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Herpes simplex virus type 1 latency-associated transcripts are evidently not essential for latent infection
I Steiner1, J G Spivack, R P Lirette
1Wistar Institute, Philadelphia, PA 19104.
The EMBO Journal
|February 1, 1989
Summary
Herpes simplex virus type 1 (HSV-1) latency-associated transcripts are not essential for establishing or maintaining latent infections. However, their absence significantly delays HSV-1 reactivation from sensory ganglia.
Area of Science:
- Virology
- Molecular Biology
- Neuroscience
Background:
- Herpes simplex virus type 1 (HSV-1) establishes lifelong latent infections in sensory ganglia.
- Latency-associated transcripts (LATs) are expressed during HSV-1 latency, but their precise role remains unclear.
Purpose of the Study:
- To investigate the role of HSV-1 latency-associated transcripts in viral latency and reactivation.
- To determine if LATs are necessary for the establishment, maintenance, or reactivation of HSV-1 latency.
Main Methods:
- Studied HSV-1 variant 1704 with deletions in LAT coding regions and upstream regulatory elements.
- Compared replication, latency establishment, and reactivation kinetics of HSV-1 1704 and wild-type (17+) in a mouse trigeminal ganglia model.
- Utilized Northern blot analysis and in situ hybridization to detect LATs during latent infection.
Main Results:
- HSV-1 variant 1704 replicated and established latent infection similarly to wild-type HSV-1.
- Reactivation of latent HSV-1 1704 from trigeminal ganglia was significantly delayed compared to wild-type HSV-1.
- LATs were undetectable in latent HSV-1 1704 infections, suggesting the deletion impacted LAT expression.
Conclusions:
- Detectable levels of HSV-1 latency-associated transcripts are not required for viral replication, establishment, or maintenance of latency in trigeminal ganglia.
- These findings suggest a crucial role for LATs in the reactivation process of HSV-1 from latency.