Herpes Zoster (Shingles): Symptoms, Vaccine, Contagion, and Treatment

What Is Herpes Zoster (Shingles)?

When the red, itchy blisters of chickenpox fade away and life returns to normal, it can feel like a complete victory over the infection. In reality, for many people, that victory is only partial. The virus responsible for chickenpox is never truly eliminated from the body. Instead, it retreats silently into the nerve cells, where it can lie dormant for decades, waiting for the right moment to strike again.

This second eruption of the varicella-zoster virus (VZV) causes a disease known as herpes zoster, commonly called shingles.

The popular name “St. Anthony’s Fire”**, used widely in European traditions, reflects the historical practice of invoking Saint Anthony the Abbot. He was believed to possess miraculous healing powers, and people called upon him to seek relief from the intense pain and burning sensations caused by the disease. During the Middle Ages and early modern period, this term was used to describe a wide range of inflammatory skin conditions that physicians of the era could not yet differentiate diagnostically.

The hallmark symptoms of herpes zoster include:

• Appearance of small fluid-filled blisters (vesicles)
• Skin redness and inflammation
• General malaise and sometimes fever
• Burning sensation and/or itching
• Tingling or pins-and-needles sensation

The most common and feared complication is postherpetic neuralgia (PHN), a persistent and often debilitating pain. This pain lingers in the affected area long after the rash has healed. This pain can last for weeks, months, or in some cases, years.

Other possible complications include:

• Involvement of the eyes (herpes ophthalmicus)
• Spread to other organs, potentially causing serious conditions such as meningoencephalitis, pneumonia, or hepatitis

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Causes

The virus responsible for both chickenpox and shingles is the Varicella-Zoster Virus (VZV), a member of the Herpesviridae family.

Some etymological context is useful for understanding the disease:

• The word varicella derives from the Latin variola (smallpox). Smallpox is a different and far more dangerous infectious disease that killed or disfigured millions of people, particularly during the Middle Ages.
• Zoster comes from the Greek word for “belt” or “girdle”, reflecting the characteristic belt-like rash that typically wraps around one side of the torso.

VZV belongs to the herpesvirus family, which also includes:

• Herpes simplex virus (HSV-1 and HSV-2): responsible for cold sores and genital herpes, a sexually transmitted disease
• Epstein-Barr virus (EBV): associated with infectious mononucleosis

Like all herpesviruses, VZV can establish latency. This means it hides in the nervous system after the initial infection and may reactivate years or even decades later.

How Does Reactivation Work?

During the primary infection (chickenpox), viral particles migrate from the bloodstream into clusters of nerve cells called sensory ganglia, located near the spinal cord and brain. Here, the virus remains dormant in an inactive (latent) state, sometimes for a lifetime. The sensory ganglia transmit information to the brain about:

• Heat and cold
• Touch
• Pain

When VZV reactivates, typically due to a weakening of immune defenses, it travels along the nerve fibers, known as axons, from the ganglia to the skin. There, it multiplies and causes the characteristic painful rash of herpes zoster. At this stage, the nervous system is far more profoundly affected than during the original chickenpox infection, which explains why shingles symptoms are typically more severe and complex.

The historical link between chickenpox and shingles was first suspected in 1909 and was conclusively confirmed in 1958, when detailed viral analysis of samples from patients with both conditions proved they were caused by the same pathogen.

Importantly, every adult who has ever had chickenpox, even an unnoticed mild case, is potentially at risk of developing shingles.

Risk Factors

Herpes zoster becomes more common after the age of 40, with incidence rising sharply with advancing age. The disease is 10 times more likely in adults over 60 than in children under 10. A significant proportion of the world population will experience at least one episode of shingles in their lifetime.

Key risk factors include:

• Older age: The immune system naturally weakens with age (immunosenescence), making reactivation more likely
• Immunosuppressive medications: Such as corticosteroids, chemotherapy agents, or post-transplant immunosuppressants
• Serious underlying illnesses: Including cancers, particularly hematological malignancies
• HIV infection: HIV significantly compromises cell-mediated immunity, which is the primary defense against VZV reactivation
• Chronic stress: Psychological and physical stress are recognized triggers for immune suppression

Interestingly, regular exposure to VZV, like that experienced by parents of young children with chickenpox, has been shown to act as a natural immune booster. This may potentially reduce the risk of reactivation.

Herpes zoster shows no significant seasonal variation and does not cause epidemic outbreaks, distinguishing it clearly from chickenpox.

Children at increased risk include those born to mothers who contracted chickenpox in the last 21 days of pregnancy and those who had chickenpox themselves during early infancy. Their immature immune systems may not maintain effective viral latency.

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Contagion

A frequently misunderstood aspect of herpes zoster is its transmissibility. Here is what the science says:

Can someone with shingles infect others? Yes, but only in a specific way. A person with active shingles can transmit VZV to someone who has never had chickenpox and is not vaccinated. However, that person will develop chickenpox, not shingles. Transmission requires direct contact with the fluid from open blisters. If the lesions are covered, or the contact person is immune (either through prior chickenpox or vaccination), there is no risk.

Is airborne transmission possible with shingles? Shingles, unlike chickenpox, does not usually spread through the air. Chickenpox infects the upper respiratory tract, making it highly contagious that way. During a shingles outbreak, the virus remains localized to the skin along the affected nerve. This is why patients with shingles can generally leave their home, provided the lesions are kept covered and contact with vulnerable individuals is avoided.

Can chickenpox cause shingles in others? No. Chickenpox patients can transmit VZV to unimmunized individuals, who will then develop chickenpox. However, they cannot directly cause shingles in anyone.

Key principle: Shingles is a reactivation of a dormant virus already present in the body. It is not “caught” from another person. The external trigger is internal immune suppression, not external exposure.

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Symptoms

The clinical presentation of herpes zoster typically unfolds in stages:

Prodromal Phase (Days Before the Rash)

Several days before the rash appears, patients may experience non-specific systemic symptoms:

• Headache
• Fever (usually low-grade)
• Chills
• General malaise and fatigue
• Sensitivity to light (photophobia)

Early Neurological Phase

The first specific symptom of shingles is typically pain, burning, tingling, or itching in a localized area of skin. This discomfort often occurs before any visible skin changes appear. This can occasionally be mistaken for other conditions (such as pleuritis, cardiac pain, or muscle strain) if the rash has not yet emerged.

Rash Phase

Within 2 to 5 days, the characteristic rash appears in the same painful area. The rash:

• Follows a dermatomal pattern, covering only the strip of skin supplied by the affected nerve
• Appears on one side of the body only (unilateral)
• Begins as red patches that progress to clusters of fluid-filled vesicles
• Is most commonly located on the chest, flank, or abdomen (forming the classic “belt”)
• Can also affect the neck, face, scalp, and, critically, the eyes

The rash may also occasionally be accompanied by enlarged lymph nodes.

Pain intensity varies widely: some patients experience only mild discomfort or itching, while others describe excruciating pain triggered even by the lightest touch (allodynia).

In most otherwise healthy individuals, the vesicles crust over and heal without leaving permanent marks. Occasionally, in cases of very large blisters, permanent scarring or skin discoloration may occur.

Zoster Sine Herpete

Zoster sine herpete is an atypical but clinically important presentation of shingles in which the patient experiences the characteristic neuropathic pain without any visible skin rash. The pain can be intense, persistent, and last for weeks or months. This condition is caused by VZV reactivation in the sensory nerves, even though no external vesicular eruption occurs. It is frequently underdiagnosed due to the absence of the classic rash, and requires specific laboratory testing (PCR) for confirmation.

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Duration

The typical timeline of herpes zoster:

In young, immunocompetent individuals, the disease typically resolves within a month. In older or immunocompromised patients, both the rash and subsequent pain can be far more prolonged.

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Risks and Complications

Postherpetic Neuralgia (PHN)

The most common and debilitating complication of herpes zoster is postherpetic neuralgia. This neuropathic pain persists in the area of the original rash long after the skin has healed. It is described as:

• Burning, throbbing, or stabbing
• Constant or intermittent
• Triggered or worsened by light touch, wind, or temperature changes

PHN can last for months or years and often does not respond to conventional pain medications, requiring specialized neuropathic pain treatments. The risk of PHN increases significantly with age. In fact, it occurs in up to 30% of patients over 60 who develop shingles.

Herpes Ophthalmicus

When shingles affects the ophthalmic branch of the trigeminal nerve, it leads to a condition called herpes ophthalmicus. This affects the forehead, eyelids, and the eye itself. This is a serious condition that can lead to:

• Corneal ulceration and scarring
• Uveitis (inflammation inside the eye)
• Partial or complete vision loss if not treated promptly

Any patient with shingles affecting the eye area should be seen immediately by an ophthalmologist.

Ramsay Hunt Syndrome

When VZV reactivates in the facial nerve (cranial nerve VII) and the adjacent vestibulocochlear nerve, it causes Ramsay Hunt Syndrome, which can present with:

• Ear pain and vesicles in the ear canal
• Facial paralysis on the affected side
• Hearing loss and balance disturbances (vertigo)

Neurological Complications

In rare cases, particularly in immunocompromised patients, VZV can spread to the brain or spinal cord. This may cause:

• Viral meningitis (inflammation of the membranes surrounding the brain)
• Encephalitis (brain inflammation)
• Stroke or transient ischemic attack (VZV can cause vasculitis affecting cerebral blood vessels)

Any new neurological symptoms outside the original affected area require immediate medical evaluation.

Immunocompromised Patients

Patients with weakened immune systems (due to HIV, cancer, or immunosuppressive therapies such as chemotherapy, corticosteroids, or post-transplant drugs) face a much higher risk of:

• Disseminated zoster: the rash spreads beyond a single dermatome and can affect multiple organs
• Longer-lasting or recurrent outbreaks
• More severe complications

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Shingles During Pregnancy

Pregnant women are understandably concerned about any infection during pregnancy. Here is what current evidence shows regarding VZV during pregnancy:

First Trimester to 30 Weeks

If a pregnant woman contracts chickenpox (primary infection) in the first 30 weeks, there is a small risk of congenital varicella syndrome in the fetus, including malformations affecting the skin, limbs, eyes, and brain. However, shingles during pregnancy (a rare event) carries a significantly lower risk of fetal harm than primary chickenpox infection, as the virus is far less likely to cross the placenta during reactivation.

Between 21 and 5 Days Before Delivery

If a mother develops chickenpox in this critical window, the newborn may be born with chickenpox or develop it within the first few days of life. However, the interval usually allows the mother’s immune system to produce some protective antibodies that are transferred to the baby. Still, a small percentage of these infants may develop shingles in the first 5 years of life, as their immature immune systems cannot maintain full viral latency.

At the Time of Delivery

This is the highest-risk scenario. The mother’s immune system has not had time to mount a protective antibody response, and the newborn’s immune system is immature. Neonatal varicella acquired at birth can be life-threatening. In these cases, the newborn is treated with Varicella-Zoster Immune Globulin (VZIG). This preparation is derived from blood rich in antibodies from recently recovered adults, providing passive immunity.

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Diagnosis

In the vast majority of cases, the diagnosis of herpes zoster is purely clinical. A general practitioner or dermatologist can recognize the condition based on:

1. Visual inspection of the characteristic unilateral, dermatomal rash
2. Medical history, including a prior history of chickenpox and any recent immune-suppressing events
3. The typical pain pattern involves burning or tingling pain that either precedes or accompanies the rash. This pain is usually confined to one side of the body

When Is Laboratory Testing Needed?

Diagnostic tests are reserved for cases where the clinical picture is unclear:

• Zoster sine herpete: No rash is present, but neuropathic pain suggests VZV reactivation
• Immunocompromised patients: Atypical, disseminated, or persistent presentations
• Differential diagnosis: Distinguishing herpes zoster from localized herpes simplex, contact dermatitis, or other vesicular skin conditions

The Gold Standard Test

The Polymerase Chain Reaction (PCR) performed on fluid from vesicles or a lesion swab is the most accurate and rapid diagnostic tool available. It identifies VZV DNA with high sensitivity and specificity. Other older methods, such as the Tzanck smear or serological antibody testing (IgM), are now considered less accurate and largely superseded by molecular techniques.

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Treatment

The main goals of herpes zoster treatment are:

1. Inhibiting viral replication to limit the extent and duration of the outbreak
2. Accelerating healing of skin lesions
3. Reducing pain to improve quality of life and prevent postherpetic neuralgia

Antiviral Therapy

Antiviral medications are the cornerstone of treatment and are most effective when started within 72 hours of rash onset. Treating early significantly reduces both the severity of the acute episode and the risk of PHN.

Standard antiviral options include:

• Valacyclovir and Famciclovir: These are the preferred first-line agents due to their high oral bioavailability and convenient dosing schedules (typically three times daily), which improves patient adherence compared to older alternatives.

• Brivudine: A highly effective option with the significant convenience of once-daily dosing for 7 days. Critical warning: Brivudine must never be used in patients currently receiving chemotherapy with fluoropyrimidines, such as 5-fluorouracil or capecitabine, or in those who have recently completed such treatment. This combination can be potentially lethal. This is due to a dangerous pharmacological interaction.

• Acyclovir aciclovir: The original antiviral remains a valid option, particularly in intravenous form for hospitalized patients with severe or complicated disease.

Pain Management

Pain management in herpes zoster frequently requires a multimodal approach, as the neuropathic nature of VZV-related pain does not always respond to standard analgesics.

Mild to moderate pain:

• Paracetamol (acetaminophen) for general discomfort and fever
• Non-steroidal anti-inflammatory drugs (NSAIDs) for their combined analgesic and anti-inflammatory effects

Neuropathic pain: Because VZV damages nerve fibers directly, conventional painkillers are often insufficient. The following are used for neuropathic pain:

• Gabapentin and Pregabalin (Lyrica): These anticonvulsants modulate nerve signal transmission and are first-line drugs for both acute zoster pain and postherpetic neuralgia
• Tricyclic antidepressants (such as amitriptyline): Used at low doses for their well-established analgesic effect on neuropathic pain

Topical treatments:

• Lidocaine patches (5%): Applied directly to the healed skin over the painful area, they provide localized, safe pain relief with minimal systemic absorption
• Capsaicin cream (derived from chili pepper): Desensitizes pain receptors in the skin; available in both low-concentration cream (applied repeatedly) and high-concentration patch (applied by healthcare professionals)

Corticosteroids: In selected patients, a short course of corticosteroids may be prescribed alongside antivirals to reduce acute nerve inflammation. Their role in preventing long-term PHN remains debated in the literature.

Lifestyle and Practical Tips

Good daily care of the affected skin is essential to prevent secondary bacterial infections and minimize discomfort:

• Keep lesions clean and dry: Wash gently with mild soap and water; pat dry rather than rubbing
• Wear loose-fitting clothing made of soft, natural fibers (cotton or silk) to minimize friction against irritated skin
• Cool, damp compresses can provide temporary relief from intense burning
• Avoid scratching the blisters, which can introduce bacteria and cause secondary infection or scarring
• Do not apply unprescribed powders, creams, or traditional remedies to the blisters, as these can trap moisture, delay healing, and promote bacterial superinfection
• Rest adequately: Sufficient sleep and rest support immune function and recovery

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Vaccination

Chickenpox Vaccine

The chickenpox vaccine prevents primary VZV infection. Importantly, individuals vaccinated against chickenpox have a significantly lower risk of developing shingles in later life, because the attenuated (weakened) viral strain used in the vaccine is far less likely to reactivate than the wild-type virus acquired through natural infection.

Shingles Vaccine (Shingrix)

Preventive vaccination against herpes zoster has undergone a revolution in recent years. Most national health authorities now recommend vaccination for adults over 50 and for younger individuals with immune-compromising conditions.

Shingrix: The Recombinant Adjuvanted Vaccine

The current gold standard for shingles prevention is the recombinant adjuvanted subunit vaccine Shingrix. Unlike its predecessor (Zostavax, a live-attenuated vaccine that has been largely phased out), Shingrix contains only a specific protein fragment of VZV combined with a powerful immune-stimulating adjuvant system (AS01B), with no live virus.

Key facts about Shingrix:

• Efficacy: Over 90% effective at preventing shingles and postherpetic neuralgia. This includes adults over 70 and immunocompromised individuals, making it a remarkable achievement compared to older vaccines
• Dosing: Two doses administered 2 to 6 months apart via intramuscular injection
• Eligibility: Recommended for adults aged 50 and over; indicated for immunocompromised individuals from age 18
• Duration of protection: Studies show high protection lasting at least 10 years
• Side effects: Common but generally mild and short-lived, lasting 1 to 3 days. They include pain and redness at the injection site, fatigue, headache, and flu-like symptoms. These effects reflect the robust immune activation produced by the adjuvant

In some countries, Shingrix is offered free of charge or at reduced cost to older adults and individuals with specific risk conditions, such as immunodeficiency, diabetes, chronic heart disease, or chronic respiratory disease. Eligibility and reimbursement policies vary by country and healthcare system.

Vaccination is currently the single most effective tool available to prevent the chronic, disabling complications of herpes zoster, particularly postherpetic neuralgia.

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Frequently Asked Questions

What is shingles (herpes zoster)?

Shingles, medically known as herpes zoster, is a viral infection caused by the reactivation of the varicella-zoster virus (VZV). This is the same virus responsible for chickenpox. After a chickenpox infection, the virus lies dormant in nerve tissue and can reactivate years or decades later, causing the characteristic painful skin rash of shingles.

What are the main symptoms of shingles?

The first signs are typically burning, tingling, or pain in a localized area of skin, often accompanied by general symptoms such as headache, fatigue, and low-grade fever. Within a few days, a distinctive one-sided rash appears in the painful area, progressing from red patches to clusters of fluid-filled blisters. The most common sites are the chest, flank, neck, and face.

How long does shingles last?

The active rash typically lasts 2 to 4 weeks. However, pain can persist much longer. Sometimes it lasts for months or even years, developing into a condition called postherpetic neuralgia. Recurrences are possible, particularly in immunocompromised individuals.

Is shingles contagious? How does transmission occur?

A person with shingles can transmit VZV to someone who has never had chickenpox or been vaccinated. However, the contact person will develop chickenpox, not shingles. Transmission requires direct contact with the fluid from active, open blisters. Shingles does not spread through the air. Once all lesions have crusted over, the person is no longer contagious.

Can you go out in public if you have shingles?

Yes. As long as the lesions are completely covered and close contact with high-risk individuals (pregnant women, newborns, immunocompromised people) is avoided, there is no need for isolation. The virus does not spread through the air during a shingles outbreak.

Can you go to the beach with shingles?

It is advisable to avoid beach exposure during an active shingles outbreak. Sun exposure can worsen skin irritation, and heat and moisture can increase discomfort. Additionally, covering active lesions while at the beach is important to prevent transmission to non-immune individuals.

How is shingles treated?

Treatment focuses on:

1. Antiviral drugs (valacyclovir, famciclovir, acyclovir, or brivudine) are most effective when started within 72 hours of rash onset
2. Pain management: paracetamol or NSAIDs for mild pain; gabapentin, pregabalin, or tricyclic antidepressants for neuropathic pain; lidocaine patches or capsaicin for topical relief
3. Rest and good wound care to support healing

Can shingles be prevented?

Yes. The most effective prevention is vaccination. The Shingrix vaccine offers over 90% protection against shingles and its complications, including postherpetic neuralgia. It is recommended for adults aged 50 and over, and for younger immunocompromised individuals. The vaccine requires two doses, given 2 to 6 months apart.

What causes the persistent pain after shingles?

Persistent pain after a shingles outbreak is called postherpetic neuralgia (PHN). It is caused by nerve damage inflicted by the virus during reactivation. The pain may be burning, stabbing, or throbbing, and can last for months or years. Conventional pain relievers are often insufficient; specialized neuropathic pain medications are usually required. PHN should be reported to a doctor promptly to begin appropriate treatment.

Can stress trigger a shingles outbreak?

Yes. Significant physical or psychological stress can temporarily suppress immune function, potentially triggering the reactivation of dormant VZV. Other factors that can provoke reactivation include illness, certain medications (immunosuppressants), advancing age, and conditions such as HIV or cancer that compromise the immune system. Maintaining a healthy lifestyle with balanced nutrition, regular exercise, adequate sleep, and effective stress management may help reduce the risk of reactivation.

Can you get shingles more than once?

Yes, although it is uncommon in immunocompetent individuals. Most people who recover from shingles develop renewed immunity that prevents recurrence for many years. However, immunocompromised patients are at higher risk of multiple episodes. The Shingrix vaccine can also be administered to people who have previously had shingles, to help prevent future recurrences.

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Sources and Bibliography

• National Institute on Aging (NIA). Shingles. Available from: https://www.nia.nih.gov/health/shingles
• Centers for Disease Control and Prevention (CDC). Shingles (Herpes Zoster). Available from: https://www.cdc.gov/shingles/index.html
• European Centre for Disease Prevention and Control (ECDC). Varicella and herpes zoster. Available from: https://www.ecdc.europa.eu
• Ministero della Salute Italiano. Piano Nazionale Prevenzione Vaccinale (PNPV) 2023–2025. Available from: https://www.salute.gov.it
• Schmader K. Herpes Zoster. Ann Intern Med. 2018;169(3):ITC19–ITC31. doi:10.7326/AITC201808070
• Cohen JI. Clinical practice: Herpes zoster. N Engl J Med. 2013;369(3):255–263. doi:10.1056/NEJMcp1302674
• Cunningham AL, et al. Efficacy of the Herpes Zoster Subunit Vaccine in Adults 70 Years of Age or Older. N Engl J Med. 2016;375:1019–1032. doi:10.1056/NEJMoa1603800
• Oxman MN, et al. A Vaccine to Prevent Herpes Zoster and Postherpetic Neuralgia in Older Adults. N Engl J Med. 2005;352:2271–2284
• BMC Infectious Diseases. Incidence of herpes zoster. Available from: https://bmcinfectdis.biomedcentral.com/articles/10.1186/s12879-022-07479-z
• PubMed. Exposure to varicella as immune booster. Available from: https://pubmed.ncbi.nlm.nih.gov/14267505/
• PubMed. Scarring after herpes zoster. Available from: https://pubmed.ncbi.nlm.nih.gov/10794584/