The Biology of Varicella-Zoster Virus Replication in the Skin

Viruses

Judith Breuer¹  Cristina Tommasi² 

[1] Department of Infection, Institute of Child Health, University College London, London WC1N 1EH, UK;School of Cellular and Molecular Medicine, University of Bristol, Bristol BS8 1TD, UK;

关键词: varicella-zoster virus;    skin;    epidermis;    keratinocytes;    epidermal differentiation;    cutaneous blistering lesions;   

DOI  :  10.3390/v14050982

来源: DOAJ

【 摘 要 】

The replication of varicella-zoster virus (VZV) in skin is critical to its pathogenesis and spread. Primary infection causes chickenpox, which is characterised by centrally distributed skin blistering lesions that are rich in infectious virus. Cell-free virus in the cutaneous blistering lesions not only spreads to cause further cases, but infects sensory nerve endings, leading to the establishment of lifelong latency in sensory and autonomic ganglia. The reactivation of virus to cause herpes zoster is again characterised by localised painful skin blistering rash containing infectious virus. The development of in vitro and in vivo models of VZV skin replication has revealed aspects of VZV replication and pathogenesis in this important target organ and improved our understanding of the vaccine strain vOKa attenuation. In this review, we outline the current knowledge on VZV interaction with host signalling pathways, the viral association with proteins associated with epidermal terminal differentiation, and how these interconnect with the VZV life cycle to facilitate viral replication and shedding.

【 授权许可】

Unknown