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Effect of input multiplicity on the establishment of simian virus 40 persistent infections in rhesus monkey kidney
Abstract:
Monolayer cultures of LLC-MK2 rhesus monkey kidney cells become persistently infected with simian virus 40 after infection at input multiplicities of 100, 10, or 1 plaque-forming unit per cell. After 3 weeks, all cells of the cultures infected at a multiplicity of 1 plaque-forming unit per cell produced the simian virus 40 T antigen. In contrast, 8 to 11 weeks elapsed before all the cells in the cultures infected at a multiplicity of 100 plaque-forming units per cell produced T antigen. Defective interfering particles and interferon production were not evident during this time.
Insights
Simian virus 40 infection of monkey kidney cells leads to persistent infection. Higher virus doses delay T antigen production in LLC-MK2 cells, with no evidence of defective interfering particles or interferon.
Area of Science:
- Virology
- Cell Biology
- Infectious Diseases
Background:
- Simian virus 40 (SV40) is a polyomavirus that can establish persistent infections in host cells.
- Understanding the kinetics of SV40 T antigen expression is crucial for studying viral replication and pathogenesis.
- LLC-MK2 cells, derived from rhesus monkey kidneys, are a common model for studying primate viruses.
Purpose of the Study:
- To investigate the impact of simian virus 40 (SV40) input multiplicity on the establishment and progression of persistent infections in LLC-MK2 cells.
- To determine the time course of SV40 T antigen expression in relation to varying viral infection doses.
- To assess the potential involvement of defective interfering particles and interferon in the observed infection dynamics.
Main Methods:
- Monolayer cultures of LLC-MK2 cells were infected with SV40 at different input multiplicities (100, 10, and 1 plaque-forming unit per cell).
- Persistent infection was monitored over several weeks.
- The production of SV40 T antigen in infected cells was assessed over time.
Main Results:
- LLC-MK2 cells infected at a multiplicity of 1 plaque-forming unit per cell showed complete T antigen production within 3 weeks.
- Cultures infected at a higher multiplicity of 100 plaque-forming units per cell required 8 to 11 weeks for all cells to produce T antigen.
- No evidence of defective interfering particles or interferon production was observed during the study period.
Conclusions:
- The input multiplicity of simian virus 40 significantly influences the kinetics of T antigen expression in persistently infected LLC-MK2 cells.
- A high viral dose delays the widespread production of T antigen, suggesting a dose-dependent effect on viral spread or replication.
- The absence of defective interfering particles and interferon indicates these factors are not primary drivers of the observed delayed T antigen expression in this model.