The cold sore virus takes over its host’s transcription machinery to replicate itself. Inhibiting a host enzyme can halt infection. 



Summary

The herpes simplex virus (HSV), responsible for cold sores, hijacks the host cell’s machinery to replicate. Specifically, HSV manipulates the host’s transcription processes, forcing the cell to produce viral components instead of its own. Research suggests that inhibiting a key host enzyme involved in this transcription process can effectively halt the viral infection. This offers a potential therapeutic strategy for treating cold sores by targeting host factors rather than the virus itself, potentially reducing the risk of resistance development.

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