Varicella zoster virus
Herpesvirus causing chickenpox and shingles in humans.
Varicella zoster virus (VZV), also called human herpesvirus 3, is one of nine herpes viruses that can infect people. It causes chickenpox, which mostly affects children and young adults, and later can cause shingles in adults (rarely in children). A rare late complication is Ramsay Hunt syndrome type 2. The virus only infects humans and can survive outside the body for a few hours.
VZV multiplies in the tonsils and produces a range of symptoms. After the initial chickenpox infection, the virus goes dormant in nerve cells, including those in the cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Years later, it can reactivate and cause shingles.
Chickenpox appears after an incubation period of 10 to 21 days (average 14 days). The virus enters through the respiratory system and targets the skin and peripheral nerves. Illness lasts about three to four days, and people are most contagious one to two days before the rash appears. Symptoms include pus-filled blisters that burst, scab, and heal, often on the face, throat, lower back, chest, and shoulders. Complications can include encephalitis, pneumonia (viral or bacterial), and bronchitis (viral or bacterial). Even after symptoms clear, the virus stays dormant in the trigeminal and dorsal root ganglia.
Shingles occurs when VZV reactivates, which happens in about one-third of cases. The lifetime risk of developing shingles is 20 to 30 percent (roughly one in four people), but for those aged 85 and older, the risk rises to one in two. A 2015 Swedish study estimated 315 cases per 100,000 people per year overall, and 577 per 100,000 for those 50 and older. VZV can also infect the central nervous system; a 2013 Swiss study reported 1.02 such infections per 100,000 people between 2003 and 2010. Shingles lesions and burning nerve pain usually appear on one side of the body, along one or two adjacent sensory nerves. Skin lesions heal over weeks, but pain often lasts longer. In 10 to 15 percent of cases, pain persists beyond three months, a condition called postherpetic neuralgia. Other serious complications include Mollaret's meningitis, zoster multiplex, brain artery inflammation leading to stroke, myelitis, herpes zoster ophthalmicus, and zoster sine herpete. In Ramsay Hunt syndrome type II, the virus affects the geniculate ganglion, causing painful blisters on the tongue and ear, along with one-sided facial weakness and hearing loss. Infection early in pregnancy can severely harm the fetus. Reye's syndrome, which causes continuous vomiting and brain dysfunction (drowsiness or aggression), can occur after initial infection, mostly in children and teenagers; using aspirin during infection raises this risk, and it can lead to coma or death.
The virus is closely related to herpes simplex viruses (HSV) and shares much of its genome. Its envelope glycoproteins (gB, gC, gE, gH, gI, gK, gL) match those in HSV, but VZV lacks an equivalent of HSV's gD protein and does not produce latency-associated transcripts (LAT). VZV virions are spherical, 180 to 200 nanometers in diameter, with a lipid envelope enclosing a 100-nanometer nucleocapsid made of 162 capsomeres arranged in an icosahedral shape. Its DNA is a single, linear, double-stranded molecule about 125,000 nucleotides long. The capsid is surrounded by a tegument of loosely associated proteins that help start virus reproduction, and the tegument is covered by a lipid envelope studded with glycoproteins about 8 nanometers long.
The genome was first sequenced in 1986. It is a linear duplex DNA molecule; a laboratory strain has 124,884 base pairs. The genome has two main isomers (P and IS) depending on the orientation of the S segment, each equally common, together making up 90 to 95 percent of molecules. The L segment can also invert, producing four linear isomers total. This distribution differs from HSV's equal probabilities, and the reason is unknown. A small number of molecules are circular, though little is known about them (HSV circularizes upon infection). There are at least 70 open reading frames.
VZV shares a common ancestor with HSV1 and HSV2; five of its roughly 70 genes have no HSV counterpart. It is less closely related to other human herpes viruses, but many homologous genes and conserved gene blocks exist. At least five clades of the virus have been identified.
- field
- Virology
- known_for
- Causing chickenpox and shingles
- incubation_period
- 10–21 days (average 14 days)
Lore & Background
Varicella zoster virus (VZV) virions are spherical, measuring 180–200 nanometers in diameter. A lipid envelope, studded with glycoprotein spikes about 8 nanometers long, encloses a 100-nanometer nucleocapsid composed of 162 capsomeres arranged in an icosahedral shape. Within the capsid lies a single, linear, double-stranded DNA molecule approximately 125,000 nucleotides long. Between the capsid and envelope lies the tegument, a layer of loosely associated proteins critical for initiating viral reproduction in infected cells. The virus is species-specific to humans and can survive in external environments for only a few hours. VZV multiplies in the tonsils and enters the body through the respiratory system, with an incubation period of 10–21 days. Primary infection causes chickenpox, targeting the skin and peripheral nerves; lesions most commonly appear on the face, throat, lower back, chest, and shoulders. After recovery, the virus remains dormant in neurons of the cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Reactivation later in life produces shingles, with lesions and burning neuropathic pain typically occurring on one side of the body along one or two adjacent sensory nerves. The individual lifetime risk of shingles is 20–30%, rising to 1 in 2 for those aged 85 and over. The genome, first sequenced in 1986, is a linear duplex DNA molecule; a laboratory strain contains 124,884 base pairs. It has at least 70 open reading frames and exists in two predominant isomers, with a small percentage of circular genomes also observed. VZV is closely related to herpes simplex viruses, sharing much genome homology, though it lacks an equivalent of the HSV gD protein and does not produce latency-associated transcripts.
Reader's Guide
Varicella zoster virus is significant as the causative agent of two common diseases: chickenpox, a highly contagious childhood illness, and shingles, a painful reactivation in older adults. Its ability to establish lifelong latency in neurons and reactivate decades later distinguishes it from many pathogens. After primary infection, the virus multiplies in the tonsils and then lies dormant in cranial, dorsal root, and autonomic ganglia. In about one-third of cases, it reactivates later in life as shingles, with lesions and burning neuropathic pain typically confined to one side of the body. Serious complications include postherpetic neuralgia, which persists beyond three months in 10–15% of cases, as well as encephalitis, pneumonia, bronchitis, Mollaret's meningitis, stroke from arterial inflammation, myelitis, and Ramsay Hunt syndrome type II, which affects the geniculate ganglion causing facial weakness and hearing loss. Infection during early pregnancy can severely injure the fetus, and Reye's syndrome, marked by vomiting and brain dysfunction, may occur in children and teenagers, especially if aspirin is used. The virus is species-specific to humans and can survive only a few hours outside the body. Morphologically, VZV is a spherical virion 180–200 nm in diameter, with a lipid envelope enclosing a 100 nm icosahedral nucleocapsid and a linear double-stranded DNA genome of about 125,000 nucleotides. Its genome, first sequenced in 1986, contains at least 70 open reading frames and exists in four linear isomers, distinct from the equiprobable distribution seen in herpes simplex virus. VZV is closely related to herpes simplex viruses, sharing much genome homology and many envelope glycoproteins, though it lacks the HSV gD protein and does not produce latency-associated transcripts. At least five clades of the virus have been identified, and its common ancestry with HSV1 and HSV2 is evident, though five of its genes have no counterpart in those viruses.
Did You Know?
- VZV can survive in external environments for a few hours.
- The virus lies dormant in neurons after chickenpox and can reactivate to cause shingles in about one-third of cases.
- Ramsay Hunt syndrome type II involves VZV affecting the geniculate ganglion, causing painful blisters on the tongue and ear with facial weakness and hearing loss.
- The VZV genome has two predominant isomers (P and IS) present with equal frequency, totaling 90–95% of genomes.
Frequently Asked Questions
Who is Varicella zoster virus?
VZV, also called human herpesvirus 3, is a species-specific pathogen that exclusively infects humans. It is one of the nine recognized human herpesviruses and sits squarely in the virology canon.
What are Varicella zoster virus's powers or role?
VZV produces two very different clinical episodes: chickenpox (varicella) during primary infection and shingles (herpes zoster) when it reactivates later in life, most often in adults. In rare late-stage cases it can also trigger Ramsay Hunt syndrome type 2.
How does Varicella zoster virus's story end?
It never truly leaves the body; after the initial rash resolves, the virus settles into a lifelong latent state within sensory nerve ganglia. Decades later it may reactivate as shingles, but the pathogen persists indefinitely in the host.
Why is Varicella zoster virus important to the canon?
Because it touches virtually every unvaccinated person at some point—first as a childhood illness and later as a painful adult reactivation—it remains a central figure in both pediatric and geriatric medicine. Its dual-phase lifecycle and rare neurological complications make it a persistent clinical challenge.
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