Herpes simplex virus (HSV) establishes latency in sensory ganglia. During reactivation, the latency-associated transcript (LAT) plays which role in neuronal survival?

• A LAT encodes ICP0 protein that transactivates immediate-early HSV genes during reactivation
• B LAT encodes thymidine kinase, allowing acyclovir activation to suppress lytic cycle
• C LAT is a non-coding RNA that suppresses apoptosis in latently infected neurons by blocking the intrinsic apoptosis pathway (possibly via microRNA-H2/H6 targeting of caspase 8 and PUMA) ✓
• D LAT is translated into a structural capsid protein that maintains the episomal latent genome

Explanation

The HSV latency-associated transcript (LAT) is the only abundantly transcribed RNA during latency; it is a non-coding RNA (ncRNA) that is not translated into protein. LAT promotes neuronal survival during latency by suppressing apoptosis — LAT-encoded microRNAs (miR-H2 targeting ICP0, miR-H6 targeting ICP4, and others targeting caspase 8 and PUMA) inhibit both lytic gene expression and apoptotic pathways, thereby preserving the reservoir of latently infected neurons. ICP0 is an immediate-early transactivator encoded by the lytic cycle genome. HSV thymidine kinase is encoded by UL23, not LAT. LAT does not encode structural capsid proteins.

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

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