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Homologous interference induced by a temperature-sensitive mutant derived from an HVJ (Sendai virus) carrier culture
Abstract:
Homologous interference between a temperature-sensitive small plaque mutant (HVJ-pB) derived from an HVJ (haemagglutinating virus of Japan - the Sendai strain of parainfluenza I virus) carrier culture of BHK cells and the original wild-type virus (HVJ-W) has been investigated. Prior infection of LLCMK2, HeLa, BHK or mouse L cells with HVJ-pB, both at permissive and non-permissive temperatures, for 24 h resulted in a reduced yield of superinfecting HVJ-W, reflecting a smaller number of cells capable of producing the superinfecting virus. However, HVJ-pB did not interfere with the replication of vesicular stomatitis virus, Sindbis virus or Newcastle disease virus. Interference in this system seems to be due to inhibition of the attachment of superinfecting HVJ-W as a result of intracellular mechanisms operating at a late stage in the replication of the interfering virus. There is also blocking or destruction of cellular receptors by extra-cellular particles of the interfering virus. Protein synthesis coded for by the complete virus genome is required to establish and maintain the interference, and treatment with actinomycin D has no effect on the interference phenomenon.
Insights
A temperature-sensitive mutant of Haemagglutinating virus of Japan (HVJ-pB) interferes with wild-type HVJ-W replication by inhibiting viral attachment. This interference requires new protein synthesis and affects cellular receptors.
Area of Science:
- Virology
- Cell Biology
Background:
- Haemagglutinating virus of Japan (HVJ), also known as Sendai virus, is a paramyxovirus.
- Carrier cultures can harbor persistent viral infections, influencing viral properties.
Purpose of the Study:
- To investigate homologous interference between a temperature-sensitive HVJ mutant (HVJ-pB) and wild-type HVJ (HVJ-W).
- To elucidate the mechanisms underlying this interference phenomenon.
Main Methods:
- Infection of various cell lines (LLCMK2, HeLa, BHK, mouse L) with HVJ-pB at permissive and non-permissive temperatures.
- Assessing the yield of superinfecting wild-type HVJ (HVJ-W).
- Testing interference against heterologous viruses (vesicular stomatitis virus, Sindbis virus, Newcastle disease virus).
- Evaluating the role of protein synthesis and actinomycin D treatment.
Main Results:
- Prior infection with HVJ-pB significantly reduced the yield of superinfecting HVJ-W.
- Interference was observed at both permissive and non-permissive temperatures.
- HVJ-pB did not interfere with the replication of unrelated viruses.
- Mechanisms involved inhibition of HVJ-W attachment, potentially via intracellular pathways and/or blocking/destruction of cellular receptors by extracellular HVJ-pB particles.
- Interference establishment and maintenance required de novo protein synthesis coded by the complete viral genome.
- Actinomycin D did not affect the interference.
Conclusions:
- Homologous interference in HVJ infection is mediated by mechanisms affecting viral attachment.
- Both intracellular events late in viral replication and extracellular interactions with cellular receptors contribute to interference.
- Viral protein synthesis is essential for establishing and maintaining this interference phenomenon.