Selection of gp33 mutants did
not occur in PKO mice; this is consistent with the observation
that protection did not occur by immunization of such mice.
This further supports the notions that gp33 mutants arise as a
result of selective pressure and that perforin activity is an
important immune mechanism for controlling MHV infection.
There also was maintenance of EGFP expression in the majority
of animals infected with RA59-gfp, whether they were
immunized with rLm-gp33 or rLm-np118; this is as would be
expected, because there was no selective pressure for deletion
mutants.