As a common skin disease, herpes actually causes considerable damage to the skin, but people don't take it seriously enough. Herpes is mainly caused by viral infection. Although the treatment is relatively mature, it is easy to relapse. Therefore, if you do not want the disease to occur, you must understand the cause of the disease and take preventive measures. 1. Causes of disease The disease is caused by the varicella-zoster virus. The virus enters the human body through the respiratory mucosa, spreads through the blood, and causes chickenpox on the skin. However, most people do not develop chickenpox after infection. This is a latent infection and they become carriers of the virus. This virus is neurotropic. After invading the sensory nerve endings of the skin, it can move along the nerves to the ganglia of the posterior roots of the spinal cord and lurk there. When the host's cellular immune function is low, such as when suffering from a cold, fever, systemic lupus erythematosus, and malignant tumors, the virus is stimulated again, causing inflammation and necrosis of the ganglia. At the same time, the reactivated virus can move along the peripheral nerve fibers to the skin to cause herpes. In rare cases, the herpes virus can spread to the anterior horn cells of the spinal cord and visceral nerve fibers, causing motor nerve paralysis, such as eye and facial nerve paralysis, as well as gastrointestinal and urinary tract symptoms. VZV is a herpes virus and a neurotropic virus. The complete VZV is spherical, with a diameter of about 150 to 200 nm. The nucleic acid is double-stranded DNA, composed of a regular icosahedral nucleocapsid. The outer layer is formed by a loose lipoprotein envelope with virus-encoded glycoproteins scattered around. Only the outer shell of the virus particle is infectious. Varicella and shingles are clinically different diseases but are caused by the same virus. After primary infection with VZV, approximately 70% of children will present clinically with varicella, and approximately 30% will have latent infection, and both are carriers of the virus. 2. Pathogenesis VZV enters nerve fibers from the skin and mucous membranes, invades sensitive ganglia, and forms a latent infection that does not cause harm to the body. However, once VZV obtains the conditions for reactivation, it will infect and cause disease again. The mechanism of VZV reactivation is currently unclear. However, many factors are related to the occurrence of herpes zoster, such as excessive fatigue, mental trauma, Hodgkin's disease and other malignant tumors, long-term use of immunosuppressants and corticosteroids, radiotherapy, major surgery, heavy metal poisoning and other inducements that can reduce the body's resistance to the lowest level. VZV cannot be controlled, that is, it proliferates and spreads in the ganglion, leading to nerve necrosis and increased inflammation, and severe neuralgia occurs clinically. VZV is transmitted back to sensitive nerves, causing severe neuritis, and spreading to the sensitive nerve endings of the skin, forming clusters of herpes. On the first day of the rash appearing, the skin nerve fibers undergo degeneration, indicating that the infection in the sensitive ganglion has invaded the skin. The infection of the ganglion can extend to adjacent areas and spread along the posterior roots of the nerves to the meninges, leading to meningitis, segmental myelitis, and infection of the anterior horn motor nerve, causing complications such as motor nerve paralysis. As age increases, the cellular immune response to VZV weakens. The cell-mediated immune response to VZV in the elderly is selective and gradually decreases. Therefore, the incidence, severity and complications of herpes zoster in the elderly are higher. After recovery, the patient will have lifelong immunity and relapse is rare. |
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