Expert Reviews in Molecular Medicine: http://www.expertreviews.org/
DOI: 10.1017/S146239940500966X; 10 August 2005
Citation details: Mark Quinlivan and Judith Breuer (2005) Molecular and therapeutic aspects of varicella–zoster virus infection.
Expert Rev. Mol. Med. Vol. 7, Issue 15, DOI: 10.1017/S146239940500966X

Molecular and therapeutic aspects of varicella–zoster virus infection

Mark Quinlivan and Judith Breuer

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Varicella–zoster virus (VZV) is a highly species-specific member of the Herpesviridae family. The virus exhibits multiple cell tropisms, infecting peripheral blood mononuclear cells and skin cells before establishing latency in sensory neurons. Such tropisms are essential both for primary infection, which manifests itself as chickenpox (varicella), and subsequent reactivation to cause herpes zoster (shingles). The highly cell-associated nature of the virus, coupled with its narrow host range, has resulted in the lack of an animal model that mimics its diseases in humans, thereby greatly hindering the study of events in VZV pathogenesis. Despite this, extensive studies both in vitro and in vivo in small-animal models have provided a fascinating insight into molecular events that govern VZV diseases. In addition, VZV has become the first human herpes virus for which a live attenuated vaccine has been developed.

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Figure 1. Structure of the varicella–zoster virus particle.
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Figure 2. Organisation of the varicella–zoster virus genome.
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Figure 3. Varicella–zoster virus cell attachment and fusion.
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Figure 4. Intracellular transport and maturation of varicella–zoster virus.
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Table 1. The varicella–zoster virus glycoproteins.
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Table 2. Viral proteins essential for replication of varicella–zoster virus in human T cells and/or human skin.
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Table 3. Genes of varicella–zoster virus to which a function has been assigned.
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