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Studies on the adaptation of mumps virus to chick embryo
Abstract:
About 15 serial passages of wild type mumps virus (Sasazaki strain) in the amnion sac of chick embryo (CE) yielded a CE-adapted strain which was poorly replicative and did not form plaques in Vero cells where the wild strain grew well. In the course of this limited replication of the CE-adapted strain in Vero cells, we have analysed the viral protein and RNA synthesis. It was found that protein synthesis took place very efficiently at least early in infection by 12 h. The subsequent rate of synthesis remained, however, at a low level without showing the progressively increasing synthesis observed with the wild strain. Furthermore, 50S genomic RNA was synthesized early in the limited infection, but the subsequent synthesis was markedly suppressed. In addition, the other virus-specific RNA species could not be detected throughout. Thus the amplified RNA synthesis observed in the permissive CE cells and in the wild strain-infection of Vero cells seemed not to occur in the limited replication. Neither interferon nor DI (defective interfering) RNA was involved in the limited virus growth. When Vero cells were infected with the wild strain 6 to 8 h before inoculation of CE-adapted strain, growth restriction was overcome and the yield of the latter virus was greatly enhanced by a factor more than 10(3). These results suggest that through adaptation to CE, mumps virus may be altered in such a way that there is a restriction, probably at a step (s) involved in amplification of the viral RNA synthesis in Vero cells and that the restriction may be overcome by the simultaneous genome expression of the prototype wild strain.
Insights
Adapting mumps virus to chick embryos (CE) limited its replication in Vero cells by suppressing viral RNA synthesis. This restriction was overcome by co-infection with the wild-type mumps virus.
Area of Science:
- Virology
- Molecular Biology
- Cell Biology
Background:
- Mumps virus adaptation to different hosts can alter its replication characteristics.
- Understanding viral replication mechanisms is crucial for controlling viral infections.
Purpose of the Study:
- To investigate the replication defects of a chick embryo-adapted mumps virus strain in Vero cells.
- To analyze viral protein and RNA synthesis during limited replication.
- To identify mechanisms underlying the replication restriction and potential ways to overcome it.
Main Methods:
- Serial passage of wild-type mumps virus (Sasazaki strain) in chick embryo (CE) amnion sacs.
- Analysis of viral protein and RNA synthesis in Vero cells infected with the CE-adapted strain.
- Co-infection experiments with wild-type and CE-adapted mumps virus strains in Vero cells.
Main Results:
- The CE-adapted mumps virus strain showed poor replication and no plaque formation in Vero cells, unlike the wild strain.
- Viral protein and 50S genomic RNA synthesis were initially efficient but subsequently suppressed in CE-adapted strain-infected Vero cells.
- Co-infection with the wild-type strain 6-8 hours prior to CE-adapted strain inoculation enhanced the latter's yield by over 1000-fold, overcoming the restriction.
Conclusions:
- Adaptation to chick embryos alters mumps virus, likely restricting viral RNA synthesis amplification in Vero cells.
- The observed restriction is not due to interferon or defective interfering RNA.
- Simultaneous genome expression with the wild-type strain can overcome the replication restriction in Vero cells.