Herpes zoster is caused by the varicella-zoster virus. The virus enters the sensory nerve terminals of the skin and moves centrally along the nerve fibers of the posterior spinal cord roots or trigeminal ganglia, where it persistently lurks in the neurons of the posterior spinal cord root ganglia. In response to various triggering stimuli, the virus can reactivate, grow and multiply, causing inflammation and necrosis of the invaded ganglion, resulting in neuralgia. At the same time, the reactivated virus can move along the peripheral nerve fibers to the skin, producing the segmental blistering rash characteristic of herpes zoster. The rash is distributed along a peripheral nerve, arranged in a band, and occurs on one side of the body, not exceeding the midline, and sometimes on the opposite side of the midline, where there may be a few rashes due to the involvement of small branches of the nerve crossing the opposite side. The preferred sites are the intercostal nerves, cervical nerves, trigeminal nerves and lumbosacral nerves. Unilateral sensory ganglia are usually invaded and bilateral involvement is extremely rare. Local lymph nodes are often enlarged. Neuralgia is one of the features of the disease, and the rash usually occurs at the same time as or later than the neuralgia, but it may occur 4-6 days after the neuralgia. The pain varies in severity and does not correlate with the severity of the rash. Usually, children with shingles have no pain or very mild pain, while older and frailer patients have severe, even unbearable pain. In some patients, neuralgia remains after the lesions have completely resolved, and this residual neuralgia can last for months. The full course of the disease is usually 2-3 weeks in children and young people, and about 3-4 weeks in the elderly.