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HSV- and chemical carcinogen-induced amplification of SV40 DNA sequences in transformed cells is cell-line-dependent
Abstract:
Eleven simian virus 40-transformed cell lines from 5 different species were tested for their ability to amplify integrated simian virus 40 DNA upon infection with herpes simplex virus type I or treatment with various chemical carcinogens. Four cell lines were positive only for virus-induced gene amplification and two lines were positive for both carcinogen- and virus-induced gene amplification. Individual cell lines were assayed for the presence of an intact SV40 origin of replication, the expression of a functional SV40 T-antigen, and permissivity to herpes simplex virus replication. These parameters were found to be positive in all 6 amplification-competent cell lines. The ability of herpes simplex virus to amplify SV40 DNA sequences in transformed cells is greater than that of chemical carcinogens and can be suppressed by specific inhibitors of the herpes virus-encoded DNA polymerase.
Insights
Herpes simplex virus type I can induce simian virus 40 (SV40) DNA amplification in transformed cells, a process more potent than chemical carcinogens. This viral gene amplification is dependent on functional SV40 replication origins and T-antigen expression.
Area of Science:
- Molecular Biology
- Virology
- Cell Biology
Background:
- Simian virus 40 (SV40) DNA amplification in transformed cells is a key area of research.
- Understanding the mechanisms of viral DNA amplification is crucial for virology and cancer research.
Purpose of the Study:
- To investigate the ability of herpes simplex virus type I (HSV-I) and chemical carcinogens to induce SV40 DNA amplification.
- To identify cellular and viral factors influencing SV40 DNA amplification.
Main Methods:
- Testing eleven SV40-transformed cell lines from five species for DNA amplification.
- Assaying for SV40 origin of replication, SV40 T-antigen expression, and HSV replication permissivity.
- Evaluating the effect of HSV-I infection and chemical carcinogens on SV40 DNA amplification.
Main Results:
- Six of the eleven cell lines showed amplification of integrated SV40 DNA.
- Four cell lines amplified SV40 DNA upon HSV-I infection, while two amplified it with both HSV-I and chemical carcinogens.
- All amplification-competent cell lines possessed an intact SV40 origin of replication, expressed functional SV40 T-antigen, and were permissive to HSV replication.
Conclusions:
- HSV-I is a potent inducer of SV40 DNA amplification in transformed cells, surpassing chemical carcinogens.
- HSV-I-induced SV40 DNA amplification is dependent on viral DNA polymerase activity and specific cellular factors related to SV40 replication.