Exposure to VZV in a healthy child initiates the production of host immunoglobulin G (IgG), immunoglobulin M (IgM), and immunoglobulin A (IgA) antibodies; IgG antibodies persist for life and confer immunity. Cell-mediated immune responses are also important in limiting the scope and the duration of primary varicella infection. After primary infection, VZV is hypothesized to spread from mucosal and epidermal lesions to local sensory nerves. VZV then remains latent in the dorsal ganglion cells of the sensory nerves. Reactivation of VZV results in the clinically distinct syndrome of herpes zoster (i.e., shingles), postherpetic neuralgia, and sometimes Ramsay Hunt syndrome type II. Varicella zoster can affect the arteries in the neck and head, producing stroke, either during childhood, or after a latency period of many years. Shingles After a<unk>  infection, the virus remains dormant in the body's nerve tissues for about 50 years. This, however, does not mean that VZV cannot be contracted later in life. The immune system usually keeps the virus at bay, however it can still manifest itself at any given age between 1 and 60, causing a different form of the viral infection called shingles (also known as herpes zoster). Since the human immune system efficacy decreases with age, the United States Advisory Committee on Immunization Practices (ACIP) suggests that every adult over the age of 50 years get the herpes zoster vaccine. Shingles affects one in five adults infected with<unk>  as children, especially those who are immune-suppressed, particularly from cancer, HIV, or other conditions. Stress can bring on shingles as well, although scientists are still researching the connection. Adults over the age of 60 who had<unk>  but not shingles are the most prone age demographic.
Chickenpox
Monkeypox
Sealpox
Smallpox
Cowpox
Stevens–Johnson syndrome
Toxic epidermal necrolysis
Mumps