Shingles is caused by the varicella-zoster virus (VZV), the same virus responsible for chickenpox. If you had chickenpox at any point in your life, the virus never fully left your body. It retreated into nerve cells near your spine and skull, where it has been sitting dormant ever since. Shingles happens when that virus wakes back up, sometimes decades later.
The Virus Behind Both Chickenpox and Shingles
Varicella-zoster virus belongs to the herpesvirus family. During a childhood chickenpox infection, the virus replicates in your skin and produces the familiar itchy, blistered rash. But while your immune system clears the rash, it doesn’t eliminate the virus entirely. VZV slips into nerve fibers in your skin and travels along them, moving deeper into the body until it reaches clusters of nerve cells called ganglia. These are located along your spinal cord (dorsal root ganglia) and at the base of your skull (cranial nerve ganglia). Once there, it goes quiet.
Researchers have identified two ways the virus makes this journey. It can travel directly from infected skin into nearby nerve endings, riding along the nerve fiber back to the ganglion. Or it can hitch a ride inside immune cells (T cells) that carry it through the bloodstream during the initial chickenpox infection. Both routes lead to the same result: the virus embeds itself in neurons and stays latent, potentially for the rest of your life.
Why the Virus Reactivates
Your immune system is what keeps VZV locked down. Specifically, a branch called cell-mediated immunity uses specialized T cells to patrol for signs of viral activity in those nerve cells. As long as this surveillance stays strong, the virus remains dormant. Reactivation happens when that immune control weakens.
Age is the biggest factor. VZV-specific T cell immunity declines significantly as you get older, which is why shingles risk climbs with each decade of life. About 1 in 3 people in the United States will develop shingles at some point, and the vast majority of cases occur after age 50. Conditions and treatments that suppress the immune system also raise risk considerably: organ transplantation, chemotherapy, HIV, and long-term use of medications like corticosteroids can all create an opening for the virus.
Physical trauma to a specific area of the body is another trigger, though less widely known. A case-control study published in the BMJ found that mechanical trauma severe enough to cause bruising was associated with an eightfold increased risk of shingles developing at that same site within the following month. Recent trauma at the rash site carried a 12-fold increased risk. The leading explanation is that injury to a nerve stimulates the virus sitting in the ganglion connected to that nerve, nudging it out of dormancy. Notably, trauma didn’t increase shingles risk anywhere else on the body, only at the injury location.
Psychological stress and other acute illnesses are frequently cited as triggers, though they’re harder to measure in controlled studies. The common thread across all these triggers is the same: anything that temporarily or permanently dips your immune defenses gives VZV an opportunity to replicate again.
What Happens When the Virus Wakes Up
Once reactivated, VZV begins replicating inside the nerve cell and travels back down the nerve fiber toward the skin, reversing the path it took years or decades earlier. This journey, called anterograde axonal transport, delivers the virus to the patch of skin supplied by that particular nerve. That’s why shingles appears as a band or strip of rash on one side of the body, following the path of a single nerve. This strip of skin is called a dermatome.
Before the rash shows up, you may feel pain, tingling, itching, or burning in the affected area for several days. Some people also develop headaches, sensitivity to light, or a general feeling of being unwell during this early phase. Then the rash emerges: red patches that quickly develop into clusters of fluid-filled blisters. New blisters continue forming for three to five days before the rash begins to dry out and scab over. Full healing typically takes two to four weeks, though some people are left with permanent skin discoloration or scarring.
The rash most commonly appears on the torso, wrapping from the spine partway around one side of the chest or abdomen. The face is the second most common location, particularly around the eye and forehead. The rash almost never crosses the body’s midline, which is one of the features that distinguishes shingles from other skin conditions.
Can You Spread Shingles to Others?
You cannot give someone shingles directly. However, the fluid inside shingles blisters contains active varicella-zoster virus. If someone who has never had chickenpox or the chickenpox vaccine comes into direct contact with that fluid, they can develop chickenpox (not shingles). Once the blisters have crusted over completely, you’re no longer contagious. Shingles is far less contagious than chickenpox itself, since the virus isn’t airborne in the same way during a shingles episode.
Postherpetic Neuralgia: The Most Common Complication
For many people, the pain of shingles doesn’t end when the rash heals. Postherpetic neuralgia (PHN) is persistent nerve pain, often described as burning or stabbing, that lingers in the same area where the rash appeared. It’s defined as pain lasting three months or more after the initial outbreak. About 13% of shingles patients aged 50 and older develop PHN, and the risk increases sharply with age. Among people who get shingles at age 60, roughly 60% experience postherpetic neuralgia. By age 70, that figure rises to 75%.
The good news is that most cases do improve over time. At one month after the shingles rash, 9 to 14% of patients have significant nerve pain. By three months, that drops to about 5%. At the one-year mark, 3% still report severe pain. But for that small percentage, PHN can be debilitating and difficult to manage, which is a major reason prevention matters.
How the Vaccine Prevents Reactivation
The recombinant zoster vaccine (sold as Shingrix) works by boosting the exact immune response that fades with age. It essentially retrains your T cells to recognize and suppress VZV before it can replicate and travel back to the skin. In clinical trials, the vaccine reduced shingles risk by 97.2% in adults aged 50 and older. Even in people 70 and above, efficacy remained high at roughly 90%.
Real-world data, which accounts for the messier conditions of everyday life, shows overall effectiveness of about 85.5%. For adults 50 to 79, effectiveness was around 87%. For those 80 and older, it was about 80%. Even people who had previously received the older, less effective shingles vaccine still saw strong protection after switching to the newer one, with adjusted effectiveness around 85%.
The vaccine is given as two doses, spaced two to six months apart. Both doses are needed for full protection. It’s recommended for adults 50 and older, as well as for younger adults whose immune systems are compromised.