Abstract
Evidence is presented that adaptation of IPN virus (strain VR 299) to FHM cells entails the selection of a variant virus type that differs significantly from the parental, and most representative, RTG-2 virus type in being able to adsorb efficiently to, and form plaques in, FHM cells.
The plaque titre of FHM-non-adapted virus stocks (RTG-2 viruses) was reduced by at least 99.99% in FHM cells, while FHM-adapted virus stocks (FHM viruses) produced plaques at equally high titres in both RTG-2 and FHM cells.
FHM viruses and RTG-2 viruses differed also in their behaviour in RTG-2 cells in respect to plaque size distribution and growth characteristics, but both virus-types were shown to be morphologically identical, and no significant difference in reactivity against specific antiserum could be detected.
Analysis of virus in individual RTG-2 plaque isolates or plaque progeny shows that a mutation of relatively high frequency (10-4 to 10-5) probably causes the ability to infect the FHM cells efficiently. Only these mutant virus-types were found in FHM plaque isolates.