Ultrastructural changes during herpes simplex virus type 2 latency and reactivation in vitro

Area of Science:

• Virology
• Cell Biology
• Microbiology

Background:

• Herpes simplex virus type 2 (HSV2) establishes lifelong latent infections.
• Understanding HSV2 latency and reactivation is crucial for developing antiviral therapies.

Purpose of the Study:

• To investigate the ultrastructural changes in HSV2-infected cells during latency and reactivation.
• To identify cellular and viral factors involved in HSV2 reactivation.

Main Methods:

• An in vitro latency system using HSV2-infected human embryonic lung cells.
• Treatment with cytosine arabinoside (ara-C) to induce latency.
• Observation of cellular ultrastructure via electron microscopy during different stages: ara-C treatment, latent period, and reactivation.

Main Results:

• During ara-C treatment, 'empty', nonenveloped, herpesvirus-like particles and fragmented chromatin were observed.
• No complete virions were detected during the latent period after ara-C removal and temperature elevation.
• Reactivation by human cytomegalovirus led to increased protein synthesis, viral matrix formation, and nucleocapsid assembly.

Conclusions:

• HSV2 latency is characterized by the absence of complete virions.
• Reactivation involves significant cellular changes and viral replication machinery.
• The specific proteins required for HSV2 reactivation remain unknown, potentially involving viral and/or host factors.