Varicella-Zoster Virus (VZV) belongs to the Alphaherpesvirinae subfamily of the Herpesviridae family, and is a double-stranded DNA virus with high host specificity that only naturally infects humans. First successfully isolated and identified in 1953, its genome is relatively compact among herpesviruses, with high species specificity and genetic conservation. The gene sequences of global VZV epidemic strains have high homology, and currently, they can be divided into at least 5 genotypes (clade 1-5) based on genomic differences. Different genotypes have geographical distribution differences worldwide, but their core biological characteristics are highly consistent. As a latent infectious virus, the genomic stability of VZV provides an important foundation for the research on the molecular mechanisms of its latency and reactivation.

VZV has typical structural characteristics of the Herpesviridae family. The viral particles are spherical with a diameter of approximately 150~200nm, and their structure consists of a core, capsid, tegument, and envelope from the inside out. The core is a linear double-stranded DNA genome with a full length of about 125kb, containing more than 70 open reading frames (ORFs) that encode a variety of structural and non-structural proteins. The capsid is a symmetrical icosahedral structure assembled from the major capsid protein (VP5) and minor capsid proteins (VP1, VP2, VP3, VP4). The tegument is located between the capsid and the envelope, a protein matrix with no fixed shape, containing a variety of virus-encoded enzymes and regulatory proteins that participate in the process of viral replication and assembly. The envelope is a lipid bilayer structure derived from the host cell membrane, with various glycoproteins such as gB, gC, gE, and gH embedded on the surface. These glycoproteins play a key role in the process of viral adsorption and invasion of host cells.

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