Coxsackie B4 Virus

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Hitoshi Suzuki - One of the best experts on this subject based on the ideXlab platform.

  • renal effects of Coxsackie B4 Virus in hyper iga mice
    Journal of The American Society of Nephrology, 2006
    Co-Authors: Yukihiko Kawasaki, Hosoya Mitsuaki, Masato Isome, Ruriko Nozawa, Hitoshi Suzuki
    Abstract:

    For clarification of the pathogenetic role of viral infection in chronic glomerulonephritis, the renal effects of Coxsackie B4 Virus (CB4) were examined in hyper-IgA (HIGA) mice. In experiment 1, HIGA mice ( n = 75) were inoculated intravenously with live CB4 and inactivated CB4 once a month from 1 to 12 mo of age. In experiment 2, HIGA mice ( n = 45) were inoculated intravenously with live CB4 and inactivated CB4 once at 6 wk of age. In experiment 3, 60 mice were inoculated intravenously with carbon and live or inactivated CB4 once at 6 wk of age. Mice in the control group were inoculated with vehicle. The kidneys were extirpated from five mice of each group killed with time after inoculation for histologic evaluation. The scores for mesangial IgA deposition, PCNA-positive cells, and matrix at 20 wk were higher in mice with live CB4 than in mice with inactivated CB4 or without CB4. On electron microscopic examination, swelling and detachment of endothelial cells from 24 h after inoculation and increase of serum IFN-γ concentration were found in mice with live CB4. Many carbon particles were present in peripheral and central zones of the mesangium from 5 to 10 d in mice with carbon and live CB4. These results suggest that CB4 provokes exacerbation of renal pathologic findings in HIGA mice via endothelial injury, IFN-γ production, and dysfunction of the mesangial pathway.

  • experimental iga nephropathy induced by Coxsackie B4 Virus in mice
    American Journal of Nephrology, 1997
    Co-Authors: Kazuo Yoshida, Junzo Suzuki, Shigeo Suzuki, Kazunari Kume, Shigeo Mutoh, Kazuo Kato, Hitoshi Suzuki
    Abstract:

    Viruses have been suspected to be etiological agents of IgA nephropathy. Recently, Viruses were detected in renal tissues from patients with IgA nephropathy. We tried to cause lesions similar to IgA nephropathy by inoculating Virus into mice and to detect Virus RNA in the lesion by in situ hybridization. A group of mice were inoculated intravenously with Coxsackie B4 Virus once a month from 1 to 5 months of age and sacrificed monthly from 6 to 12 months of age. Mesangial proliferation and deposits that stained positive with periodic acid-Schiff in light microscopy and electron-dense deposits in electron microscopy were found from 6 months of age. Positive findings for IgG and IgA deposition in the mesangium were noted and the intensity of IgA deposition was predominant after 10 months of age. The signals of Coxsackie B4 Virus by in situ hybridization were observed in the lesions. These observations indicate that Coxsackie B4 Virus inoculated repeatedly into mice induces lesions similar to IgA nephropathy. The depositions of the lesions may be immune complexes of Coxsackie B4 Virus and these immune complexes injure renal tissues.

  • detection of Coxsackie B4 Virus rna in infected mouse kidneys by in situ hybridization
    Nephron, 1994
    Co-Authors: Shigeo Mutoh, Kazunari Kume, Kazuo Kumada, Junzou Suzuki, Tomoyuki Yokota, Hitoshi Suzuki
    Abstract:

    We describe a method for detecting Virus-specific RNA sequences using a nonradioactive enzyme system, and analyze Coxsackie B4 Virus (cox. B4) RNA sequences in infected mouse kidney with pathological

Hans Diderholm - One of the best experts on this subject based on the ideXlab platform.

  • differences in inhibition of replication between Coxsackie B4 Virus strains in various cell lines by antibodies to some cell surface proteins
    Virus Research, 2001
    Co-Authors: Gun Frisk, Katarina Jansson, Marianne Ericsson, Hans Diderholm
    Abstract:

    Abstract Monoclonal antibodies that interact with the decay accelerating factor (DAF, CD55), the lymphocyte homing receptor (CD44) or the intercellular adhesion molecule I (ICAM- 1) were found to inhibit the replication of different strains of CoxsackieVirus serotype B4 (CBV-4) to various extent. By adding antibodies to CD55 the replication of two (V345 and VD2921) of seven strains in HeLa cells, three (V89-4557, VD2921 and T318) of seven in A549-10C cells and one (VD2921) of five strains in RD cells was blocked totally. Consequently, the replication of one strain (VD2921) was blocked in all cells indicating that this strain uses CD55 as a receptor or as a co-receptor on all cell lines and is unable to use another cell surface protein. The binding of this strain to the cell surface was inhibited by the antibodies to CD55. None of the CBV-4 strains was blocked totally by adding antibodies to CD44 to HeLa and A549-10C cells, whereas in RD cells the replication of one (T318) of the CBV-4 strains was blocked totally. The antibodies to ICAM-1 did not inhibit totally the replication of any strain in HeLa and RD cells, but it blocked totally the replication of one strain (CBV-4-E) in A549-10C cells. In HeLa and A549-10C cells the degree of replication correlated highly with the degree of cytopathic effect (CPE). In RD cells, four of the strains replicated without CPE. The adding of antibodies to the integrin α v β 3 led to slightly enhanced replication of three of the CBV-4 strains in all cell lines. It is concluded that the receptor usage by different strains of CBV-4 varies not only within the same cells but also between different cell lines.

  • antibody responses to different strains of Coxsackie B4 Virus in patients with newly diagnosed type i diabetes mellitus or aseptic meningitis
    Journal of Infection, 1997
    Co-Authors: Gun Frisk, Hans Diderholm
    Abstract:

    Considerable differences in antibody responses measured by capture-IgM RIA and neutralization tests (NT) were seen in children with newly diagnosed type I (insulin-dependent) diabetes mellitus (IDDM) when five different strains of Coxsackie B4 Virus (CBV-4) were used. The IgM positivity of the 160 patients varied between 3.7 and 10.0% ( P P

Yasuhiro Sumida - One of the best experts on this subject based on the ideXlab platform.

Erik Thorsby - One of the best experts on this subject based on the ideXlab platform.

  • T lymphocyte responses to Coxsackie B4 and mumps Virus. II: Immunorégulation by HLA-DR3 and DR4 associated restriction elements
    Tissue Antigens, 2008
    Co-Authors: Øystein Bruserud, Margurethe Stenersen, Erik Thorsby
    Abstract:

    A major part of the Tlymphocyte response to mumps and Coxsackie B4 Virus appears to be restricted by HLA-DR associated restriction elements. This was further corroborated in inhibition experiments using monoclonal antibodies reactive with different HLA class II molecules. Only antibodies reactive with DR molecules significantly inhibited the response. The frequencies of DR restricted antigen-reactive Tlymphocytes (ARTL) to mumps and Coxsackie B4 Virus were then investigated, using a limiting dilution assay. A decreased frequency of DR3 restricted ARTL to mumps and Coxsackie B4 was found compared to ARTL restricted by other DR associated elements. In contrast, an increased frequency of DR4 restricted ARTL to mumps and Coxsackie B4 was found. The results were similar for healthy individuals and Type 1 diabetic patients. No correlation was found between DR restriction elements and the frequencies of ARTL to varicella-zoster or PPD. The studies indicate that HLA-DR3 and DR4, which are associated with Type 1 diabetes, have a different regulatory function on the proliferative Tlymphocyte response to mumps and Coxsackie B4.

Gun Frisk - One of the best experts on this subject based on the ideXlab platform.

  • differences in inhibition of replication between Coxsackie B4 Virus strains in various cell lines by antibodies to some cell surface proteins
    Virus Research, 2001
    Co-Authors: Gun Frisk, Katarina Jansson, Marianne Ericsson, Hans Diderholm
    Abstract:

    Abstract Monoclonal antibodies that interact with the decay accelerating factor (DAF, CD55), the lymphocyte homing receptor (CD44) or the intercellular adhesion molecule I (ICAM- 1) were found to inhibit the replication of different strains of CoxsackieVirus serotype B4 (CBV-4) to various extent. By adding antibodies to CD55 the replication of two (V345 and VD2921) of seven strains in HeLa cells, three (V89-4557, VD2921 and T318) of seven in A549-10C cells and one (VD2921) of five strains in RD cells was blocked totally. Consequently, the replication of one strain (VD2921) was blocked in all cells indicating that this strain uses CD55 as a receptor or as a co-receptor on all cell lines and is unable to use another cell surface protein. The binding of this strain to the cell surface was inhibited by the antibodies to CD55. None of the CBV-4 strains was blocked totally by adding antibodies to CD44 to HeLa and A549-10C cells, whereas in RD cells the replication of one (T318) of the CBV-4 strains was blocked totally. The antibodies to ICAM-1 did not inhibit totally the replication of any strain in HeLa and RD cells, but it blocked totally the replication of one strain (CBV-4-E) in A549-10C cells. In HeLa and A549-10C cells the degree of replication correlated highly with the degree of cytopathic effect (CPE). In RD cells, four of the strains replicated without CPE. The adding of antibodies to the integrin α v β 3 led to slightly enhanced replication of three of the CBV-4 strains in all cell lines. It is concluded that the receptor usage by different strains of CBV-4 varies not only within the same cells but also between different cell lines.

  • antibody responses to different strains of Coxsackie B4 Virus in patients with newly diagnosed type i diabetes mellitus or aseptic meningitis
    Journal of Infection, 1997
    Co-Authors: Gun Frisk, Hans Diderholm
    Abstract:

    Considerable differences in antibody responses measured by capture-IgM RIA and neutralization tests (NT) were seen in children with newly diagnosed type I (insulin-dependent) diabetes mellitus (IDDM) when five different strains of Coxsackie B4 Virus (CBV-4) were used. The IgM positivity of the 160 patients varied between 3.7 and 10.0% ( P P

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