Further characterization of the complementation group B temperature-sensitive mutant of respiratory syncytial virus

Abstract

A temperature-sensitive and plaque morphology mutant, ts-2, of respiratory syncytial virus and sole representative of complementation group B, was compared with members of the other complementation groups of respiratory syncytial virus (group A [ts-1] and group C [ts-7]). Mutant ts-2 was 10- to 1000-fold more restricted in growth and ability to spread at restrictive temperatures (37.degree., 38.degree. and 39.degree. C) than at the permissive temperature (32.degree. C). In temperature shift-up experiments, the ts defect of ts-1 and other members of complementation group A affected a late function that was required for at least 13 h in the replicative cycle. The ts lesion of ts-7 affected a function early in the replication cycle. In contrast, ts-2 was not temperature sensitive when studied by the shift-up technique. The discrepancy between the ts plaque property and failure to detect temperature sensitivity during the shift-up experiment was resolved when it was shown that ts-2 had a defect in adsorption and/or penetration at the restrictive temperature. Clonal analysis of revertant ts-2 showed a coordinate restoration of ts+ phenotype and syncytium-forming capacity. Apparently, ts-2 has a defect in a protein that is involved in adsorption and/or penetration of virus and is also responsible for [human laryngeal carcinoma HEp-2] cell fusion activity.