Simian varicella vims

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... 

It was concluded previously (11) that FMAU is a most potent and selective antiviral compound for the treatment of mouse encephalitis caused by HSV-2 and therefore deserved consideration as a potential agent in human trials for the treatment of HSV encephalitis in neonates and adults at low dose levels. The preliminary data described in Tables I and II for FEAU suggested (10) that this compound may also be worthy of similar consideration. Based upon these earlier findings (10) and on our preliminary biochemical report (12). further comparative biochemical and antiviral studies were undertaken with FMAU and FEAU, including their relative activities against Simian varicella vims in the African green monkey and against hepatitis vims in the woodchuck animal model. In these studies (13) an alternative synthesis of FEAU is also described. 

Table VII. Evalnation of Oral Dosage of FEAD in the Treatment of Simian Varicella Vims Infection in the African Green Monkey ...

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