When Was Shingles Discovered and What Causes It?

Shingles has been recognized as a distinct illness since antiquity, though centuries passed before anyone understood what actually caused it. The culprit is varicella-zoster virus (VZV), the same pathogen behind chickenpox, which hides silently in nerve cells for decades before flaring back to life. The story of how doctors connected these two seemingly different diseases, and how the virus manages its long disappearing act, is more interesting than most people expect.

Recognized for Centuries, Understood Only Recently

Ancient physicians described the painful, blistering rash we now call shingles, and the condition appears in medical texts stretching back thousands of years. But a critical piece of the puzzle stayed hidden for a remarkably long time: the relationship between shingles and chickenpox. While herpes zoster (the medical name for shingles) was recognized since antiquity, chickenpox was routinely confused with smallpox well into the 1800s, and the two diseases were not clearly distinguished until that century.¹ Without understanding that chickenpox was its own separate illness, there was no way to see that it shared a cause with shingles.

The connection between the two diseases came together gradually. In the early twentieth century, clinicians noticed that children who were exposed to adults with shingles sometimes developed chickenpox, hinting that one virus might be responsible for both. By mid-century, laboratory work confirmed that the virus isolated from shingles blisters was the same one found in chickenpox lesions. This was a genuinely surprising finding at the time, because the two conditions look and behave so differently. Chickenpox is a widespread, itchy rash that hits mostly children. Shingles is a localized, burning eruption that strikes adults, usually on one side of the body, and can cause severe nerve pain lasting months or longer.

How the Virus Gets In and Stays Hidden

When you first catch VZV, usually as a child with chickenpox, the virus does something that makes the later development of shingles almost inevitable: it sneaks into your nerve cells and goes quiet. During the chickenpox rash, infectious virus particles are released from infected skin cells. Sensory nerve endings sit right there in the skin, and they become bathed in those particles.² The virus enters those nerve endings and travels backward along the nerve fiber toward the nerve cell body, a process researchers have directly observed in laboratory models using specialized chamber systems that separate axons from cell bodies.³

Once VZV reaches the nerve cell body, it settles into clusters of nerve cells called ganglia, particularly the trigeminal ganglia (near the face) and the dorsal root ganglia (along the spine). There it enters a dormant state called latency. The virus isn’t actively replicating or causing symptoms. It is, in a sense, sleeping. Studies using techniques that amplify tiny traces of viral DNA have found VZV genetic material in the nerve cell nuclei of people who had no symptoms at all. The neuron itself is the primary hideout: only occasional non-nerve cells in the ganglia contained the virus.⁴ This means nearly everyone who has ever had chickenpox is carrying dormant VZV in their nerve cells, and roughly one in three will eventually develop shingles when the virus wakes up.

What Wakes the Virus Up

The immune system is the main thing keeping latent VZV in check. Specifically, a branch of the immune system called cell-mediated immunity, which involves specialized immune cells that can recognize and suppress virus-infected cells. As long as this arm of the immune system stays strong enough, the virus remains dormant. The trouble is that immune function naturally declines with age, a process called immunosenescence. Research on aged skin cells has shown that this age-related immune weakening plays an important role in allowing VZV to reactivate.⁵ This is why shingles overwhelmingly affects older adults: the immune surveillance that kept the virus bottled up for decades gradually loses its grip.

Age is the single biggest risk factor, but it is not the only one. Anything that significantly weakens the immune system can give VZV an opening. People undergoing chemotherapy, organ transplant recipients on immunosuppressive drugs, and people living with HIV are all at higher risk. Severe physical or emotional stress, while harder to pin down in studies, is also widely considered a contributing factor. But even in otherwise healthy adults, shingles can strike seemingly at random once immune function dips below whatever threshold was holding the virus in check. This unpredictability is part of what makes the disease frustrating: anyone who had chickenpox is a potential candidate.⁶

What Shingles Actually Does to the Body

When VZV reactivates, it travels back down the nerve fiber toward the skin, replicating as it goes. This produces the classic shingles presentation: a painful, blistering rash that follows the path of a single nerve, wrapping around one side of the torso or appearing on the face. But the rash is almost secondary to what is happening inside the nerve. The virus’s replication causes inflammation and cell death along the nerve and in the surrounding tissue.⁶ This nerve damage is why shingles hurts so much, often far more than you would expect from looking at the skin.

The pain itself has a neurological basis that goes beyond simple inflammation. Studies of skin biopsies from shingles patients have shown that the severity of lasting pain correlates with how many small sensory nerve fibers are destroyed in the affected area. Autopsies have also shown that persistent pain is linked to shrinkage of the part of the spinal cord that processes sensation from the affected nerve.⁷ In other words, shingles doesn’t just irritate nerves temporarily. In severe cases, it damages or destroys them, and the spinal cord itself can change in response. The sharp, shooting pains that some patients experience may result from damaged nerve fibers short-circuiting against each other, a phenomenon called ephaptic transmission.

Complications Beyond the Rash

The complication people hear about most is postherpetic neuralgia, or PHN, which is chronic pain in the area where the rash appeared that persists long after the blisters heal. PHN can last months or even years, and its cause remains poorly understood despite decades of research.⁶ It tends to be more common and more severe in older patients, and it is notoriously difficult to treat. For people who develop it, the pain can be constant, burning, or stabbing, and it can interfere with sleep, mood, and daily function in ways that ripple outward to affect the whole household.

PHN gets most of the attention, but the list of possible shingles complications is longer than many people realize. Reactivation of VZV can cause cranial nerve palsies (weakness or paralysis of facial muscles), a condition called zoster paresis (weakness in limb muscles served by the affected nerve), inflammation of the brain and spinal cord, cerebellar dysfunction, and a range of eye problems when the virus affects the ophthalmic branch of the trigeminal nerve. There is also a vascular complication in which VZV inflames blood vessels in the brain, which can mimic other conditions and is sometimes misdiagnosed.⁸ These complications are less common than PHN but underscore that shingles is not simply a skin disease. It is fundamentally a neurological event.

Shingles Without a Rash

One of the more unsettling findings in shingles research is that VZV can reactivate and cause neurological problems without ever producing the telltale rash. This condition is known as zoster sine herpete, and it can present as chronic nerve pain, facial paralysis, encephalitis, or other neurological disorders with no visible skin lesions to tip off the doctor.⁹ Diagnosing it requires specific laboratory testing for VZV, and because the rash is the main thing clinicians look for when they suspect shingles, cases of zoster sine herpete are likely underdiagnosed. If you develop unexplained nerve pain along a specific area of the body, especially if you are older, VZV reactivation is worth considering even in the absence of blisters.

Why Early Treatment Matters

Antiviral drugs like acyclovir and valacyclovir are the standard treatment for shingles, and the timing of when you start them makes a real difference. In clinical trials, patients who began acyclovir within 48 hours of the rash appearing saw their pain resolve in a median of about 28 days, compared to roughly 60 days for those who received a placebo. Valacyclovir performed even better than acyclovir in head-to-head comparisons. Encouragingly, antivirals still shortened pain duration even when treatment was delayed up to 72 hours after the rash appeared, though the benefit was greatest with earlier treatment.¹⁰

The practical takeaway is straightforward: if you develop a painful, blistering rash on one side of your body, see a doctor quickly. The 72-hour window is not a hard cutoff after which treatment becomes useless, but every hour counts in terms of reducing the total duration of pain. Antivirals work by stopping the virus from replicating, so the sooner they are on board, the less nerve damage accumulates. They don’t cure the disease or guarantee protection against PHN, but they meaningfully shorten the ordeal.

Modern Vaccines and How They Work

Prevention has changed dramatically with the development of the recombinant zoster vaccine (sold as Shingrix), which replaced the older live-virus vaccine in most guidelines. Shingrix uses a single viral protein from VZV combined with an adjuvant system that stimulates the immune system. It provokes strong, long-lasting antibody and T-cell responses against VZV, and its effectiveness holds up even in older adults and people with weakened immune systems.¹¹ Clinical trials showed protection above 90 percent in adults over 50, a level of efficacy that held across age groups, which was a significant improvement over the older vaccine.

Because Shingrix is not a live vaccine, it can be given to people whose immune systems are suppressed, a population that the older vaccine could not safely cover. The two-dose series does come with a notable downside: the side effects, while temporary, can be more intense than with many vaccines. Sore arms, fatigue, muscle pain, and sometimes fever are common in the days following each shot. These reactions are a sign that the adjuvant is doing its job of provoking a strong immune response. For most people, a couple of rough days after each dose is a very reasonable trade for substantially lower odds of developing shingles and its complications.

The Chickenpox Vaccine Debate and Shingles Rates

When widespread childhood chickenpox vaccination programs began, some researchers worried about an unintended consequence. The idea, originally proposed by the epidemiologist R. Edgar Hope-Simpson, was that periodic re-exposure to chickenpox in the community might help boost adults’ immunity against VZV and keep shingles at bay. If childhood vaccination eliminated circulating chickenpox, the theory went, adults would lose that natural boosting, and shingles rates might rise.

Modeling studies have lent some theoretical support to this concern. A Norwegian simulation found that universal varicella vaccination alone, without accompanying zoster vaccination for adults, would lead to a marked increase in shingles incidence.¹² But when researchers looked at what actually happened in the United States after the chickenpox vaccine was introduced, the picture was more reassuring. Despite rapid, dramatic declines in circulating VZV, there was no clear evidence that shingles rates in the general population increased as a result of the vaccination program.¹³ Several explanations have been offered for why the feared rise did not materialize: the original hypothesis may overstate the importance of external boosting, the body’s own subclinical reactivations may provide enough internal immune stimulation, or the adults who truly benefited from chickenpox contact may have been a small subset like parents of young children rather than the population at large.

The debate has not been fully settled, and it is possible that the impact simply takes longer to emerge than the surveillance window so far. But the data accumulated to date suggest that chickenpox vaccination has not created the shingles wave that some predicted, and the availability of Shingrix for older adults provides a safety net regardless.

The Ancient Virus Behind It All

VZV itself has a long evolutionary history with humans. It is the smallest of the human herpesviruses, and its various genetic lineages, or clades, have been traced using molecular clock methods. Researchers using Bayesian evolutionary analysis estimated that the major VZV clades diverged around 8,000 years ago, and the most likely geographic origin for that divergence was Europe rather than Africa, as some earlier models had suggested.¹⁴ This is more recent than human migration out of Africa, which complicates the simple idea that VZV lineages split as human populations dispersed. The virus appears to have undergone its own waves of diversification and migration, possibly tracking shifts in human settlement patterns, trade routes, and population density that occurred after agriculture emerged.

The Toll on Daily Life and Mental Health

The medical literature tends to focus on the rash, the nerve damage, and the immune mechanisms, but for the people who go through shingles, the experience is defined as much by its emotional and social impact as by its physical symptoms. A qualitative study of patients and their families in Germany found pervasive feelings of helplessness, frustration, and depression. Former patients described the experience as one in which their lives stopped, while their family members described the opposite problem: their lives became busier and more stressful as they took on caregiving responsibilities. Both patients and family members said they never forgot the illness and its considerable impact, especially when PHN was involved.¹⁵

Quantitative data from a large cross-sectional study in China showed that quality of life during shingles drops substantially, and the drop is steepest for patients over 70, who reported the most severe declines in mobility and self-care ability. Shingles-related pain was independently associated with lower quality of life, and patients with other chronic conditions fared even worse.¹⁶ The psychological dimension is also relevant to outcomes: a prospective study found that patients who went on to develop PHN had reported greater somatosensory amplification and greater limitations in physical and social functioning even in the early stages of their shingles episode, suggesting that psychological factors may influence how the nervous system processes and perpetuates pain after the acute infection resolves.¹⁷

None of this means that PHN is “in your head.” The nerve damage is real and measurable. But the interplay between physical nerve injury and psychological state appears to matter for how the brain processes pain signals over time. People who are more attuned to bodily sensations and who experience greater functional disruption early on may be at higher risk for chronic pain, which has practical implications: early attention to pain management and psychological support during a shingles episode could potentially reduce the likelihood of PHN taking hold, though more research is needed to confirm that.