recovered from brain lysates of such protected mice,
at 5 days postinfection, had lost the ability to express EGFP and had deletions in their genomes
encompassing EGFP and gp33-41.
In addition, genomes of viruses from about half the plaques that retained
the EGFP gene had mutations within the gp33-41 epitope. On the other hand, gp33-41-specific cells failed to
protect perforin-deficient mice from infection by the recombinant MHV expressing gp33, indicating that
perforin-mediated mechanisms were needed. Virus recovered from perforin-deficient mice did not exhibit loss
of EGFP expression and the gp33-41 epitope. These observations suggest that the cytotoxic T-cell response to
gp33-41 exerts a strong immune pressure that quickly selects epitope escape mutants to gp33-41.