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Varicella-zoster virus (VZV), also known as Human alphaherpesvirus 3, is a double-stranded DNA virus that causes varicella (chickenpox) and herpes zoster (shingles) (StatPearls: NBK448191). It establishes lifelong latency in the sensory ganglia following primary infection, with the potential for reactivation later in life as immunity wanes (NIH: Shingles). The virus encodes several key proteins, including a DNA polymerase that is the primary target for nucleoside analog antivirals such as acyclovir and valacyclovir (PubChem: Acyclovir). In addition to being a target for therapeutic intervention, VZV is utilized in a live-attenuated form (e.g., the Oka strain) to elicit protective humoral and cellular immune responses (CDC: Varicella). These vaccines are critical for preventing primary infection and reducing the incidence of shingles and its complications, such as postherpetic neuralgia (CDC: Varicella). Understanding VZV's mechanisms of latency and replication is essential for developing next-generation vaccines and more effective antiviral therapies (UniProt: 10335).
Inhibition of viral DNA polymerase and induction of adaptive humoral and cellular immune responses
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