When primary VZV infection occurs, the virus is first inoculated into the upper respiratory tract mucosa, then replicated in the local lymph nodes and released into the blood to form the first viremia. When the virus is transported to the organs of reticuloendothelial system such as liver and spleen, it completes the second round of replication, forming the second viremia and spreading widely throughout the body. About 14 to 16 days after infection, the virus can penetrate the capillary endothelial cells to the epidermis, then move along the nerve fibers of the posterior spinal cord or trigeminal ganglion to the center, and persistently lurk in the neurons of the posterior spinal root ganglion. The onset of VZV is usually divided into three stages: the first stage is in the latent period, in which the latent VZV reactivates in neurons and the immune surveillance function is impaired; the second stage is in the clinical eruption period, when the virus is released from ganglion along the nerve pathway to skin, the memory immune response of the host is enhanced, and the VZV infection is confined to the primary lesion, once the memory immune response is weakened. The third stage is in clinical dissemination. The virus not only affects the skin, but also spreads to the central nervous system and other internal organs.
All herpes viruses have latency, and latency is almost lifelong. The latency of most herpes viruses is an important form of escape from epidemic surveillance. It has been found that VZVDNA exists in cells in the form of free genes, and there are transcripts and synthetic proteins of viral genes in latent infection. VZV ORF and microRNAs play an important role in maintaining latent infection of VZV. According to the doctor's advice, nearly half of the patients recovered within 2 to 3 weeks, and most of the elderly recovered within 3 to 4 weeks. Sequelae of neuralgia are elderly patients with chronic diseases. However, recurrent seizures are also common.
