Shingles (Herpes Zoster) is a painful rash caused by the reactivation of the Varicella-Zoster Virus (VZV). It is not possible to develop shingles without VZV already being present in your body. This virus first causes the illness known as chickenpox. After the initial infection resolves, VZV remains in a dormant state within the nervous system, establishing the foundation for a potential shingles outbreak years or decades later.
The Varicella-Zoster Virus Connection
Shingles is a direct consequence of the two-stage lifecycle of the Varicella-Zoster Virus. The primary infection, chickenpox, usually occurs in childhood, causing a characteristic widespread rash. Even after the immune system clears the visible symptoms, the VZV does not leave the body.
Instead, the virus travels along nerve fibers and retreats into sensory nerve structures near the spinal cord and brain, called ganglia. Here, the VZV enters a state of latency, remaining inactive and undetected. This latent virus is the necessary precursor for shingles.
Shingles develops when the dormant VZV reactivates, traveling back down the nerve fibers to the skin, causing a localized, painful rash. Reactivation often occurs when the immune system’s ability to suppress the virus is weakened, such as by age, stress, or medical conditions. Most people born before the chickenpox vaccine became common have been exposed to VZV, even if they do not recall having chickenpox.
Shingles Risk After Vaccination
The Varicella vaccine, which protects against chickenpox, has created a new context for the risk of shingles. The vaccine contains a live, attenuated form of the VZV. This weakened virus is still capable of establishing latency in the nervous system and can reactivate later in life.
The risk of developing shingles after vaccination is lower compared to the risk following a natural chickenpox infection. Studies show the incidence of shingles in vaccinated children is reduced, with one study finding the rate to be 78% lower than in unvaccinated children. This is because the vaccine virus is less likely to reactivate than the wild-type virus acquired through natural infection.
While the vaccine provides a high level of protection, the risk of shingles is not zero. Cases in vaccinated individuals tend to be milder and less frequent than those who had the natural disease. The public health goal of widespread childhood vaccination is to reduce the burden of both chickenpox and the later development of shingles.
VZV Transmission and Contagion
A person with an active shingles rash cannot transmit shingles directly to another person. Shingles is a reactivation within an individual’s body, not a new external infection. However, the fluid-filled blisters contain the active Varicella-Zoster Virus, which is contagious.
If a non-immune person comes into direct contact with the fluid from the shingles blisters, they can contract the VZV. The exposed person will develop the primary infection, which is chickenpox, not shingles. Only after developing chickenpox would they carry the latent VZV that could reactivate as shingles later in life.
Transmission of the virus is restricted to direct contact with the weeping lesions. The patient remains contagious only while the blisters are open. Once the rash has fully crusted over, the person is no longer able to spread the virus. Patients are advised to cover the rash and avoid contact with non-immune individuals (infants, pregnant women, and those with weakened immune systems).