You get shingles from a virus already inside your body. If you’ve ever had chickenpox, the virus that caused it never fully left. It settled into nerve clusters near your spine and brain, where it can sit quietly for decades before reactivating as shingles. About 1 in 3 people in the United States will experience this reactivation at some point in their lives.
The Virus That Causes Shingles
Chickenpox and shingles are caused by the same virus: varicella-zoster. When you recover from chickenpox as a child, your immune system clears the infection from your skin and bloodstream, but the virus retreats into sensory nerve clusters called dorsal root ganglia. There, it essentially turns off most of its own genes while keeping just one regulatory gene active, enough to maintain itself without triggering an immune response.
This isn’t a new infection waiting to happen. It’s the original virus, parked in your nervous system, held in check by your immune system’s ongoing surveillance. The virus doesn’t need outside help to persist. Research has shown that it maintains latency through its own internal mechanism, independent of the immune system’s involvement.
Why the Virus Reactivates
Shingles happens when your immune system’s grip on the dormant virus weakens enough for it to start replicating again. The reactivated virus travels along nerve fibers from a single nerve cluster to the patch of skin that nerve serves, which is why shingles typically appears as a band or strip of blisters on one side of the body.
The single biggest risk factor is age. Your risk rises sharply after 50 as the immune cells specifically trained to suppress varicella-zoster decline in number and effectiveness. But age isn’t the only trigger. Several conditions that weaken the immune system significantly increase your chances:
- Organ or bone marrow transplants, which require long-term immune-suppressing medications
- Cancers affecting the immune system, particularly leukemia and lymphoma
- HIV infection
- Immunosuppressive medications, including steroids used for autoimmune conditions
Stress as a Trigger
Physical and emotional stress can also tip the balance. A French study of 250 people with shingles found that those who had experienced a recent negative life event were about 3.4 times more likely to develop an outbreak. The proposed mechanism is straightforward: stress hormones suppress immune function, and the weakened surveillance gives the virus an opening.
One striking example comes from NASA research on astronauts. Before spaceflight, only one out of eight astronauts had detectable levels of varicella-zoster virus in their saliva. After spaceflight, all eight tested positive. None of the ground-based controls showed any sign of the virus. The physical and psychological stress of space travel was enough to nudge the virus toward reactivation, even in healthy adults.
Can Someone Give You Shingles?
You cannot catch shingles from another person. Shingles is always a reactivation of virus already living in your own nerve tissue. However, someone with active shingles blisters can spread the varicella-zoster virus to a person who has never had chickenpox or the chickenpox vaccine. That person would develop chickenpox, not shingles, and could then be at risk for shingles later in life.
Transmission happens through direct contact with fluid from the blisters or by breathing in viral particles released from them. Once the blisters crust over, the person is no longer contagious.
Do You Need to Have Had Chickenpox?
Yes. Shingles requires a prior varicella-zoster infection. But “prior infection” doesn’t always mean you remember having chickenpox. Some people had such mild cases as children that no one noticed, or they were infected before they could form memories. Others may have been exposed to the virus through vaccination with the older live chickenpox vaccine, which uses a weakened form of the same virus. If varicella-zoster is in your nerve tissue, shingles is possible, whether or not you recall the original illness.
What Shingles Feels Like
Shingles often announces itself before any rash appears. The earliest stage, called the prodromal phase, involves tingling, itching, or burning pain in a localized area of skin. Some people also experience flu-like symptoms: headaches, chills, fatigue, light sensitivity, and a general foggy feeling. At this point there’s nothing visible on the skin, which can make the symptoms confusing.
The rash follows, typically as a band of red, fluid-filled blisters on one side of the torso, face, or neck. The blisters eventually crust over and heal, usually within two to four weeks. The pain, however, doesn’t always follow the same timeline.
The Risk of Lasting Nerve Pain
The most common complication of shingles is postherpetic neuralgia, pain that persists in the affected area long after the rash has healed. It’s defined as pain lasting 90 days or more after diagnosis. Overall, about 5.8% of shingles patients develop it, but the rate climbs with age: roughly 12.5% of shingles patients aged 50 and older are affected. The pain can last months or years and ranges from a constant burning sensation to sharp, stabbing episodes triggered by light touch.
Vaccination Lowers Your Risk
The shingles vaccine is recommended for adults 50 and older as a two-dose series, with the second dose given two to six months after the first. Adults 19 and older with weakened immune systems can also receive it, with the option to shorten the gap between doses to one to two months when needed. Even if you’ve already had shingles, vaccination helps prevent future episodes, since the virus remains in your nerve tissue and can reactivate more than once.