First, herpes zoster does not have life-long immunity. Otherwise, how can there be so many people in the clinic, and then suffer from herpes zoster again? Second, people who have not had chickenpox before, that is, those who have been infected with varicella-zoster virus for the first time, may not be herpes zoster, but manifest as chickenpox. Third, whether the performance of skin lesions is chickenpox or herpes zoster has nothing to do with the age at the time of onset. In other words, if a child has had a chickenpox once, the body will get life-long immunity to chickenpox, he will not Suffering from chickenpox, and if after a year or two, he is unfortunately infected again, it is caused by the virus that is lurking in his body, and it can be manifested as herpes zoster. VZV is composed of double-stranded DNA, capsid, cortex and capsule. The innermost layer is the nucleocapsid containing the DNA genome, and the outermost layer is the capsule membrane containing the viral glycoprotein from the host cell membrane, with the cortex in the middle. It is mainly composed of three immediate early proteins (IEs), which are encoded by ORF4, ORF62 and ORF63, respectively.
The genome of VZV can be divided into four parts: long single sequence (UL), short single sequence (US), internal repeat (IR) and terminal repeat (TR), containing 71 ORFs and promoter-related sequences. The 2/3 ORF and 8 glycoproteins are involved in viral DNA replication, splicing, packaging, metabolism, and nucleocapsid assembly. Most of the VZV genes are involved in viral replication, and the encoded products are expressed in immediate early protein (IE), early protein, and late protein sequences. When the virus is latently infected, only the early protein gene encodes IE62 and IE63, and the late protein gene mainly encodes some capsids and glycoproteins, which are not expressed when latent infection. Viral glycoproteins mediate viral adsorption, enter human host cells, express on the cell membrane of infected cells and promote the spread of viruse