Summary auto-generated
This study examined how herpes simplex virus type 1 (HSV-1) infection affects cellular DNA polymerase activities in thymidine kinase-deficient mouse cells. Researchers used pulse-labeling with radioactive thymidine and chromatographic analysis to track viral and cellular DNA synthesis, along with measuring three main cellular DNA polymerases (α, β, and γ) at various time points during infection. Viral DNA synthesis peaked around 8 hours post-infection, while cellular DNA synthesis was progressively inhibited but remained detectable throughout the infection cycle. The drug phosphonoacetic acid effectively blocked viral DNA synthesis only when added before viral replication began. Analysis of individual cellular polymerases revealed that α polymerase activity decreased during infection, β polymerase activity increased significantly, and γ polymerase activity showed slight elevation. These findings suggest that cellular DNA repair mechanisms, particularly those involving β polymerase, may be induced during HSV-1 infection to support both viral and essential cellular DNA synthesis.
Key findings
- Viral DNA synthesis peaked at 8 hours post-infection while cellular DNA synthesis was progressively inhibited but remained appreciable throughout the infectious cycle
- Phosphonoacetic acid selectively inhibited viral DNA synthesis only when added before the onset of viral DNA replication
- Cellular α polymerase activity decreased rapidly during infection while β polymerase activity increased significantly, suggesting induction of DNA repair enzymes
- The increase in β polymerase activity indicates that cellular DNA repair mechanisms may be activated to support viral replication and maintenance of essential cellular functions
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Abstract
Thymidine kinase-deficient mouse cell cultures infected with herpes simplex virus type 1 exhibited a maximum of virus DNA synthesis around 8 h post-infection as determined by pulse labelling with 3H-thymidine. Cellular DNA synthesis was progressively inhibited, but still appreciable until 8 h post-infection and not completely abolished at any time during the infectious cycle. Phosphonoacetic acid was found to be a potent and selective inhibitor of virus DNA synthesis only when added to infected cultures before the onset of virus DNA synthesis. During the interval of increasing virus DNA synthesis the activity of cellular α polymerase decreased rapidly, whereas the polymerase activity increased significantly; a slight increase was observed for the γ polymerase activity. When infected cells were kept in the presence of phosphonoacetic acid following virus adsorption the effect on cellular DNA polymerases was less pronounced.