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Mutation of the Immunodominant CD8+ Epitope in the MHV-4 Spike Protein

  • Ming Ming Chua
  • Joanna J. Phillips
  • Su-Hun Seo
  • Ehud Lavi
  • Susan R. Weiss
Part of the Advances in Experimental Medicine and Biology book series (AEMB, volume 494)

Abstract

Our lab focuses on understanding the mechanism of murine Coronavirus mouse hepatitis virus (MHV) pathogenesis in the central nervous system (CNS). MHV strains MHV-4 (JHM) and A59 induce acute encephalitis, followed by chronic demyelination in weanling C57B1/6 (B6) mice; virus is cleared from the CNS by about 2 weeks post infection and demyelination occurs in the absence of infectious virus. We have previously used targeted recombination to select isogenic viruses differing only in the spike gene, expressing either the A59 spike (SA59R16) or the MHV-4 spike (S4R29) in the background of the A59 genome (Phillips et al., 1999). While the MHV-4 spike expressing virus (S4R29) is, like MHV-4, highly neurovirulent, the SA59R16, like MHV-A59, is significantly less neurovirulent

Keywords

Post Infection Spike Gene Mouse Hepatitis Virus Spike Protein Epitope Mutant 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer Science+Business Media New York 2001

Authors and Affiliations

  • Ming Ming Chua
    • 1
  • Joanna J. Phillips
    • 1
  • Su-Hun Seo
    • 1
  • Ehud Lavi
    • 2
  • Susan R. Weiss
    • 1
  1. 1.Department of MicrobiologyUniversity of Pennsylvania School of MedicinePhiladelphiaUSA
  2. 2.Department of Pathology and Laboratory MedicineUniversity of Pennsylvania School of MedicinePhiladelphiaUSA

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