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Ganglionic permissivity to HSV-1 replication and acyclovir-induced latency: an in vitro model
J A Millin1, E M Opremcak, P A Wells
1Hilles Immunology Laboratory, Harvard Medical School, Massachusetts Eye and Ear Infirmary, Boston 02114.
Investigative Ophthalmology & Visual Science
|February 1, 1988
Summary
This study shows that Herpes Simplex Virus type 1 (HSV-1) replicates more in A/J mouse ganglia than C57BL/6J, but acyclovir equally suppresses HSV-1 infection in both, establishing latency.
Area of Science:
- Virology
- Neuroscience
- Immunology
Background:
- Herpes Simplex Virus type 1 (HSV-1) establishes latent infections in murine trigeminal ganglia.
- Understanding host genetic influences on HSV-1 replication and latency is crucial for developing antiviral strategies.
Purpose of the Study:
- To investigate the genetic impact of host mice on HSV-1 permissivity and latency in trigeminal ganglia.
- To establish an in vitro system for studying HSV-1 infection dynamics in murine trigeminal ganglia.
Main Methods:
- Developed an in vitro culture system using trigeminal ganglia from HSV-1 sensitive A/J and resistant C57BL/6J mice.
- Inoculated ganglia with HSV-1 strains (MP and KOS) and treated with or without acyclovir.
- Assayed for infectious viral particles and performed immunostaining for viral proteins.
Main Results:
- A/J ganglia exhibited three-fold higher HSV-1 replication compared to C57BL/6J ganglia without acyclovir treatment.
- Acyclovir treatment completely suppressed viral replication in both murine strains.
- Immunostaining confirmed latent viral protein expression in acyclovir-treated ganglia, with 54% spontaneous reactivation upon desuppression.
Conclusions:
- HSV-1 can establish active infection in whole murine trigeminal ganglia in vitro.
- Significant genetic variation exists in HSV-1 replication permissivity between A/J and C57BL/6J mouse strains.
- Acyclovir effectively suppresses in vitro HSV-1 ganglionic infection in both strains, inducing a latent state.