Varicella-Zoster Virus: Molecular Biology

Varicella-zoster virus (VZV) is a member of the Herpesviridae and one of the eight herpesviruses that infect humans as their natural host. VZV is the causative agent of varicella (chickenpox) during primary infection and zoster (shingles) after reactivation from latency. The site of latent VZV infection lies primarily in the dorsal root ganglia and trigeminal ganglia. Based on this, and in conjunction with the structure of the viral genome, VZV is designated as a neurotropic alphaherpesvirus, as are herpes simplex virus types 1 and 2. The biology of VZV infection involves numerous organs and cell types of the infected host, including the lungs, skin, neurons, and T lymphocytes. In each of these organs and cell types, a careful balance is struck between the need for viral replication and propagation and the ability of the infected cell and the human host to survive the infection. Our understanding at the molecular level of the mechanisms by which VZV manages this balance has expanded rapidly over the past decade owing to intensive study of specific processes and the development of new genetic techniques and models of infection. This article describes our current understanding of the molecular biology of VZV infection with a concentration on recently obtained information.