Varicella-zoster virus (VZV) establishes latency in sensory ganglia and reactivates as herpes zoster. The key viral protein that maintains latency by suppressing lytic gene expression in dorsal root ganglion neurons is:

• A Latency-associated transcript (LAT) RNA — same as HSV-1
• B Thymidine kinase, which sequesters viral DNA in a non-replicating state
• C VZV ORF63 protein (IE63), which accumulates in neuronal nuclei and inhibits viral gene transactivation ✓
• D gE glycoprotein, which downregulates MHC class I on neurons

Explanation

During VZV latency in sensory and cranial nerve ganglia, ORF63 protein (IE63) is the predominant viral protein expressed. IE63 accumulates in neuronal nuclei, suppresses the viral immediate-early transcriptional activator IE62, and maintains the genome in a quiescent state. VZV does not produce a true LAT RNA equivalent as HSV does. Reactivation triggers zoster rash in the corresponding dermatome and postherpetic neuralgia, especially in the immunocompromised and elderly.

Reference: Ananthanarayan & Paniker's Textbook of Microbiology, 11th ed.

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Written and medically reviewed by the StethoPrep medical team.