Defective interfering particles of human parainfluenza virus type 3 are associated with persistent infection in cell
1Department of Pediatrics, Mount Sinai School of Medicine, New York, New York 10029-6574.
Abstract:
CV-1 cell lines persistently infected with human parainfluenza virus type 3 (HPF3) contain one or more distinct subgenomic RNAs in addition to standard viral genomes. These RNAs are shown to be the genomes of defective-interfering (DI) particles of the virus; they are present in particles in the culture fluid, and they interfere with the growth of wild-type virus. Removal of the particles from the culture fluid by ultracentrifugation yields a supernatant fluid free from inhibitory activity, demonstrating that the anti-viral effect is not mediated by soluble factors. A role for the DI particles in persistence of HPF3 is considered.
Insights
Defective-interfering (DI) particles containing subgenomic RNAs were found in persistent human parainfluenza virus type 3 (HPF3) infections. These DI particles interfere with wild-type virus growth, suggesting a role in HPF3 persistence.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Persistent infections with human parainfluenza virus type 3 (HPF3) are characterized by the presence of viral RNA.
- Subgenomic RNAs have been observed in CV-1 cell lines persistently infected with HPF3.
Purpose of the Study:
- To identify the nature of subgenomic RNAs in persistently infected cells.
- To investigate the role of these RNAs in viral interference and persistence.
Main Methods:
- Ultracentrifugation to isolate viral particles.
- Analysis of RNA content in infected cell lines.
- Interference assays with wild-type virus.
Main Results:
- Distinct subgenomic RNAs, identified as defective-interfering (DI) particle genomes, were found in persistently infected CV-1 cells.
- DI particles were present in the culture fluid and interfered with wild-type HPF3 growth.
- Removal of DI particles eliminated inhibitory activity, indicating the effect is particle-mediated, not soluble factors.
Conclusions:
- Defective-interfering particles play a significant role in the biology of persistent HPF3 infections.
- DI particles may contribute to the maintenance of viral persistence by interfering with wild-type virus replication.
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