya Kanto, Michiyo Inoue, Hideki Miyatake, Aki Sato, Mitsuru Sakakibara, Takayuki Yakushijin, Chika Oki, Ichiyo Itose, Naoki Hiramatsu, Tetsuo Takehara, Akinori Kasahara, and Norio Hayashi 1919 Parenteral Influenza Vaccination Influences Mucosal and Systemic T CellMediated Immunity in Healthy Adults Terry Guthrie, Christopher G. L. Hobbs, Victoria Davenport, Rachel E. Horton, Robert S. Heyderman, and Neil A. Williams 1927 AntiG Protein Antibody Responses to Respiratory Syncytial Virus Infection or Vaccination Are Associated with Inhibition of G Protein CX3C-CX3CR1 Binding and Leukocyte Chemotaxis Jennifer L. Harcourt, Ruth A. Karron, and Ralph A. Tripp 1936Variable Resistance to Palivizumab in Cotton Rats by Respiratory Syncytial Virus Mutants Xiaodong Zhao, Fu-Ping Chen, A. George Megaw, and Wayne M. Sullender 1941 HIV/AIDS Time to Virological Failure of 3 Classes of Antiretrovirals after Initiation of Highly Active Antiretroviral Therapy: Results from the 1947

  • comparison of the transcription profile of Simian Parvovirus with that of the human erythrovirus b19 reveals a number of unique features
    Journal of Virology, 2004
    Co-Authors: Zhengwen Liu, Kevin E. Brown, Gerard M Osullivan, Yonglie Chu, Jianming Qiu, Fang Cheng, Yuko Yoto, David J Pintel
    Abstract:

    Simian Parvovirus (SPV) is a member of the genus Erythrovirus and is closely related to the human Parvovirus B19. Natural and experimental infection of monkeys with SPV resembles B19 infection of human. We report a detailed characterization of the viral RNAs and proteins generated following transfection of cloned SPV into COS cells and SPV infection of the human erythroid progenitor line UT-7/Epo-S1. SPV and B19 are 50% identical at the nucleotide level, and although their basic transcription and protein expression profiles were generally similar, there were also significant differences. SPV pre-mRNAs contain three introns, compared to two found for B19: an additional intron was found within the capsid-coding region. RNAs in which this intron was spliced were abundant and encoded the SPV 14-kDa protein (analogous to the B19 11-kDa protein), which initiated at an AUG in the exon preceding the third intron. Unlike B19, SPV RNAs were also spliced between the donor of the first intron and the acceptor of the second intron. The third intron was additionally spliced from a portion of these molecules; these mRNAs encoded the 14-kDa protein. A portion was not spliced further and encoded VP2. Like B19, SPV has a polyadenylation signal [AAUAAA (pA)p] in the middle of the genome, which directed efficient polyadenylation of both spliced and unspliced mRNAs (encoding a putative 10-kDa protein, analogous to the B19 7.5-kDa protein, and SPV NS1, respectively). The 14-kDa protein was localized to both in the nucleus and cytoplasm.

  • Simian Parvovirus infection: a potential zoonosis
    2004
    Co-Authors: Kevin E. Brown, Zhengwen Liu, Giorgio A Gallinella, Susan A Wong, Ian P. Mills, Gerard M. O’sullivan
    Abstract:

    Introduction. Simian Parvovirus (SPV) causes severe anemia in immunocompromised macaques. The closely related erythrovirus, Parvovirus B19, causes anemia in susceptible humans and can be grown in human bone marrow mononuclear cells in vitro. We hypothesized that SPV may infect humans and replicate in human bone marrow mononuclear cells. Methods. Serum samples from handlers of an SPV-seropositive macaque colony were tested by Western blo

  • the cloning expression and identification of Simian Parvovirus vp2 protein
    Journal of Xi'an Jiaotong University, 2004
    Co-Authors: Zhengwen Liu, K E Brown, Yonglie Chu
    Abstract:

    Objective To clone,express and identify Simian Parvovirus (SPV) Vp2 protein in E.coli. Methods SPV Vp2 gene was amplified by PCR using specific primers and inserted into the multiple cloning site of pThioHis A vector. The expression vector pThioHis A-Vp2 was constructed and transformed into E.coli DH5α competent cells. The positive clones were identified by restriction enzyme digestion analysis and sequencing analysis. SPV Vp2 protein expression was induced by IPTG and the expressed protein was identified by SDS-PAGE and Western blot analysis using both anti-Thio and anti-SPV Vp2 antibodies. Results The expression vector pThioHis A-Vp2 and positively transformed clones were obtained. SPV Vp2 protein was expressed by the positive clones under the induction of IPTG. Western blot analyses showed that the expressed protein specifically reacted with both anti-Thio and anti-SPV Vp2 antibodies. Conclusion SPV Vp2 can be highly expressed by the constructed pThioHis A-Vp2 transformed E.coli. The successful expression of SPV Vp2 is of great significance for the further investigation of SPV infection and related studies.

Spencer W. Green - One of the best experts on this subject based on the ideXlab platform.

  • experimental infection of cynomolgus monkeys with Simian Parvovirus
    Journal of Virology, 1997
    Co-Authors: M G Osullivan, Spencer W. Green, Neal S. Young, D K Anderson, J A Goodrich, H Tulli, Kevin E. Brown
    Abstract:

    Simian Parvovirus is a recently discovered Parvovirus that was first isolated from cynomolgus monkeys. It is similar to human B19 Parvovirus in terms of virus genome, tropism for erythroid cells, and characteristic pathology in natural infections. Cynomolgus monkeys were infected with Simian Parvovirus to investigate their potential usefulness as an animal model of human B19 Parvovirus. Six adult female cynomolgus monkeys were inoculated with purified Simian Parvovirus by the intravenous or intranasal route and monitored for evidence of clinical abnormalities; this included the preparation of complete hematological profiles. Viremia and Simian Parvovirus-specific antibody were determined in infected monkeys by dot blot and Western blot assays, respectively. Bone marrow was examined at necropsy 6, 10, or 15 days postinfection. All of the monkeys developed a smoldering, low-grade viremia that peaked approximately 10 to 12 days after inoculation. Peak viremia coincided with the appearance of specific antibody and was followed by sudden clearance of the virus and complete, but transient, absence of reticulocytes from the peripheral blood. Clinical signs were mild and involved mainly anorexia and slight weight loss. Infection was associated with a mild decrease in hemoglobin, hematocrit, and erythrocyte numbers. Bone marrow showed marked destruction of erythroid cells coincident with peak viremia. Our findings indicate that infection of healthy monkeys by Simian Parvovirus is self-limited and mild, with transient cessation of erythropoiesis. Our study has reproduced Koch's postulates and further shown that Simian Parvovirus infection of monkeys is almost identical to human B19 Parvovirus infection of humans. Accordingly, this animal model may prove valuable in the study of the pathogenesis of B19 virus infection.

  • clinical and epidemiological features of Simian Parvovirus infection in cynomolgus macaques with severe anemia
    Laboratory Animal Science, 1996
    Co-Authors: M G Osullivan, Spencer W. Green, Neal S. Young, D K Anderson, J E Lund, W P Brown, Kevin E. Brown
    Abstract:

    We recently identified a Simian Parvovirus (SPV) in cynomolgus monkeys with severe anemia. We describe here the clinical and epidemiological findings in the original outbreak and in a second episode of anemia involving monkeys in a drug safety study at a separate facility. The major clinical findings associated with SPV infection were a severe normocytic, normochromic anemia. In the original episode the anemia was predominantly nonregenerative, whereas in the second outbreak there was an initial strong, regenerative response. In the absence of predisposing factors, SPV infection was mild or inapparent. However, the presence of concurrent acute infection with type D Simian retrovirus in the original episode is believed to have been a major predisposing factor for the development of immunodeficiency and persistent SPV infection, culminating in severe anemia. It is unclear whether Simian retrovirus infection played a role in the second episode, but it is possible that the drug used may have been a factor, because severely anemic monkeys were in the high drug dosage group. We conclude that SPV should be considered in the differential diagnosis of severe anemia in monkeys.

  • Cloning and sequencing of the Simian Parvovirus genome.
    Virology, 1995
    Co-Authors: Kevin E. Brown, Spencer W. Green, M. Gerard O'sullivan, Neal S. Young
    Abstract:

    We recently reported the identification of a novel Simian Parvovirus in cynomolgus monkeys with severe anemia. We now describe the cloning and sequencing of 4986 nucleotides of the viral DNA. Like the human Parvovirus B19, Simian Parvovirus encapsidates both positive and negative single-stranded DNA. The positive strand contains two large open reading frames, with the left open reading frame encoding the nonstructural protein(s) and the right reading frame encoding the two capsid proteins. Simian Parvovirus has little homology with the autonomous Parvoviruses or the dependovirus AAV-2 but 50% overall homology with Parvovirus B19 DNA. At the amino acid level there was 70% homology with B19 capsid proteins and 50% homology with B19 nonstructural protein. Based on this genetic similarity and with the known tropism of the virus for cynomolgus erythroid precursors, we suggest that this new virus should be classified as a new member of the Erythrovirus genus of the Parvoviridae.