Chickenpox (varicella) and shingles (herpes zoster) are caused by the same agent, the Varicella-Zoster Virus (VZV). Chickenpox is the initial infection, while shingles is a distinct, painful rash that occurs years or decades later. Both conditions are directly linked to the presence of VZV within the body.
The Varicella-Zoster Virus and Viral Latency
The connection between chickenpox and shingles is the Varicella-Zoster Virus (VZV), a member of the herpesvirus family. Chickenpox is the primary, highly contagious infection causing a characteristic blistering rash. After recovery, VZV is not eliminated but establishes a hidden, dormant state known as latency.
The virus travels to the sensory nerve root ganglia, clusters of nerve cells located near the spinal cord and brain. In these nerve cells, the virus can remain inactive for a person’s entire life. Latency is essentially the virus going into a deep sleep within the nervous system, waiting for an opportunity to reawaken.
Shingles occurs when latent VZV reactivates, typically due to a decline in cell-mediated immunity associated with age or immunosuppression. The reactivated virus travels along the nerve fibers to the skin, causing the painful, localized rash. This mechanism confirms that a person must have been exposed to VZV at some point to develop shingles later on.
Shingles Risk Without Prior Chickenpox
If you truly never had any exposure to VZV, either through natural infection or vaccination, you cannot develop shingles because there is no latent virus to reactivate. However, “never having chickenpox” needs careful clarification. Many people had a subclinical infection as children, meaning they were infected with VZV but experienced very mild or no noticeable symptoms. These individuals still harbor the latent virus and are at risk for shingles.
The introduction of the Varicella vaccine, which protects against chickenpox, created a new scenario regarding shingles risk. The chickenpox vaccine uses a weakened, live form of VZV. This weakened virus is still capable of establishing latency in the nerve cells, just like the natural virus.
Individuals vaccinated against chickenpox but who never had the disease can still develop shingles later in life. However, the risk of shingles is significantly lower after vaccination compared to natural VZV infection, and the resulting shingles is often less severe. Vaccination replaces natural infection as the source of the latent virus, creating a possibility for shingles, albeit a reduced one.
Preventing Shingles Reactivation
Preventing shingles involves proactively boosting the immune system’s ability to keep latent VZV suppressed. The most effective approach is the shingles vaccine, which is distinct from the chickenpox vaccine. This vaccine, currently a recombinant, non-live formulation, is highly effective at preventing shingles and its most common complication, postherpetic neuralgia.
The Centers for Disease Control and Prevention recommends two doses of the recombinant shingles vaccine for all healthy adults aged 50 and older. It is also recommended for adults aged 19 and older who have weakened immune systems due to disease or therapy. The vaccine works by significantly raising the body’s cellular immune response against the latent VZV.
Even individuals who have previously had shingles, received the older live shingles vaccine, or received the chickenpox vaccine should still get the current recombinant vaccine. Vaccination provides over 90% protection against shingles in adults aged 50 and older. Maintaining a robust immune status through vaccination is the primary defense against viral reactivation.