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Herpesvirus-induced availability of host DNA to exogenous endonuclease
Acta Virologica
|September 1, 1975
Abstract:
Deoxyribonuclease I penetrates herpesvirus-infected L cells and degrades host DNA without interfering with viral multiplication. The DNA of uninfected control monolayers of L cells, disrupted by scraping, is similarly attacked. In contrast, undisturbed L cells are not affected. This suggests that altered cell membrane permeability allows the nuclease to enter the cell, thereby permitting access of exogenous deoxyribonuclease to cellular DNA.
Insights
Deoxyribonuclease I enters herpesvirus-infected cells and degrades host DNA without hindering viral replication. This indicates that changes in cell membrane permeability enable the enzyme
Area of Science:
- Cell Biology
- Virology
- Enzymology
Background:
- Herpesvirus infections can alter host cell properties.
- Exogenous enzymes may interact with infected cells.
- Cell membrane integrity is crucial for cellular processes.
Purpose of the Study:
- To investigate the effect of deoxyribonuclease I on herpesvirus-infected L cells.
- To determine if deoxyribonuclease I can degrade host DNA within infected cells.
- To explore the role of cell membrane permeability in enzyme entry.
Main Methods:
- Treatment of herpesvirus-infected L cells with deoxyribonuclease I.
- Assessment of viral multiplication post-treatment.
- Analysis of host DNA integrity in treated and untreated cells.
- Comparison with uninfected, disrupted, and undisturbed L cells.
Main Results:
- Deoxyribonuclease I penetrated herpesvirus-infected L cells.
- Host DNA was degraded by deoxyribonuclease I.
- Viral multiplication was not affected by the enzyme.
- Undisturbed L cells remained unaffected, while disrupted cells showed DNA degradation.
Conclusions:
- Altered cell membrane permeability in infected cells facilitates deoxyribonuclease I entry.
- Exogenous deoxyribonuclease I can access and degrade host DNA without impacting viral replication.
- Cellular integrity plays a key role in susceptibility to exogenous nucleases.