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Amplification of herpes simplex virus resistance in mouse neuroblastoma (Cl300) cells
Abstract:
Clones of mouse neuroblastoma (Cl300) cells with increased resistance to herpes simplex virus (HSV) were obtained among survivors after prolonged exposure of partially HSV resistent Cl300 cells to successively increasing multiplicities of infection (MOI) of HSV. The increased restrictedness to HSV of these Cl300 R clones (Cl300 RI and Cl300 RII) as compared to the parental Cl300 cells was demonstrated by a tolerance to higher MOIs of HSV, judged by the appearance of cytopathic effects; by lower yields of progeny virus; and by higher activities of a non-interferon HSV inhibitor. Morphological appearance, cellular growth rate as well as HSV adsorptive capacity of the Cl300 R cells did not differ from that of Cl300 cells. Neither was virus penetration affected. These neuroblastoma Cl300 R cells, demonstrating an amplified resistance to HSV, might serve useful in studies on the regulation of virus replication in HSV latency establishment in neurons.
Insights
Researchers developed herpes simplex virus (HSV)-resistant mouse neuroblastoma (Cl300) cells. These Cl300 R clones show increased tolerance to HSV infection, offering a new model for studying virus replication and latency.
Area of Science:
- Virology
- Cell Biology
- Neuroscience
Background:
- Herpes Simplex Virus (HSV) establishes latency in neurons, a process not fully understood.
- Mouse neuroblastoma (Cl300) cells are a model for neuronal studies.
- Developing tools to study HSV latency is crucial for understanding viral persistence.
Purpose of the Study:
- To generate and characterize mouse neuroblastoma cell clones with enhanced resistance to HSV.
- To investigate the mechanisms underlying HSV resistance in these selected clones.
- To provide a model system for studying HSV replication and latency establishment.
Main Methods:
- Selection of Cl300 cell clones surviving prolonged exposure to increasing multiplicities of infection (MOI) of HSV.
- Assessing HSV resistance by evaluating cytopathic effects, progeny virus yields, and HSV inhibitor activity.
- Comparing morphological appearance, growth rate, and HSV adsorption/penetration between parental and resistant cells.
Main Results:
- Successfully obtained Cl300 cell clones (Cl300 R) exhibiting significantly increased resistance to HSV.
- Cl300 R clones demonstrated tolerance to higher HSV MOIs and produced lower yields of progeny virus.
- Enhanced activity of a non-interferon HSV inhibitor was observed in Cl300 R cells.
- No significant differences were found in cell morphology, growth rate, or HSV adsorption/penetration.
Conclusions:
- The generated Cl300 R cell clones possess amplified resistance to HSV without altering fundamental cellular properties.
- These resistant neuroblastoma cells offer a valuable tool for investigating HSV replication regulation.
- The model system is promising for future studies on the establishment of HSV latency in neuronal cells.