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  • 1
    Online Resource
    Online Resource
    Genetic Determinants of Mouse Hepatitis Virus Strain 1 Pneumovirulence
    American Society for Microbiology ; 2010
    In:  Journal of Virology Vol. 84, No. 18 ( 2010-09-15), p. 9278-9291
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 84, No. 18 ( 2010-09-15), p. 9278-9291
    Abstract: We report here investigation into the genetic basis of mouse hepatitis virus strain 1 (MHV-1) pneumovirulence. Sequencing of the 3′ one-third of the MHV-1 genome demonstrated that the genetic organization of MHV-1 was similar to that of other strains of MHV. The hemagglutinin esterase (HE) protein was truncated, and reverse transcription-PCR (RT-PCR) studies confirmed previous work that suggested that the MHV-1 HE is a pseudogene. Targeted recombination was used to select chimeric viruses containing either the MHV-1 S gene or genes encoding all of the MHV-1 structural proteins, on an MHV-A59 background. Challenge studies in mice demonstrated that expression of the MHV-1 S gene within the MHV-A59 background (rA59/S MHV-1 ) increased the pneumovirulence of MHV-A59, and mice infected with this recombinant virus developed pulmonary lesions that were similar to those observed with MHV-1, although rA59/S MHV-1 was significantly less virulent. Chimeras containing all of the MHV-1 structural genes on an MHV-A59 background were able to reproduce the severe acute respiratory syndrome (SARS)-like pathology observed with MHV-1 and reproducibly increased pneumovirulence relative to rA59/S MHV-1 , but were still much less virulent than MHV-1. These data suggest that important determinants of pneumopathogenicity are contained within the 3′ one-third of the MHV-1 genome, but additional important virulence factors must be encoded in the genome upstream of the S gene. The severity of the pulmonary lesions observed correlates better with elevated levels of inflammatory cytokines than with viral replication in the lungs, suggesting that pulmonary disease has an important immunological component.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.00330-10
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2010
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  • 2
    Online Resource
    Online Resource
    Murine Coronavirus Spike Protein Determines the Ability of the Virus To Replicate in the Liver and Cause Hepatitis
    American Society for Microbiology ; 2001
    In:  Journal of Virology Vol. 75, No. 5 ( 2001-03), p. 2452-2457
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 75, No. 5 ( 2001-03), p. 2452-2457
    Abstract: Recombinant mouse hepatitis viruses (MHV) differing only in the spike gene, containing A59, MHV-4, and MHV-2 spike genes in the background of the A59 genome, were compared for their ability to replicate in the liver and induce hepatitis in weanling C57BL/6 mice infected with 500 PFU of each virus by intrahepatic injection. Penn98-1, expressing the MHV-2 spike gene, replicated to high titer in the liver, similar to MHV-2, and induced severe hepatitis with extensive hepatocellular necrosis. S A59 R13, expressing the A59 spike gene, replicated to a somewhat lower titer and induced moderate to severe hepatitis with zonal necrosis, similar to MHV-A59. S 4 R21, expressing the MHV-4 spike gene, replicated to a minimal extent and induced few if any pathological changes, similar to MHV-4. Thus, the extent of replication and the degree of hepatitis in the liver induced by these recombinant viruses were determined largely by the spike protein.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.75.5.2452-2457.2001
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2001
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  • 3
    Online Resource
    Online Resource
    Pathogenesis of Chimeric MHV4/MHV-A59 Recombinant Viruses: the Murine Coronavirus Spike Protein Is a Major Determinant of Neurovirulence
    American Society for Microbiology ; 1999
    In:  Journal of Virology Vol. 73, No. 9 ( 1999-09), p. 7752-7760
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 73, No. 9 ( 1999-09), p. 7752-7760
    Abstract: The mouse hepatitis virus (MHV) spike glycoprotein, S, has been implicated as a major determinant of viral pathogenesis. In the absence of a full-length molecular clone, however, it has been difficult to address the role of individual viral genes in pathogenesis. By using targeted RNA recombination to introduce the S gene of MHV4, a highly neurovirulent strain, into the genome of MHV-A59, a mildly neurovirulent strain, we have been able to directly address the role of the S gene in neurovirulence. In cell culture, the recombinants containing the MHV4 S gene, S4R22 and S4R21, exhibited a small-plaque phenotype and replicated to low levels, similar to wild-type MHV4. Intracranial inoculation of C57BL/6 mice with S4R22 and S4R21 revealed a marked alteration in pathogenesis. Relative to wild-type control recombinant viruses (wtR13 and wtR9), containing the MHV-A59 S gene, the MHV4 S gene recombinants exhibited a dramatic increase in virulence and an increase in both viral antigen staining and inflammation in the central nervous system. There was not, however, an increase in the level of viral replication in the brain. These studies demonstrate that the MHV4 S gene alone is sufficient to confer a highly neurovirulent phenotype to a recombinant virus deriving the remainder of its genome from a mildly neurovirulent virus, MHV-A59. This definitively confirms previous findings, suggesting that the spike is a major determinant of pathogenesis.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.73.9.7752-7760.1999
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1999
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  • 4
    Online Resource
    Online Resource
    Altered Pathogenesis of a Mutant of the Murine Coronavirus MHV-A59 Is Associated with a Q159L Amino Acid Substitution in the Spike Protein
    Elsevier BV ; 1997
    In:  Virology Vol. 239, No. 1 ( 1997-12), p. 1-10
    Details
    In: Virology, Elsevier BV, Vol. 239, No. 1 ( 1997-12), p. 1-10
    Type of Medium: Online Resource
    ISSN: 0042-6822
    URL: Article
    DOI: 10.1006/viro.1997.8877
    RVK:
    WA 15000
    Language: English
    Publisher: Elsevier BV
    Publication Date: 1997
    detail.hit.zdb_id: 1471925-3
    SSG: 12
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  • 5
    Online Resource
    Online Resource
    Perforin-Mediated CTL Cytolysis Counteracts Direct Cell-Cell Spread of Listeria monocytogenes
    The American Association of Immunologists ; 2002
    In:  The Journal of Immunology Vol. 169, No. 9 ( 2002-11-01), p. 5202-5208
    Details
    In: The Journal of Immunology, The American Association of Immunologists, Vol. 169, No. 9 ( 2002-11-01), p. 5202-5208
    Abstract: The immune system has evolved various effector cells and functions to combat diverse infectious agents equipped with different virulence strategies. CD8 T cells play a critical role in protective immunity to Listeria monocytogenes (Lm), a bacterium that grows within the host cell cytosol and spreads directly into neighboring cells. The importance of CD8 T cells during Lm infection is currently attributed to the cytosolic niche of this organism, which allows it to evade many aspects of immune surveillance. CTL lysis of infected cells is believed to be an essential protective mechanism, presumably functioning to release intracellular bacteria, although its precise role remains to be fully defined. In this study, we examined the contribution of perforin-mediated CTL cytolysis to protective immunity against recombinant Lm capable of or defective in cell-cell spread. We found that CTL cytolysis is critical for protective immunity to Lm capable of cell-cell spread while protective immunity against spread-defective Lm is largely independent of CTL cytolysis. These results demonstrate that an important function of CTL cytolysis is to counter the microbial virulence strategy of direct cell-cell spread. We propose a model that advances the current view of the role of CTL cytolysis in immunity to intracellular pathogens.
    Type of Medium: Online Resource
    ISSN: 0022-1767 , 1550-6606
    URL: Article
    DOI: 10.4049/jimmunol.169.9.5202
    RVK:
    XA 54100
    RVK:
    XA 10000
    Language: English
    Publisher: The American Association of Immunologists
    Publication Date: 2002
    detail.hit.zdb_id: 1475085-5
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  • 6
    Online Resource
    Online Resource
    Water binding and hygroscopicity in π-conjugated polyelectrolytes
    Springer Science and Business Media LLC ; 2023
    In:  Nature Communications Vol. 14, No. 1 ( 2023-07-05)
    Details
    In: Nature Communications, Springer Science and Business Media LLC, Vol. 14, No. 1 ( 2023-07-05)
    Abstract: The presence of water strongly influences structure, dynamics and properties of ion-containing soft matter. Yet, the hydration of such matter is not well understood. Here, we show through a large study of monovalent π-conjugated polyelectrolytes that their reversible hydration, up to several water molecules per ion pair, occurs chiefly at the interface between the ion clusters and the hydrophobic matrix without disrupting ion packing. This establishes the appropriate model to be surface hydration, not the often-assumed internal hydration of the ion clusters. Through detailed analysis of desorption energies and O–H vibrational frequencies, together with OPLS4 and DFT calculations, we have elucidated key binding motifs of the sorbed water. Type-I water, which desorbs below 50 °C, corresponds to hydrogen-bonded water clusters constituting secondary hydration. Type-II water, which typically desorbs over 50–150 °C, corresponds to water bound to the anion under the influence of a proximal cation, or to a cation‒anion pair, at the cluster surface. This constitutes primary hydration. Type-III water, which irreversibly desorbs beyond 150 °C, corresponds to water kinetically trapped between ions. Its amount varies strongly with processing and heat treatment. As a consequence, hygroscopicity—which is the water sorption capacity per ion pair—depends not only on the ions, but also their cluster morphology.
    Type of Medium: Online Resource
    ISSN: 2041-1723
    URL: Article
    DOI: 10.1038/s41467-023-39215-9
    Language: English
    Publisher: Springer Science and Business Media LLC
    Publication Date: 2023
    detail.hit.zdb_id: 2553671-0
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  • 7
    Online Resource
    Online Resource
    Replicase Genes of Murine Coronavirus Strains A59 and JHM Are Interchangeable: Differences in Pathogenesis Map to the 3′ One-Third of the Genome
    American Society for Microbiology ; 2007
    In:  Journal of Virology Vol. 81, No. 2 ( 2007-01-15), p. 1022-1026
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 81, No. 2 ( 2007-01-15), p. 1022-1026
    Abstract: The important roles of the spike protein and other structural proteins in murine coronavirus (MHV) pathogenesis have been demonstrated; however, the role of the replicase gene remains unexplored. We assessed the influence of the replicase genes of the highly neurovirulent MHV-JHM strain and the hepatotropic and mildly neurovirulent A59 strain in acute infection of the mouse. Analysis of chimeric A59/JHM recombinant viruses indicates that the replicase genes are interchangeable and that it is the 3′ end of the genome, encoding the structural proteins, rather than the replicase gene, that determines the pathogenic properties of these chimeras.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.01944-06
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2007
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  • 8
    Online Resource
    Online Resource
    Targeted Recombination within the Spike Gene of Murine Coronavirus Mouse Hepatitis Virus-A59: Q159 Is a Determinant of Hepatotropism
    American Society for Microbiology ; 1998
    In:  Journal of Virology Vol. 72, No. 12 ( 1998-12), p. 9628-9636
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 72, No. 12 ( 1998-12), p. 9628-9636
    Abstract: Previous studies of a group of mutants of the murine coronavirus mouse hepatitis virus (MHV)-A59, isolated from persistently infected glial cells, have shown a strong correlation between a Q159L amino acid substitution in the S1 subunit of the spike gene and a loss in the ability to induce hepatitis and demyelination. To determine if Q159L alone is sufficient to cause these altered pathogenic properties, targeted RNA recombination was used to introduce a Q159L amino acid substitution into the spike gene of MHV-A59. Recombination was carried out between the genome of a temperature-sensitive mutant of MHV-A59 (Alb4) and RNA transcribed from a plasmid (pFV1) containing the spike gene as well as downstream regions, through the 3′ end, of the MHV-A59 genome. We have selected and characterized two recombinant viruses containing Q159L. These recombinant viruses (159R36 and 159R40) replicate in the brains of C57BL/6 mice and induce encephalitis to a similar extent as wild-type MHV-A59. However, they exhibit a markedly reduced ability to replicate in the liver or produce hepatitis compared to wild-type MHV-A59. These viruses also exhibit reduced virulence and reduced demyelination. A recombinant virus containing the wild-type MHV-A59 spike gene, wtR10, behaved essentially like wild-type MHV-A59. This is the first report of the isolation of recombinant viruses containing a site-directed mutation, encoding an amino acid substitution, within the spike gene of any coronavirus. This technology will allow us to begin to map the molecular determinants of pathogenesis within the spike glycoprotein.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.72.12.9628-9636.1998
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 1998
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  • 9
    Online Resource
    Online Resource
    Contributions of the Viral Genetic Background and a Single Amino Acid Substitution in an Immunodominant CD8 + T-Cell Epitope to Murine Coronavirus Neurovirulence
    American Society for Microbiology ; 2005
    In:  Journal of Virology Vol. 79, No. 14 ( 2005-07), p. 9108-9118
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 79, No. 14 ( 2005-07), p. 9108-9118
    Abstract: The immunodominant CD8 + T-cell epitope of a highly neurovirulent strain of mouse hepatitis virus (MHV), JHM, is thought to be essential for protection against virus persistence within the central nervous system. To test whether abrogation of this H-2D b -restricted epitope, located within the spike glycoprotein at residues S510 to 518 (S510), resulted in delayed virus clearance and/or virus persistence we selected isogenic recombinants which express either the wild-type JHM spike protein (RJHM) or spike containing the N514S mutation (RJHM N514S ), which abrogates the response to S510. In contrast to observations in suckling mice in which viruses encoding inactivating mutations within the S510 epitope (epitope escape mutants) were associated with persistent virus and increased neurovirulence (Pewe et al., J Virol. 72:5912-5918, 1998), RJHM N514S was not more virulent than the parental, RJHM, in 4-week-old C57BL/6 ( H-2 b ) mice after intracranial injection. Recombinant viruses expressing the JHM spike, wild type or encoding the N514S substitution, were also selected in which background genes were derived from the neuroattenuated A59 strain of MHV. Whereas recombinants expressing the wild-type JHM spike (SJHM/RA59) were highly neurovirulent, A59 recombinants containing the N514S mutation (SJHM N514S /RA59) were attenuated, replicated less efficiently, and exhibited reduced virus spread in the brain at 5 days postinfection (peak of infectious virus titers in the central nervous system) compared to parental virus encoding wild-type spike. Virulence assays in BALB/c mice ( H-2 d ), which do not recognize the S510 epitope, revealed that attenuation of the epitope escape mutants was not due to the loss of a pathogenic immune response directed against the S510 epitope. Thus, an intact immunodominant S510 epitope is not essential for virus clearance from the CNS, the S510 inactivating mutation results in decreased virulence in weanling mice but not in suckling mice, suggesting that specific host conditions are required for epitope escape mutants to display increased virulence, and the N514S mutation causes increased attenuation in the context of A59 background genes, demonstrating that genes other than that for the spike are also important in determining neurovirulence.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.79.14.9108-9118.2005
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2005
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  • 10
    Online Resource
    Online Resource
    Priming of CD8 + T Cells during Central Nervous System Infection with a Murine Coronavirus Is Strain Dependent
    American Society for Microbiology ; 2008
    In:  Journal of Virology Vol. 82, No. 13 ( 2008-07), p. 6150-6160
    Details
    In: Journal of Virology, American Society for Microbiology, Vol. 82, No. 13 ( 2008-07), p. 6150-6160
    Abstract: Virus-specific CD8 + T cells are critical for protection against neurotropic coronaviruses; however, central nervous system (CNS) infection with the recombinant JHM (RJHM) strain of mouse hepatitis virus (MHV) elicits a weak CD8 + T-cell response in the brain and causes lethal encephalomyelitis. An adoptive transfer model was used to elucidate the kinetics of CD8 + T-cell priming during CNS infection with RJHM as well as with two MHV strains that induce a robust CD8 + T-cell response (RA59 and SJHM/RA59, a recombinant A59 virus expressing the JHM spike). While RA59 and SJHM/RA59 infections resulted in CD8 + T-cell priming within the first 2 days postinfection, RJHM infection did not lead to proliferation of naïve CD8 + T cells. While all three viruses replicated efficiently in the brain, only RA59 and SJHM/RA59 replicated to appreciable levels in the cervical lymph nodes (CLN), the site of T-cell priming during acute CNS infection. RJHM was unable to suppress the CD8 + T-cell response elicited by RA59 in mice simultaneously infected with both strains, suggesting that RJHM does not cause generalized immunosuppression. RJHM was also unable to elicit a secondary CD8 + T-cell response in the brain following peripheral immunization against a viral epitope. Notably, the weak CD8 + T-cell response elicited by RJHM was unique to CNS infection, since peripheral inoculation induced a robust CD8 + T-cell response in the spleen. These findings suggest that the failure of RJHM to prime a robust CD8 + T-cell response during CNS infection is likely due to its failure to replicate in the CLN.
    Type of Medium: Online Resource
    ISSN: 0022-538X , 1098-5514
    URL: Article
    DOI: 10.1128/JVI.00106-08
    Language: English
    Publisher: American Society for Microbiology
    Publication Date: 2008
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