Title: Coronavirus induction of class I major histocompatibility complex expression in murine astrocytes is virus strain specific Document date: 1994_9_1
ID: 4bf8eiix_24
Snippet: The Ability_ of MHV to Induce Class I Is Not Dependent on Replication Efficiency. In our laboratory, A59 grows to higher titer in vitro than the JHMV strains in DBT cells, often ex-ceeding JHMV growth 10-20-fold. In addition, recombinant viruses containing A59 leader predominate over those containing JHMV leader, suggesting that A59 leader provides a growth advantage (52) . Thus, it was important to determine whether the lack of class I inducing .....
Document: The Ability_ of MHV to Induce Class I Is Not Dependent on Replication Efficiency. In our laboratory, A59 grows to higher titer in vitro than the JHMV strains in DBT cells, often ex-ceeding JHMV growth 10-20-fold. In addition, recombinant viruses containing A59 leader predominate over those containing JHMV leader, suggesting that A59 leader provides a growth advantage (52) . Thus, it was important to determine whether the lack of class I inducing activity by JHMV was due to poor replication efficiency in primary astrocytes. For this purpose, the number of astrocytes staining for viral antigen was determined by immunoperoxidase staining, and the yield of infectious viral particles/cell was measured in infectious center assays. The data, presented in Table 3 , indicate that on day 3 p.i., 53% of the JHM-DL-infected astrocytes were positive for viral antigen, compared with 45% of cells infected with A59. In addition, cells infected with the recombinant virus CA13, which retains 3' JHMV and 5' A59 sequences and does not stimulate class I expression, showed 48% antigen positive staining. Cells infected with CA13 produced the highest level of infectious virus at 0.51 plaques/cell, in spite of its inability to stimulate class I expression (Table 3) . By contrast, EL3, which was an effective class I inducer, replicated at relatively low efficiency at 0.08 plaques/cell. Thus, class 1-inducing activity was not a function of the ability of the virus to infect or replicate in pri-
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