Murine sarcoma virus defectiveness: serological detection of only helper virus reverse transcriptase in sarcoma virus rescued from nonmurine S + L-cells.

Abstract

Abstract Murine sarcoma virus (MSV) defectiveness was studied by examining MSV rescued by RD-114 virus superinfection of both dog and human heterologous host cells nonproductively transformed by the S+L− strain of Moloney MSV (S+L− cells). Biological assays showed that the rescued MSV pseudotype was present in excess over the RD-114 helper virus. The biologically determined virus ratio corresponded to that determined by virus nucleic acid hybridizations. Antisera distinguishing the DNA polymerase of murine type C virus from that of RD-114 virus demonstrated that the only detectable RNA-dependent DNA polymerase present in the rescued MSV virions was that of RD-114 helper virus. No murine virus polymerase was detectable within the virions. Previous data have demonstrated that no murine-viral polymerase is associated with S+L− heterologous human, dog, and mink host cells. The work presented here demonstrates that cells producing infectious MSV and helper virions still do not express murine polymerase within released MSV virions. These findings suggest that heterologous host-cell control mechanisms are not preventing MSV polymerase expression in these cells. Instead, the rescued MSV virions acquire the polymerase protein from the rescuing helper virus. These data provide evidence that the MSV genome lacks the information necessary for polymerase, and requires for the production of infectious progeny the functioning of a helper virus replication gene set supplying at least viral envelope antigen(s) and virion core protein polymerase.