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Herpes simplex virus type 2 establishes latency in the mouse footpad
G B Clements1, J H Subak-Sharpe
1Institute of Virology, Glasgow, U.K.
The Journal of General Virology
|February 1, 1988
Summary
Latent herpes simplex virus type 2 (HSV-2) can reactivate from ganglia and footpad tissue in mice, even without illness. Antiviral treatment and nerve sectioning did not prevent this reactivation from the footpad.
Area of Science:
- Virology
- Immunology
- Neuroscience
Background:
- Herpes simplex virus type 2 (HSV-2) establishes lifelong latent infections in sensory neurons.
- Reactivation of latent HSV-2 can lead to recurrent disease and transmission.
Purpose of the Study:
- To investigate the persistence and reactivation potential of latent HSV-2 in mouse ganglia and peripheral tissues.
- To evaluate the efficacy of acycloguanosine treatment and nerve sectioning in preventing HSV-2 reactivation from peripheral sites.
Main Methods:
- BALB/c mice were inoculated with HSV-2 in the footpad to establish latent infection.
- Latent virus was reactivated by explantation and culturing of ganglia and footpad tissue.
- Mice received oral acycloguanosine or underwent femoral and sciatic nerve sectioning, or both, to assess preventative effects.
Main Results:
- Latent HSV-2 was successfully reactivated from both ganglia and footpad tissue 3 months post-infection, in the absence of clinical signs.
- Virus recovery from the footpad was not inhibited by acycloguanosine treatment (40 mg/kg) for up to 6 months.
- Neither femoral and sciatic nerve sectioning nor the combination of nerve sectioning and antiviral treatment prevented footpad virus recovery.
Conclusions:
- HSV-2 can maintain a latent state in peripheral tissues like the footpad, with potential for reactivation.
- Current antiviral strategies and surgical interventions may not be sufficient to eradicate or prevent reactivation of HSV-2 from all infected sites.