A mutant of rous sarcoma virus with a thermolabile defect in the virus envelope

Abstract

A mutant of Prague strain Rous sarcoma virus, ts LA30m PR-A (referred to here as LA30A), has a temperature-sensitive ( ts) defect early in infection. The defect appears to reside in a structural component of the virus, for mutant virions are heat labile. Two observations show that the mutated virion components function very early during infection. First, LA30A passes through the ts stage of its life cycle more rapidly than another early mutant which has a ts RNA-dependent DNA polymerase, indicating that the defective LA30A function operates before reverse transcription. Second, once LA30A has penetrated the cell, the infection is no longer ts. Pseudotypes of both Bryan high-titer strain Rous sarcoma virus and of vesicular stomatitis virus with envelopes donated by LA30A show heat lability typical of the mutant. All these data strongly suggest that LA30A possesses a ts defect in the viral envelope glycoproteins. If the mutant undergoes phenotypic mixing with Rous-associated viruses (RAV), the ts defect is stabilized even when infecting cells which lack receptors for RAV envelope glycoproteins, The possible reasons for this effect are discussed.