Chickenpox (varicella) is a highly contagious viral illness caused by the Varicella-Zoster Virus (VZV). While the acute phase of the infection, including the characteristic rash and other symptoms, resolves on its own, the virus does not leave the body. Instead, VZV establishes a lifelong, dormant presence within the nervous system. This continued existence poses a risk of future illness, which takes the form of shingles (herpes zoster).
The Initial Infection: Chickenpox
The acute phase of VZV infection is marked by a distinctive, itchy rash that progresses through three stages: raised red bumps, fluid-filled blisters, and scabs. The rash is usually accompanied by non-specific symptoms such as fever and headache, which start one to two days before the rash appears. The virus spreads easily through the air from coughs or sneezes and by contact with the fluid from the blisters.
A person remains contagious until all the blisters have dried up and formed scabs, which typically takes four to seven days after the rash first appears. Once the immune system controls the active infection, visible symptoms clear up within one to two weeks. The body develops immunity, making a second case of chickenpox very rare.
How the Varicella-Zoster Virus Becomes Latent
After the chickenpox rash heals, VZV transitions into a latent state within specific nerve structures. The virus travels from the skin and mucous membranes to the sensory nerve ganglia, which are clusters of nerve cells located near the spinal cord and the brain. These ganglia include the dorsal root ganglia along the spine and the cranial nerve ganglia in the head.
During latency, the VZV genome remains present within the nerve cell bodies, but the virus is not actively replicating. The virus hides from the immune system within the neurons, which are protected from constant immune surveillance. This allows VZV to remain in the body for the person’s entire life.
Reactivation: The Development of Shingles
The latent VZV can reactivate later in life, causing shingles (herpes zoster). Reactivation occurs when the virus is no longer suppressed by the body’s immune system, typically due to a decline in cellular immunity. This decline is triggered by the natural process of aging, or by conditions that compromise the immune system, such as HIV, cancer, or the use of immunosuppressant medications. Stress and physical trauma may also temporarily weaken the immune response.
Once reactivated, the virus travels down the nerve fibers to the skin, causing a painful, localized rash. The shingles rash appears as a single stripe of blisters on one side of the body, following the path of the specific nerve (a dermatome). Two to four days before the rash erupts, people often experience tingling, itching, or burning pain in the affected area. This pain can be significant and may persist for weeks.
A common complication of shingles, especially in older adults, is post-herpetic neuralgia (PHN). PHN is persistent nerve pain lasting more than three months after the rash has healed, resulting from nerve damage caused by the replicating virus. This condition can be debilitating, affecting 5 to 30 percent of shingles patients aged 50 and older. If VZV reactivates in the facial nerves, it can cause zoster ophthalmicus, leading to a rash near the eye and carrying a risk of vision loss.
Prevention Strategies for VZV
Preventative measures are available to manage both the initial VZV infection and the risk of its later reactivation as shingles. The Varicella vaccine prevents chickenpox or significantly reduces the illness’s severity in those who have not previously had the disease. This vaccine is typically given to children in a two-dose series, leading to a significant decline in chickenpox incidence.
For adults, particularly those over the age of 50, the Zoster vaccine is available to prevent shingles. The recombinant zoster vaccine (RZV) is highly effective at preventing shingles and reducing the risk of developing post-herpetic neuralgia. It is recommended for most adults in this age group to boost declining cellular immunity, which otherwise allows VZV to reactivate.
Antiviral medications, such as acyclovir, valacyclovir, and famciclovir, are used to treat acute cases of both chickenpox and shingles. These drugs interfere with the virus’s ability to replicate, shortening the duration and lessening the severity of the illness, especially if treatment begins shortly after symptoms appear. For shingles, early antiviral treatment also helps reduce the duration of post-herpetic neuralgia.