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  • American Society for Microbiology  (7)
  • 1995-1999  (7)
Medientyp
Verlag/Herausgeber
  • American Society for Microbiology  (7)
Sprache
Erscheinungszeitraum
  • 1995-1999  (7)
Jahr
  • 1
    Online-Ressource
    Online-Ressource
    American Society for Microbiology ; 1998
    In:  Journal of Virology Vol. 72, No. 2 ( 1998-02), p. 1219-1223
    In: Journal of Virology, American Society for Microbiology, Vol. 72, No. 2 ( 1998-02), p. 1219-1223
    Kurzfassung: In situ nucleic acid hybridization and immunohistochemistry were used to determine the histological localization of mouse adenovirus type 1 (MAV-1) during acute infection of adult mice infected either intraperitoneally or intranasally with 1,000 PFU of wild-type virus. Organ samples were collected from days 1 to 17 postinfection for the intraperitoneally infected mice and from days 1 to 13 for the intranasally infected mice. Endothelial cells of the brain and spinal cord showed extensive evidence of MAV-1 infection. Endothelial cells in lungs, kidneys, and other organs were also positive for MAV-1, indicating a widespread involvement of the systemic circulation. The presence of viral nucleic acid and/or antigen was also demonstrated in lymphoid tissue. The spleens, Peyer’s patches, and peripheral lymph nodes showed positive staining at various times postinfection in mice infected by either route. Virus-infected cells in the spleen exhibited a stellate shape and were localized to the red pulp and germinal centers, suggesting that they are cells of the mononuclear phagocytic system.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1998
    ZDB Id: 1495529-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 2
    Online-Ressource
    Online-Ressource
    American Society for Microbiology ; 1996
    In:  Journal of Virology Vol. 70, No. 9 ( 1996-09), p. 5867-5874
    In: Journal of Virology, American Society for Microbiology, Vol. 70, No. 9 ( 1996-09), p. 5867-5874
    Kurzfassung: Early region 3 (E3) of mouse adenovirus type 1 has the potential to produce three proteins which have identical amino termini but unique carboxy-terminal sequences. Three recombinant deletion viruses were constructed so that each could produce only one of the three E3 proteins. A fourth mutant that should produce no E3 proteins was also constructed. These recombinants were able to grow in mouse 3T6 cells and produced wild-type levels of viral mRNAs and proteins except for those specifically deleted by the mutations. Early mRNA production from the mutant viruses was analyzed by reverse transcriptase PCR and confirmed that each deletion mutant would be able to produce only one of the three E3 proteins. Late mRNA production was analyzed by Northern (RNA) blotting and found to be similar in wild-type and mutant viruses. Capsid morphology was unaltered in the mutant viruses as seen by electron microscopy. Immunoprecipitation of E3 proteins from infections of mouse 3T6 cells using an antiserum specific for all three E3 proteins was used to examine the effect of the introduced mutations on protein expression. Two mutants produced only one class of E3 protein as predicted from their specific mutations and mRNA expression profiles. One mutant virus failed to produce any detectable E3 proteins. The predicted E3-null mutant was found to be leaky and could produce low levels of E3 proteins. Outbred Swiss mice were infected with the E3 mutant viruses to determine if the E3 proteins have an effect on the pathogenicity of the virus in mice. All of the mutants showed decreased pathogenicity as determined by increased 50% lethal doses, indicating that the proteins of the E3 region are important determinants of the pathogenesis of mouse adenovirus in its natural host.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1996
    ZDB Id: 1495529-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 3
    Online-Ressource
    Online-Ressource
    American Society for Microbiology ; 1996
    In:  Journal of Virology Vol. 70, No. 8 ( 1996-08), p. 5495-5502
    In: Journal of Virology, American Society for Microbiology, Vol. 70, No. 8 ( 1996-08), p. 5495-5502
    Kurzfassung: It has been proposed that adenoviruses establish and maintain persistent infections by reducing the class I major histocompatibility complex-associated presentation of viral antigens to cytotoxic T lymphocytes, leading to ineffective cell-mediated immunity and impaired clearance of infected cells (W.S.M. Wold and L. R. Gooding, Virology 184:1-8, 1991). Early region 3 of human adenovirus types 2 and 5 encodes a 19-kDa glycoprotein that associates with the class I major histocompatibility complex (MHC) antigens in the endoplasmic reticulum and prevents their maturation and transport to the cell surface. Early region 1A of human adenovirus type 12 encodes a protein that inhibits class I MHC mRNA production at the transcriptional or posttranscriptional processing level. Unlike human adenovirus infections, however, mouse adenovirus type 1 (MAV-1) infection of a variety of cell types did not affect the surface expression of 10 different mouse class I MHC allotypes. MAV-1-infected cells also regenerated cell surface class I MHC antigens following proteolytic removal as efficiently as mock-infected cells. The ability of cells to present antigen to class I MHC (Kb)-ovalbumin-specific T-cell hybridoma cells was likewise unaltered by MAV-1 infection. Thus, the ability of MAV-1 to persist cannot be explained by the model of reduced class I MHC-associated antigen presentation proposed for human adenoviruses.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1996
    ZDB Id: 1495529-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 4
    Online-Ressource
    Online-Ressource
    American Society for Microbiology ; 1998
    In:  Journal of Virology Vol. 72, No. 8 ( 1998-08), p. 6325-6331
    In: Journal of Virology, American Society for Microbiology, Vol. 72, No. 8 ( 1998-08), p. 6325-6331
    Kurzfassung: Mouse adenovirus type 1 (MAV-1) mutants with deletions of conserved regions of early region 1A (E1A) or with point mutations that eliminate translation of E1A were used to determine the role of E1A in MAV-1 replication. MAV-1 E1A mutants expressing no E1A protein grew to titers comparable to wild-type MAV-1 titers on mouse fibroblasts (3T6 fibroblasts and fibroblasts derived from Rb +/+, Rb +/−, and Rb −/− transgenic embryos). To test the hypothesis that E1A could induce a quiescent cell to reenter the cell cycle, fibroblasts were serum starved to stop DNA replication and cellular replication and then infected with the E1A mutant and wild-type viruses. All grew to equivalent titers. Steady-state levels of MAV-1 early mRNAs (E1A, E1B, E2, E3, and E4) from 3T6 cells infected with wild-type or E1A mutant virus were examined by Northern analysis. Steady-state levels of mRNAs from the mutant-infected cells were comparable to or greater than the levels found in wild-type virus infections for most of the early regions and for two late genes. The E2 mRNA levels were slightly reduced in all mutant infections relative to wild-type infections. E1A mRNA was not detected from infections with the MAV-1 E1A null mutant, pm E109, or from infections with similar MAV-1 E1A null mutants, pm E112 and pm E113. The implications for the lack of a requirement of E1A in cell culture are discussed.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1998
    ZDB Id: 1495529-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 5
    Online-Ressource
    Online-Ressource
    American Society for Microbiology ; 1999
    In:  Journal of Virology Vol. 73, No. 10 ( 1999-10), p. 8640-8646
    In: Journal of Virology, American Society for Microbiology, Vol. 73, No. 10 ( 1999-10), p. 8640-8646
    Kurzfassung: Previous attempts to construct a mouse adenovirus type 1 early region 3 (E3) null mutant by initiator codon mutagenesis were unsuccessful because one of the E3 proteins, gp11K, is synthesized as a fusion protein from a late viral mRNA (A. N. Cauthen and K. R. Spindler, Virology 259:119–128, 1999). Therefore, a different mutagenesis strategy was employed that inserted termination codons into all three reading frames of the E3 proteins. This strategy produced a mutant, pm E314, that was null for the expression of E3 proteins as determined by immunoprecipitation with E3-specific antisera. This mutant grew as well as wild-type (wt) virus in both 3T6 mouse fibroblasts and mouse brain microvascular endothelial cells. However, the 50% lethal dose for pm E314 in adult NIH Swiss outbred mice was approximately 6 log units higher than that of wt virus, indicating that pm E314 was less virulent in mice. In situ hybridization experiments revealed that the absence of the E3 proteins did not alter the tropism of the mutant virus from that of wt virus. When the histopathology was evaluated, the characteristics of the pm E314 infection at both doses administered were strikingly different from those exhibited by wt virus. The central nervous system of wt-infected mice exhibited damage to the endothelium and recruitment of inflammatory cells, whereas the central nervous system of pm E314-infected mice showed no inflammatory response and only mild signs of endothelial damage.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1999
    ZDB Id: 1495529-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 6
    Online-Ressource
    Online-Ressource
    American Society for Microbiology ; 1995
    In:  Journal of Virology Vol. 69, No. 12 ( 1995-12), p. 8084-8088
    In: Journal of Virology, American Society for Microbiology, Vol. 69, No. 12 ( 1995-12), p. 8084-8088
    Kurzfassung: Adult Swiss outbred mice from two sources had a nearly 6,000-fold difference in susceptibility to mouse adenovirus type 1-induced disease. This difference was not attributable to differential organ tropism. Signs associated with mouse adenovirus type 1 infection that have not been previously reported are described at the clinical, gross pathological, and histological levels.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1995
    ZDB Id: 1495529-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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  • 7
    Online-Ressource
    Online-Ressource
    American Society for Microbiology ; 1998
    In:  Journal of Virology Vol. 72, No. 7 ( 1998-07), p. 5699-5706
    In: Journal of Virology, American Society for Microbiology, Vol. 72, No. 7 ( 1998-07), p. 5699-5706
    Kurzfassung: Mouse adenovirus type 1 (MAV-1) early region 1A (E1A) viral mutants were used to determine the importance of this region in pathogenesis and establishment of a persistent infection in the natural host. Lethal dose analysis with adult male Swiss outbred mice revealed a significant reduction in virulence for all of the E1A mutants. During acute infections with 10 5 PFU of virus, an E1A null mutant, pm E109, was found in the same organs (brain, spleen, and spinal cord) and the same cell types (endothelial cells and mononuclear cells in lymphoid tissue) as wild-type virus. Another null mutant, pm E112, was detected in the same organs but in lower numbers. However, when mice were given a lower dose, 1 PFU, pm E109 and pm E112 reached none of the target organs analyzed by 14 days postinfection (p.i.). The absence of E1A did not hinder the ability of MAV-1 to establish a persistent infection. Viral nucleic acid was detected by PCR amplification or in situ hybridization in the kidneys, brains, spleens, and prefemoral lymph nodes of mice infected with wild-type or mutant virus up to 55 weeks p.i. The brain, spleen, and lymph node are recognized sites of acute viral infection but are previously unrecognized sites for MAV-1 persistence. Evidence for the potential reactivation of persistent MAV-1 infections is also presented.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1998
    ZDB Id: 1495529-5
    Bibliothek Standort Signatur Band/Heft/Jahr Verfügbarkeit
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