Initial herpes zoster infection presents as chickenpox. After the initial episode of chickenpox resolves, the varicella zoster virus remains latent in the nerve cell bodies and, less frequently, the non-neuronal satellite cells of the dorsal root, cranial nerve or autonomic ganglia, without causing any symptoms. Years or decades after the initial infection, the virus may break out of nerve cell bodies and travel down nerve axons to cause viral infection of the skin in the region of the nerve. The virus may spread from one or more ganglia along nerves of an affected segment and infect the corresponding dermatome (an area of skin supplied by one spinal nerve) causing a painful rash. Although the rash usually heals within two to four weeks, some sufferers experience residual nerve pain for months or years, a condition called postherpetic neuralgia. Exactly how the virus remains latent in the body, and subsequently re-activates, is not understood.
Clinical incidence of shingles often occurs in patients with age 50 above after stress. During outbreak, the skin lesion become contagious. This might be the viral mechanism to spread and escape dying host. The virus survives in domant form in human neuron. When host signals weakness, virus reactivate to proliferate and spread to next host much like grass seeding in the fall before winter. For long time, medical communities believe weaken immune system as reason for outbreak. But it is very likely parasites escaping dying host.
This logics might be apply to many parasitic disease in human or animals.