[Varicella-zoster virus (VZV)].

Abstract

Varicella-zoster virus (VZV) causes varicella in primary infection and zoster after reactivation from latency. Both herpes simplex virus (HSV) and VZV are classified into the same alpha-herpesvirus subfamily. Although most VZV genes have their HSV homologs, VZV has many unique biological characteristics. In this review, we summarized recent studies on 1) animal models for VZV infection and outcomes from studies using the models, including 2) viral dissemination processes from respiratory mucosa, T cells, to skin, 3) cellular receptors for VZV entry, 4) functions of viral genes required uniquely for in vivo growth and for establishment of latency, 5) host immune responses and viral immune evasion mechanisms, and 6) varicella vaccine and anti-VZV drugs.

• Authors: Kyosuke Kanai, Souichi Yamada, Naoki Inoue
• Journal: Uirusu (Uirusu) Vol. 60 Issue 2 Pg. 197-207 (Dec 2010) ISSN: 0042-6857 [Print] Japan
• PMID: 21488333 (Publication Type: English Abstract, Journal Article, Review)

Chemical References

• Antiviral Agents
• Chickenpox Vaccine
• Receptors, Virus
• Vaccines, Attenuated

Topics

• Animals
• Antiviral Agents
• Chickenpox Vaccine
• Disease Models, Animal
• Drug Design
• Herpes Zoster (immunology, virology)
• Herpesvirus 3, Human (genetics, immunology, pathogenicity, physiology)
• Humans
• Immunity, Cellular
• Nervous System (virology)
• Receptors, Virus
• Respiratory System (virology)
• Skin (virology)
• T-Lymphocytes (immunology, virology)
• Vaccines, Attenuated
• Virus Latency (genetics)