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Human herpesvirus type 2 (HSV-2) is a double-stranded DNA virus responsible for genital herpes and other clinical syndromes. Following transmission via direct contact, HSV-2 infects epithelial cells and causes lytic damage through intracellular replication and release of virions, producing vesicular lesions and cell death. The virus then establishes latency in sensory neurons (most commonly sacral ganglia), periodically reactivates, and travels outward to mucocutaneous surfaces, where replication and re-lytic episodes occur. HSV-2 evades immune responses with several mechanisms, notably by reducing MHC I antigen presentation, and persists lifelong in a latent form with frequent asymptomatic shedding, contributing to its widespread transmission. While not a conventional molecular target, drugs such as acyclovir target HSV-2 proteins to inhibit viral replication and control its clinical impact.
Inhibition of viral DNA polymerase (nucleoside analogs like acyclovir are phosphorylated by viral thymidine kinase and then inhibit HSV DNA polymerase, preventing viral replication and subsequent cell lysis)
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