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The virus that causes shingles is cunning. It lies dormant inside the human body — often hiding in the nerve cells of the spinal column or the brain. Then, after decades of inactivity, it can remerge as a painful, blister-pocked skin rash.
“The way the virus is quiescent for decades and then reactivates — it’s unusual, but it makes sense from the perspective of the virus’ survival,” says Rafael Harpaz, MD, a medical epidemiologist with the CDC’s Division of Viral Diseases. Back when humans lived in small hunter-gatherer communities, Harpaz explains, viruses that depended on human hosts would have died out quickly if they infected everyone en masse. By lying in wait, shingles allows new generations of carriers to be born.
Harpaz has spent years studying the bug. A 2016 study of his in the journal Clinical Infectious Diseases helped shine a spotlight on a curious phenomenon: For at least the past 60 years, rates of shingles have been climbing. Compared to the period from 1945 to 1949, when 0.76 people per 1,000 developed shingles, rates climbed to 3.15 per 1,000 by the period from 2000 to 2007, his study found.
“[The rise] seems to be occurring across all age groups, and not just in the U.S.,” says Kosuke Kawai, ScD, an assistant professor of otolaryngology at Boston Children’s Hospital and one of Harpaz’s co-authors on the CID study. “There are studies in European countries, and also in Taiwan and Australia, that seem to show this same increase over time.”
While rates of shingles have been escalating for decades, Harpaz says the increase seems to be “plateauing” among older adults — a group that usually suffers from a higher incidence of shingles than younger people. (A new vaccine was introduced in 2006, and some experts suspect that may explain it.) But rates of shingles among those age 30 to 50 don’t seem to be leveling off.
From the late 1940s to the early 2000s, the prevalence of shingles among Americans younger than 50 more than quadrupled, Harpaz’s data shows. Some research suggests the incidence of shingles among younger adults may actually be gaining steam. At least anecdotally, shingles seems to be increasingly common among people in their twenties and thirties — a group that, historically, suffered from vanishingly low rates of the disease.
What’s fueling all this? Harpaz is stumped. “I have given this as much thought as anyone, and it remains a mystery to me,” he says.
Known medically as herpes zoster, shingles is a cousin to the viruses that cause oral and genital herpes, and it springs from the same virus that causes chickenpox, Harpaz explains. (You cannot have shingles if you haven’t been exposed to chickenpox first.)
Shingles turns up more often in women than in men, but not by much. The disease tends to manifest as a painful, blistering rash that’s usually confined to a single swath of flesh on one side of a person’s body or face. The condition, which can’t be cured, tends to resolve by itself and usually doesn’t recur, says Wilbur Chen, MD, an associate professor of medicine and infectious disease physician at the University of Maryland.
But for some people, shingles leads to complications that endure.
One of those complications, called postherpetic neuralgia, is a debilitating pain that strikes 10 percent to 18 percent of patients and can last for years, according to the CDC. “It can be life-shattering,” Harpaz says. “People end up reclusive and depressed and suicidal — just plagued with pain.” Another common complication is something called ophthalmicus. This refers to shingles that occurs in the cranial nerves around the eye, and it can lead to permanent vision loss, pain, or scarring.
As recently as the early 2000s, roughly 95 percent of all American adults had experienced chickenpox — most when they were kids. But after the introduction of the childhood chickenpox vaccine, in 1996, rates of the infection dropped by more than 70 percent, according to a recent analysis in the journal Vaccine.
“The chickenpox vaccine is an attenuated, live version of [the virus that causes chickenpox],” Kawai explains. “So those who have had the vaccination can still develop shingles later in life.”
Some experts who study shingles have long theorized that adult exposure to kids with chickenpox may provide a kind of protective “booster” effect against shingles. “So, if you vaccinate children and they’re no longer getting chickenpox, that means adults are no longer exposed, and so there’s no opportunity to have immunity against [shingles] boosted,” Harpaz explains.
Research from Europe backs up this “external boosting” theory and concludes that it could cause an uptick in shingles cases among adults in their thirties and early forties. But again, Harpaz says the data doesn’t really bear this out. “Rates of [shingles] had been increasing well before the [chickenpox] vaccine, and there doesn’t seem to be an acceleration after the vaccine,” he says.
So what else could explain the worldwide rise in shingles cases — a rise that continues apace among younger adults?
“My general sense is that more young people are undergoing organ transplants or surviving cancers — so they’re surviving, but they’re immunocompromised,” says UMD’s Chen. He says the same is true for those living with HIV. Shingles has long been linked to depressed immune function. And so, as medical science has allowed people to survive what were once deadly health conditions — albeit with weakened immune systems — it makes sense that shingles rates would increase, he says.
Harpaz’s own research has found that, indeed, rates of immunosuppression are increasing among American adults. But again, he says this wouldn’t explain the steady rise in shingles dating back all the way to the 1940s and ’50s. “We’ve looked at this explanation, and it doesn’t hold up,” Harpaz says. The same is true for theories (and some supporting evidence) linking climate change, agricultural pesticides, and antibiotic resistance to the steady rise of shingles, he says.
Chen points out that stress may also to play a role. “Shingles can happen among healthy young adults with no other underlying diseases and who are otherwise athletic, and sometimes we think it might be stress-induced,” he says.
Stress can suppress immune function and trigger outbreaks of cold sores and other herpes virus–related symptoms. “This is all speculation, but I think you could point to social media and modern culture and the emotional and physical and spiritual stress a lot of younger adults are feeling,” Chen says. “I don’t think this is driving higher rates, but it could be a factor.”
As with all things herpes zoster, Harpaz has checked out the data. Again, his findings suggest stress alone isn’t to blame. “I have been an author on papers where it seemed to show stress both was and wasn’t a factor,” he says. Harpaz points out that shingles rates were much lower during World War II — a decidedly stressful time. “So I’m skeptical stress is the cause,” he says.
“There are so many things changing in our world that it’s hard to be able to track them down and figure out how they could be related to shingles,” Harpaz says. “Systematically, one after another, the theories we’ve looked at don’t pan out. But we’ll keep looking.”