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346 related items for PubMed ID: 15919915

  • 1. Murine coronavirus evolution in vivo: functional compensation of a detrimental amino acid substitution in the receptor binding domain of the spike glycoprotein.
    Navas-Martin S, Hingley ST, Weiss SR.
    J Virol; 2005 Jun; 79(12):7629-40. PubMed ID: 15919915
    [Abstract] [Full Text] [Related]

  • 2. Targeted recombination within the spike gene of murine coronavirus mouse hepatitis virus-A59: Q159 is a determinant of hepatotropism.
    Leparc-Goffart I, Hingley ST, Chua MM, Phillips J, Lavi E, Weiss SR.
    J Virol; 1998 Dec; 72(12):9628-36. PubMed ID: 9811696
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  • 3. Murine coronavirus spike protein determines the ability of the virus to replicate in the liver and cause hepatitis.
    Navas S, Seo SH, Chua MM, Das Sarma J, Lavi E, Hingley ST, Weiss SR.
    J Virol; 2001 Mar; 75(5):2452-7. PubMed ID: 11160748
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  • 4. Hepatitis mutants of mouse hepatitis virus strain A59.
    Hingley ST, Gombold JL, Lavi E, Weiss SR.
    Adv Exp Med Biol; 1995 Mar; 380():577-82. PubMed ID: 8830545
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  • 5. In vitro properties and pathogenesis of A59/MHV4 chimeric mouse hepatitis viruses.
    Tsai JC, Weiss SR.
    Adv Exp Med Biol; 2001 Mar; 494():169-72. PubMed ID: 11774464
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  • 6. Altered pathogenesis of a mutant of the murine coronavirus MHV-A59 is associated with a Q159L amino acid substitution in the spike protein.
    Leparc-Goffart I, Hingley ST, Chua MM, Jiang X, Lavi E, Weiss SR.
    Virology; 1997 Dec 08; 239(1):1-10. PubMed ID: 9426441
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  • 9. Sequence analysis of the S gene of recombinant MHV-2/A59 coronaviruses reveals three candidate mutations associated with demyelination and hepatitis.
    Das Sarma J, Fu L, Hingley ST, Lai MM, Lavi E.
    J Neurovirol; 2001 Oct 08; 7(5):432-6. PubMed ID: 11582515
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  • 11. Amino acid substitutions and an insertion in the spike glycoprotein extend the host range of the murine coronavirus MHV-A59.
    Thackray LB, Holmes KV.
    Virology; 2004 Jul 01; 324(2):510-24. PubMed ID: 15207636
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  • 12. The virulence of mouse hepatitis virus strain A59 is not dependent on efficient spike protein cleavage and cell-to-cell fusion.
    Hingley ST, Leparc-Goffart I, Seo SH, Tsai JC, Weiss SR.
    J Neurovirol; 2002 Oct 01; 8(5):400-10. PubMed ID: 12402166
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  • 13. Multiple regions of the murine coronavirus spike glycoprotein influence neurovirulence.
    Phillips JJ, Chua M, Seo SH, Weiss SR.
    J Neurovirol; 2001 Oct 01; 7(5):421-31. PubMed ID: 11582514
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  • 14. Substitutions of conserved amino acids in the receptor-binding domain of the spike glycoprotein affect utilization of murine CEACAM1a by the murine coronavirus MHV-A59.
    Thackray LB, Turner BC, Holmes KV.
    Virology; 2005 Mar 30; 334(1):98-110. PubMed ID: 15749126
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  • 16. MHV-A59 fusion mutants are attenuated and display altered hepatotropism.
    Hingley ST, Gombold JL, Lavi E, Weiss SR.
    Virology; 1994 Apr 30; 200(1):1-10. PubMed ID: 8128613
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  • 18. Pathogenesis of chimeric MHV4/MHV-A59 recombinant viruses: the murine coronavirus spike protein is a major determinant of neurovirulence.
    Phillips JJ, Chua MM, Lavi E, Weiss SR.
    J Virol; 1999 Sep 30; 73(9):7752-60. PubMed ID: 10438865
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  • 20. Identification of H209 as Essential for pH 8-Triggered Receptor-Independent Syncytium Formation by S Protein of Mouse Hepatitis Virus A59.
    Li P, Shan Y, Zheng W, Ou X, Mi D, Mu Z, Holmes KV, Qian Z.
    J Virol; 2018 Jun 01; 92(11):. PubMed ID: 29514915
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