Zoster and Postherpetic Neuralgia

Introduction to Zoster and Postherpetic Neuralgia

Zoster is an acute skin disease caused by the varicella-zoster virus. It is a recessive infection and has become a virus carrier. This virus is addicted to neurological and the nerve can be moved to the spinal cord after the invasion of sensory nerve endings skin along. When the host cell immune function is at low conditions or certain diseases, such as colds, fever, systemic lupus erythematosus, and malignant tumor, the virus can be activated again and cause inflammation and necrosis of ganglion. At the same time, the reactivated virus can travel along the peripheral nerve fibers to the skin and cause herpes and pain. If the virus in the body and the virus transmitted to the peripheral nerve are cleared out of the body, there will be no sequelae. Otherwise, there may be positronic neuralgia.

Key Factors of Zoster and Postherpetic Neuralgia

In recent years, the research on the main factors of postherpetic neuralgia cause has received extensive attention. Understanding the potential risk factors is of great significance for the prevention, diagnosis, and intervention of postherpetic neuralgia. Up to now, many factors have been identified, which including but not limited to:

• Age. Older people with the basal metabolic disease are at greater risk for postherpetic neuralgia. It has been reported that about 20% of zoster patients will have residual neuralgia. The incidence of postherpetic neuralgia increased from 8% in the 50-55 age groups to 21% in the 80-85 age groups. The older the patients are, the more diseases they suffer from, the lower their immune function is, and the worse their ability to repair neuroinflammation is, so they are more prone to zoster and postherpetic neuralgia.
• Zoster type. Normally, large blister zoster type and bad meal zoster type are more likely to lead to sequelae. These two kinds of zosters require a longer scab time, during which virus activity is frequent, resulting in the occurrence of postherpetic neuralgia.
• Prodromal pain and acute pain degree. Precursor refers to the pain before zoster occurs, which generally lasts to the acute stage after the eruption. It is caused by the damage of peripheral ganglion and nerve fiber of viral replication and is closely associated with postherpetic neuralgia progress.

Research on Postherpetic Neuralgia

Currently, the pathogenesis of postherpetic neuralgia is not very clear. Recent studies have shown that: the varicella-zoster virus can long-term dormant in the dorsal root ganglion (DRG) and sensory ganglion. When low immunity or impaired immune defense, like extreme fatigue, malignant tumor, or chronic infectious disease, the varicella-zoster virus may be activated again and spread to the corresponding skin innervation area of the sensory nerve to form herpes zoster, leading to damage to the central or peripheral nervous system.

Moreover, the mechanism of postherpetic neuralgia is complex and often related to a variety of mechanisms that cause anatomical structure changes and functional impairment, such as peripheral sensitization, central sensitization, disablement of the downstream inhibitory system, activation of spinal cord glial cells, and changes in ion channels. Besides, a variety of companies have generated a series of products or neuroscience research tools, including but not limited to, Neural Proteins & Peptides, Neural Antibodies, as well as Animal Models to facilitate the diagnosis and treatment of zoster and postherpetic neuralgia.

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