[Herpes simplex virus type 1 latency and reactivation: an update]

Area of Science:

• Virology
• Molecular Biology
• Immunology

Context:

• Herpes simplex virus type 1 (HSV-1) establishes lifelong latent infections in sensory neurons after primary infection.
• During latency, the HSV-1 genome persists as a chromatinized episome, expressing specific transcripts and microRNAs to suppress lytic functions.

Purpose:

• To elucidate the molecular mechanisms governing HSV-1's dual life cycle, encompassing both productive lytic replication and persistent latent infection.
• To understand the epigenetic regulation controlling the switch between HSV-1 lytic and latent gene expression programs.

Summary:

• HSV-1 productively infects epithelial cells and enters sensory neurons, establishing lifelong latency via retrograde transport of its genome to the nucleus.
• Latency involves a chromatinized episomal viral genome expressing latency-associated transcripts (LAT) and microRNAs that inhibit lytic gene expression.
• The virus can periodically reactivate to initiate secondary lytic infections, facilitated by epigenetic control over alternative viral gene expression programs.

Impact:

• Understanding HSV-1 latency and reactivation is crucial for developing antiviral therapies targeting recurrent infections.
• This research sheds light on viral adaptation strategies, including immune evasion and host-to-host dissemination.
• Insights into epigenetic control of viral gene expression may have broader implications for other persistent viral infections.