Natural history of VZV infection: Pathogenesis, action mechanisms and virological criteria for antiviral drug evaluation

Varicella-zoster-virus causes chickenpox during primary infection of the host. Succeding lymphatic and blood dissemination, the VZV reach cutaneous epthelial cells. VZV exhibits tropism for lung and central nervous system when viremia and viral replication are not controlled by the host response. After primary infection, VZV establishes latency in cell of dorsal root ganglia. Once a Life, VZV is reactived and causes shingles. VZV reachs skin though sensory nerve. Shingles could be complicated by its ophtalmic localization and nervous system involvment and by dissemination in immunocompromised patients. Acyclovir and valacyclovir, foscarnet, penciclovir are virustatic antiviral drugs which inhibits VZV DNA polymerase and are active on replicative virus. In chickenpox therapeutic trials, antiviral drugs are evaluated with cutaneous criteria, general symptoms and complications. In zona therapeutic trials, primary criteria in immunocompetent subject concerns pain and in immunocompromised patient viral dissemination.