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  • American Society for Microbiology  (49)
  • 1
    Online-Ressource
    Online-Ressource
    Genomewide Association Analysis of Respiratory Syncytial Virus Infection in Mice
    American Society for Microbiology ; 2010
    In:  Journal of Virology Vol. 84, No. 5 ( 2010-03), p. 2257-2269
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 84, No. 5 ( 2010-03), p. 2257-2269
    Kurzfassung: Respiratory syncytial virus (RSV) is the major cause of lower respiratory tract infection in infants, with about half being infected in their first year of life. Yet only 2 to 3% of infants are hospitalized for RSV infection, suggesting that individual susceptibility contributes to disease severity. Previously, we determined that AKR/J (susceptible) mice developed high lung RSV titers and showed delayed weight recovery, whereas C57BL/6J (resistant) mice demonstrated low lung RSV titers and rapid weight recovery. In addition, we have reported that gene-targeted mice lacking the cystic fibrosis transmembrane conductance regulator ( Cftr ; ATP-binding cassette subfamily C, member 7) are susceptible to RSV infection. For this report, recombinant backcross and F2 progeny derived from C57BL/6J and AKR/J mice were infected with RSV, their lung titers were measured, and quantitative trait locus (QTL) analysis was performed. A major QTL, designated Rsvs1 , was identified on proximal mouse chromosome 6 in both recombinant populations. Microarray analysis comparing lung transcripts of the parental strains during infection identified several candidate genes that mapped to the Rsvs1 interval, including Cftr . These findings add to our understanding of individual RSV susceptibility and strongly support a modifier role for CFTR in RSV infection, a significant cause of respiratory morbidity in infants with cystic fibrosis.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.00584-09
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2010
    ZDB Id: 1495529-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 2
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    Dual RNA-seq identifies genes and pathways modulated during Clostridioides difficile colonization
    American Society for Microbiology ; 2023
    In:  mSystems
    Details
    In: mSystems, American Society for Microbiology
    Kurzfassung: The initial interactions between the colonic epithelium and the bacterium are likely critical in the establishment of Clostridioides difficile infection, one of the major causes of hospital-acquired diarrhea worldwide. Molecular interactions between C. difficile and human gut cells have not been well defined mainly due to the technical challenges of studying cellular host–pathogen interactions with this anaerobe. Here we have examined transcriptional changes occurring in the pathogen and host cells during the initial 24 hours of infection. Our data indicate several changes in metabolic pathways and virulence-associated factors during the initial bacterium-host cell contact and early stages of infection. We describe canonical pathways enriched based on the expression profiles of a dual RNA sequencing in the host and bacterium, and functions of bacterial factors that are modulated during infection. This study thus provides fresh insight into the early C. difficile infection process.
    Materialart: Online-Ressource
    ISSN: 2379-5077
    URL: Article
    DOI: 10.1128/msystems.00555-23
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2023
    ZDB Id: 2844333-0
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 3
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    Two deletions within genes for simian virus 40 structural proteins VP2 and VP3 lead to formation of abnormal transcriptional complexes
    American Society for Microbiology ; 1981
    In:  Journal of Virology Vol. 38, No. 1 ( 1981-04), p. 91-103
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 38, No. 1 ( 1981-04), p. 91-103
    Kurzfassung: The procedure developed by R. M. Fernandez-Muñoz et al. (J. Virol. 29:612-623, 1979) for isolating simian virus 40 (SV 40) chromatin free of disrupted previrions was optimized for preparing late transcriptional complexes, and these complexes were partially characterized. Transcriptional complexes derived from wild-type virus and from several deletion and temperature-sensitive mutants could be activated more than five-fold either by the anionic detergent Sarkosyl or by 300 mM ammonium sulfate, in agreement with the properties of SV40 transcriptional complexes prepared by other procedures. In contrast, complexes from cells infected with deletion mutants dl1261 or dl1262 were not activated at all by a high salt concentration, even though the extent of their activation by Sarkosyl was normal. Mutants dl1261 and dl1262 carry deletions of 54 and 36 base pairs, respectively, at an approximate map position of 0.91, which is within the overlapping genes for the virion proteins VP2 and VP3. The effects of these deletions on transcription in vitro indicate that VP2 or VP3 or both are bound to late transcriptional complexes in a way that affects the progress of initiated RNA polymerase. The properties of late transcriptional complexes derived from wild-type SV40 can be explained by the presence of the following two different kinds of complexes: (i) a minority class (about 20%), which is free of VP2 or VP3, active at low concentrations of ammonium sulfate in vitro, and responsible for late transcription in vivo, and (ii) a majority class (about 80%) with VP2 or VP3 bound, which is inactive at low salt concentrations both in vitro and in vivo but capable of being activated by high salt concentrations or by Sarkosyl. We propose that mutant VP2 and VP3 proteins from dl1261 and dl1262 bind to the majority class of late transcriptional complexes in a way that can be reversed by Sarkosyl but not by a high salt concentration.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.38.1.91-103.1981
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1981
    ZDB Id: 1495529-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 4
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    Online-Ressource
    RNase of classical swine fever virus: biochemical characterization and inhibition by virus-neutralizing monoclonal antibodies
    American Society for Microbiology ; 1996
    In:  Journal of Virology Vol. 70, No. 1 ( 1996-01), p. 352-358
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 70, No. 1 ( 1996-01), p. 352-358
    Kurzfassung: The structural glycoprotein E0 of classical swine fever virus (CSFV) possesses an intrinsic RNase activity. Here we present the first comprehensive biochemical characterization of E0, using a recombinant glycoprotein expressed in insect cells. We were able to show that the presence of neither carbohydrate moieties nor disulfide bonds is a prerequisite for RNase activity. In addition, virus-neutralizing and nonneutralizing anti-E0 monoclonal antibodies were tested for their ability to influence RNase activity. In these experiments, the antibodies which effectively blocked the infection of STE cells also exerted a high degree of E0 RNase inhibition. This correlation suggests that the RNase activity of CSFV E0 plays a role in the viral life cycle.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.70.1.352-358.1996
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1996
    ZDB Id: 1495529-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 5
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    Online-Ressource
    Down-Regulation of p53 by Double-Stranded RNA Modulates the Antiviral Response
    American Society for Microbiology ; 2005
    In:  Journal of Virology Vol. 79, No. 17 ( 2005-09), p. 11105-11114
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 79, No. 17 ( 2005-09), p. 11105-11114
    Kurzfassung: p53 has been well characterized as a tumor suppressor gene, but its role in antiviral defense remains unclear. A recent report has demonstrated that p53 can be induced by interferons and is activated after vesicular stomatitis virus (VSV) infection. We observed that different nononcogenic viruses, including encephalomyocarditis virus (EMCV) and human parainfluenza virus type 3 (HPIV3), induced down-regulation of p53 in infected cells. Double-stranded RNA (dsRNA) and a mutant vaccinia virus lacking the dsRNA binding protein E3L can also induce this effect, indicating that dsRNA formed during viral infection is likely the trigger for down-regulation of p53. The mechanism of down-regulation of p53 by dsRNA relies on translation inhibition mediated by the PKR and RNase L pathways. In the absence of p53, the replication of both EMCV and HPIV3 was retarded, whereas, conversely, VSV replication was enhanced. Cell cycle analysis indicated that wild-type (WT) but not p53 knockout (KO) fibroblasts undergo an early-G 1 arrest following dsRNA treatment. Moreover, in WT cells the onset of dsRNA-induced apoptosis begins after p53 levels are down-regulated, whereas p53 KO cells, which lack the early-G 1 arrest, rapidly undergo apoptosis. Hence, our data suggest that the down-regulation of p53 facilitates apoptosis, thereby limiting viral replication.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.79.17.11105-11114.2005
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2005
    ZDB Id: 1495529-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 6
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    Influenza A Virus Multicycle Replication Yields Comparable Viral Population Emergence in Human Respiratory and Ocular Cell Types
    American Society for Microbiology ; 2023
    In:  Microbiology Spectrum Vol. 11, No. 4 ( 2023-08-17)
    Details
    In: Microbiology Spectrum, American Society for Microbiology, Vol. 11, No. 4 ( 2023-08-17)
    Kurzfassung: While primarily considered a respiratory pathogen, influenza A virus (IAV) is nonetheless capable of spreading to, and replicating in, numerous extrapulmonary tissues in humans. However, within-host assessments of genetic diversity during multicycle replication have been largely limited to respiratory tract tissues and specimens. As selective pressures can vary greatly between anatomical sites, there is a need to examine how measures of viral diversity may vary between influenza viruses exhibiting different tropisms in humans, as well as following influenza virus infection of cells derived from different organ systems. Here, we employed human primary tissue constructs emulative of the human airway or corneal surface, and we infected both with a panel of human- and avian-origin IAV, inclusive of H1 and H3 subtype human viruses and highly pathogenic H5 and H7 subtype viruses, which are associated with both respiratory disease and conjunctivitis following human infection. While both cell types supported productive replication of all viruses, airway-derived tissue constructs elicited greater induction of genes associated with antiviral responses than did corneal-derived constructs. We used next-generation sequencing to examine viral mutations and population diversity, utilizing several metrics. With few exceptions, generally comparable measures of viral diversity and mutational frequency were detected following homologous virus infection of both respiratory-origin and ocular-origin tissue constructs. Expansion of within-host assessments of genetic diversity to include IAV with atypical clinical presentations in humans or in extrapulmonary cell types can provide greater insight into understanding those features most prone to modulation in the context of viral tropism. IMPORTANCE Influenza A virus (IAV) can infect tissues both within and beyond the respiratory tract, leading to extrapulmonary complications, such as conjunctivitis or gastrointestinal disease. Selective pressures governing virus replication and induction of host responses can vary based on the anatomical site of infection, yet studies examining within-host assessments of genetic diversity are typically only conducted in cells derived from the respiratory tract. We examined the contribution of influenza virus tropism on these properties two different ways: by using IAV associated with different tropisms in humans, and by infecting human cell types from two different organ systems susceptible to IAV infection. Despite the diversity of cell types and viruses employed, we observed generally similar measures of viral diversity postinfection across all conditions tested; these findings nonetheless contribute to a greater understanding of the role tissue type contributes to the dynamics of virus evolution within a human host.
    Materialart: Online-Ressource
    ISSN: 2165-0497
    URL: Article
    DOI: 10.1128/spectrum.01166-23
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 2023
    ZDB Id: 2807133-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 7
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    Mutagenicity of anthraquinone and hydroxylated anthraquinones in the Ames/Salmonella microsome system
    American Society for Microbiology ; 1982
    In:  Applied and Environmental Microbiology Vol. 43, No. 6 ( 1982-06), p. 1354-1359
    Details
    In: Applied and Environmental Microbiology, American Society for Microbiology, Vol. 43, No. 6 ( 1982-06), p. 1354-1359
    Kurzfassung: The mutagenicity of anthracene, anthraquinone, and four structurally similar compounds of each was evaluated in the Ames/Salmonella microsome assay. Anthraquinone was shown to be mutagenic for strains TA1537, TA1538, and TA98 in the absence of rat liver homogenate. The four anthraquinone derivatives tested were mutagenic for TA1537 exclusively. None of the anthracenes exhibited mutagenic activity.
    Materialart: Online-Ressource
    ISSN: 0099-2240 , 1098-5336
    URL: Article
    DOI: 10.1128/aem.43.6.1354-1359.1982
    RVK:
    WA 15000
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1982
    ZDB Id: 223011-2
    ZDB Id: 1478346-0
    SSG: 12
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 8
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    A second envelope glycoprotein mediates neutralization of a pestivirus, hog cholera virus
    American Society for Microbiology ; 1992
    In:  Journal of Virology Vol. 66, No. 6 ( 1992-06), p. 3677-3682
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 66, No. 6 ( 1992-06), p. 3677-3682
    Kurzfassung: Several monoclonal antibodies (MAbs) raised against hog cholera virus (HCV) reacted with the HCV structural glycoprotein gp44/48 and neutralized the virus. The presence of HCV gp44/48 on the viral surface was directly demonstrated by immunogold electron microscopy. Eight anti-HCV gp44/48 MAbs were tested by immunoperoxidase assay against a panel of pestivirus strains. Each MAb showed a distinct pattern of reactivity with HCV strains. It is suggested that the MAbs are well suited for epidemiological investigations of HCV outbreaks.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.66.6.3677-3682.1992
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1992
    ZDB Id: 1495529-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 9
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    Constitutive production of alpha and beta interferons in mutant human cell lines
    American Society for Microbiology ; 1994
    In:  Journal of Virology Vol. 68, No. 6 ( 1994-06), p. 4057-4062
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 68, No. 6 ( 1994-06), p. 4057-4062
    Kurzfassung: Alpha and beta interferons control expression of a selectable marker in the human hypoxanthine phosphoribosyltransferase-negative cell line 2fTGH, in which transcription of gpt is regulated by the upstream region of an interferon-responsive human gene. Selection of mutagenized 2fTGH cells in hypoxanthine-aminopterin-thymidine medium yielded mutants in one recessive (C1) and two dominant (C2 and C3) complementation groups. The mutants constitutively expressed low levels of beta interferon (C1), alpha interferon (C2), or both (C3).
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.68.6.4057-4062.1994
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1994
    ZDB Id: 1495529-5
    Standort Signatur Einschränkungen Verfügbarkeit
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  • 10
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    Cytopathogenicity of a pestivirus correlates with a 27-nucleotide insertion
    American Society for Microbiology ; 1996
    In:  Journal of Virology Vol. 70, No. 11 ( 1996-11), p. 7851-7858
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 70, No. 11 ( 1996-11), p. 7851-7858
    Kurzfassung: Cytopathogenic (cp) bovine viral diarrhea virus (BVDV) strains are generated in cattle persistently infected with noncytopathogenic (noncp) BVDV.cp BVDV strains are considered crucial for the development of fatal mucosal disease. Comparative analysis of cp and noncp BVDV strains isolated from one animal suffering from mucosal disease revealed that the genomes of the cp BVDV strain (CP7) and the corresponding noncp BVDV strain (NCP7) are highly homologous. However, only the genome of CP7 contains an insertion of 27 nucleotides in the NS2 coding region. The inserted sequence represents a duplication of bases 4064 to 4090 of the viral genome, located between the formerly neighboring nucleotides 4353 and 4354. Parts of the viral polyproteins of CP7 and NCP7 were expressed in the T7 vaccinia virus system. These studies revealed that the insertion identified in the CP7 genome is necessary and sufficient for the induction of NS2-3 cleavage. Since the expression of NS3 is strictly correlated to cp BVDV, the insertion identified in the genome of BVDV CP7 represents most likely the relevant mutation leading to the evolvement of CP7 from NCP7.
    Materialart: Online-Ressource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/jvi.70.11.7851-7858.1996
    Sprache: Englisch
    Verlag: American Society for Microbiology
    Publikationsdatum: 1996
    ZDB Id: 1495529-5
    Standort Signatur Einschränkungen Verfügbarkeit
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