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Reactivation of latent Herpes simplex virus after pneumococcal pneumonia in mice
Abstract:
In attempts to reactivate latent herpes simplex virus, we instilled Diplococcus pneumoniae intratracheally into mice harboring latent infections in sacrosciatic spinal ganglia. All mice developed a severe pneumonia within 24 h and were given penicillin therapy. Representative mice that survived the penumonia were sacrificed at daily intervals, and appropriate tissues were examined for evidence of viral reactivation. Herpes simplex virus was reactivated in the ganglia and appeared to travel both proximally and distally in associated nerve trunks. Clinically apparent disease due to the virus was not detected in any mice.
Insights
Bacterial pneumonia reactivated latent herpes simplex virus (HSV) in mice. The virus traveled through nerve trunks but did not cause apparent disease, suggesting a potential mechanism for HSV latency and reactivation.
Area of Science:
- Virology
- Microbiology
- Neuroscience
Background:
- Herpes simplex virus (HSV) establishes lifelong latent infections in neurons.
- Reactivation of latent HSV can lead to recurrent disease.
- Factors influencing HSV reactivation are not fully understood.
Purpose of the Study:
- To investigate the potential of bacterial infection to reactivate latent HSV.
- To examine the behavior of reactivated HSV within the nervous system.
Main Methods:
- Latent HSV infection was established in mice.
- Intratracheal instillation of Diplococcus pneumoniae induced pneumonia.
- Penicillin therapy was administered; surviving mice were analyzed for viral reactivation in neural tissues.
Main Results:
- Diplococcus pneumoniae infection successfully reactivated latent HSV in sacrosciatic spinal ganglia.
- Reactivated HSV was detected in nerve trunks, moving proximally and distally.
- No clinically apparent HSV disease was observed in any of the infected mice.
Conclusions:
- Bacterial infections, such as pneumonia, can serve as a trigger for HSV reactivation.
- Reactivated HSV can disseminate along nerve pathways without causing overt clinical symptoms.
- This study provides insights into the complex interplay between bacterial and viral infections in maintaining HSV latency.