Persistent infection by a temperature-sensitive mutant isolated from a Sendai virus (HVJ) carrier culture: Its initiation and maintenance without aid of defective interfering particles

Abstract

Previous studies showed that there is a selective survival of is mutants in BHK-Sendai virus (HVJ) carrier culture. In addition, it is now demonstrated that the carrier culture synthesizes defective interfering (DI) size RNAs. Thus, both is mutants and DI particles have been suggested to play roles in the maintenance of the persistent infection. The present study was undertaken to clarify the role of is mutants. is virus was isolated from the carrier culture, purified so as not to contain detectable DI particles, and examined for its capacity to establish persistent infections in normal cells as well as for its interaction with wild-type Sendai virus. The is virus has extremely low cytopathogenicity, allows the infected LLCMK 2 cells to survive, and readily establishes a long-term persistent infection. The established carrier culture is resistant to challenge by wild-type Sendai virus while sensitive to a heterologous virus infection. Nearly 100% of the carrier cells exhibit virus-specific antigens. The intracellular nucleocapsids isolated from the carrier cells contain only 50 S virion-size RNA but no detectable DI RNAs at each subculture of analysis. Original is characteristics have been expressed in the carrier cells as demonstrated by temperature-dependent production of HN and M polypeptides and progeny viruses. Persistent infections were also established in a variety of the other cell lines without added DI particles. These results indicate that the to virus is able to establish persistent infection without requirement of DI particles for either its initiation or maintenance. Further, the is virus itself strongly interfered with the replication of wild-type virus and mixed infection of LLCMK 2 cells with is and wild-type viruses also readily established a long-term persistent infection.