Potential Models to Study VZV Neuropathogenesis

Unlike HSV-1, VZV does not reactivate from ganglia after experimental infection of primates or rodents. However, after footpad inocnlation of rats with VZV, the protein encoded by gene 63 can be detected in Inmbar ganglia 1 month after infection. Viral protein is also detected in neurons, both in the nnclei and cytoplasm of infected cells. An independent stndy nsing the same rat model detected VZV gene 63 DNA in 5-10% of nenrons and VZV RNA in nenrons and non-nenronal cells (Kennedy et al., 1999). Simian varicella vims may also be a valnable model to stndy the pathogenesis of varicella virns-host interactions. Finally, the application of hnmanized immnnodeficient mice (SCID-hn) to VZV has provided new information 

Therapy for herpes zoster should be aimed at accelerating healing, limiting the severity and duration of acute and chronic pain and reducing any complications associated with the infection. In patients who are immunocompromised, therapy should also be aimed at reducing the risk of viral dissemination. Acyclovir, valacyclovir, and famciclovir are all used in the United States for the treatment of herpes zoster. Acyclovir is approved in the U.S. for the treatment of both chickenpox and herpes zoster in the normal host. Oral acyclovir therapy in normal children, adolescents, and adults shortens the duration of lesion formation by about a day, reduces the total number of new lesions by abont 25%, and reduces many of the symptoms in abont a third of patients (Gnann and Whitley, 2002 Snoeck et al., 1999). 

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