Varicella Zoster: Virus and Disease

Abstract Varicella‐zoster virus (VZV) is a human‐specific virus that causes varicella (chickenpox) upon primary infection of children. During the convalescent stage of infection, VZV establishes latency in dorsal root ganglia of the nervous system and reactivates decades later in adults, causing herpes zoster (shingles). In the early 1970s, a live attenuated varicella vaccine was developed; subsequent varicella vaccination has greatly reduced VZV‐related hospitalisations and fatalities, although VZV remains commonplace in areas of the world that have not achieved high degrees of vaccination. VZV research continues to study viral mechanisms and pathogenesis. Recent experiments have discovered that VZV induces the cellular process called autophagy, which can aid in prolonging cell lifespan. Phylogenetic analyses of sequenced genomes indicate that the VZV genome originated in Africa and has coevolved with its human hosts during their migration out‐of‐Africa throughout the world. Key Concepts: Varicella‐zoster virus causes chickenpox initially, but remains latent in the body and can be reactivated, usually in the elderly, to cause the infection known as shingles. VZV is one of nine human herpesviruses; in 2012, human herpesvirus type 6 was separated into two species called A and B. VZV is evolutionarily closely most related to the herpes simplex virus (HSV); however, it causes chickenpox and shingles and cannot cause herpes. The double‐stranded DNA genome of VZV has been fully sequenced and has more than 70 open reading frames that encode nearly 70 unique proteins. A highly geometrical and complex layer of proteins known as the capsid serves as a protective housing for the viral DNA; the capsid is then covered by a tegument and a lipid bilayer called the envelope. Glycoproteins – proteins with bound sugars – are embedded within the envelope and serve functions from attachment to the host cell and cell‐to‐cell spread of the infection. VZV is thought to have originated in Africa and has spread throughout the world by coevolving with its human host. VZV is spread only during active infection; among the human herpesviruses, VZV is the only one that is spread by aerosolizing into airborne particles. Autophagy, the recycling of damaged organelles, is induced by VZV as a method of prolonging cell lifespan, which gives the virus more time to replicate. A live attenuated varicella vaccine was developed in the early 1970s and has dramatically reduced the number of VZV‐related hospitalisations and fatalities. Antiviral drugs such as aciclovir are very effective in the treatment of VZV infections.