Varicella zoster virus
Virus causing chickenpox and shingles in humans.
Varicella zoster virus, or human herpesvirus 3, is one of nine herpes viruses known to infect people. It is responsible for two distinct illnesses: chickenpox, which typically strikes children and young adults, and shingles, which mostly occurs in adults and only rarely in children. In uncommon instances, a late complication called Ramsay Hunt syndrome type 2 can develop. The virus only infects humans and can survive for a few hours outside the body.
Once inhaled, the virus multiplies in the tonsils and spreads. After the initial chickenpox infection clears, VZV goes dormant inside nerve cells, including those in the cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Years or decades later, it can reactivate, causing shingles.
Chickenpox has an incubation period of 10 to 21 days, averaging 14 days. The illness itself lasts about three to four days, targeting the skin and peripheral nerves. People are most contagious one to two days before the characteristic blisters appear. These lesions fill with pus, rupture, and scab over, commonly showing up on the face, throat, lower back, chest, and shoulders. Complications can include encephalitis, pneumonia, or bronchitis—either from the virus itself or from secondary bacterial infections.
Shingles occurs when the virus reactivates, which happens in about one-third of infected people. The lifetime risk of developing shingles is estimated at 20 to 30 percent, or roughly one in four people. For those 85 and older, the risk rises to one in two. A 2015 Swedish study found an annual incidence of 315 cases per 100,000 people overall, and 577 per 100,000 among those 50 and older. The virus can also infect the central nervous system; a Swiss hospital study from 2003 to 2010 reported 1.02 such infections per 100,000 people annually. Shingles lesions and the associated burning nerve pain usually appear on one side of the body, following one or two adjacent sensory nerves. The skin heals over several weeks, but pain often lingers. In 10 to 15 percent of cases, pain lasts more than three months—a chronic condition called postherpetic neuralgia. Other serious complications include Mollaret's meningitis, zoster multiplex, stroke from inflamed brain arteries, myelitis, herpes zoster ophthalmicus, and zoster sine herpete.
- Field
- Virology
- Known for
- Causing chickenpox and shingles
- Genome size
- 124,884 base pairs (laboratory strain)
- Virion diameter
- 180–200 nm
- Incubation period
- 10–21 days
Lore & Background
Varicella zoster virus multiplies in the tonsils and causes a wide variety of symptoms. After primary infection (chickenpox), the virus lies dormant in neurons, including cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Many years after recovery, VZV can reactivate to cause shingles. The virus enters through the respiratory system and has an incubation period of 10–21 days, with an average of 14 days. Infected individuals are most contagious 1–2 days before lesions appear. Lesions most commonly occur on the face, throat, lower back, chest, and shoulders.
In about a third of cases, VZV reactivates in later life, producing shingles. The individual lifetime risk of developing herpes zoster is thought to be between 20% and 30%. For people aged 85 and over, this risk increases to 1 in 2. Shingles lesions and associated neuropathic pain tend to occur on skin innervated by one or two adjacent sensory nerves, almost always on one side of the body. In 10–15% of cases, pain persists more than three months, a condition known as postherpetic neuralgia. Other serious complications include Mollaret's meningitis, stroke, myelitis, and Ramsay Hunt syndrome type II.
Reader's Guide
Varicella zoster virus is significant as the causative agent of two distinct diseases: chickenpox, a common childhood illness, and shingles, a painful reactivation in older adults. Its ability to establish lifelong latency in neurons and reactivate decades later makes it a unique pathogen. The development of a live attenuated vaccine (Oka/Merck strain) in the 1980s, approved in the United States in 1995, has dramatically reduced chickenpox incidence and its complications. VZV is also notable for its genomic structure—a linear double-stranded DNA molecule of about 125,000 base pairs—and its close relation to herpes simplex viruses, though it lacks the HSV gD protein and latency-associated transcripts. Epidemiological studies show genotype distribution varies by region, with European strains (E1, E2) predominating in Europe and Australia. The virus's species-specificity to humans and its ability to cause severe complications in immunocompromised individuals and during pregnancy underscore its medical importance. Treatment options include acyclovir, famciclovir, and valaciclovir, though intravenous administration of acyclovir is often required for effective serum concentration.
Did You Know?
- VZV can survive in external environments for a few hours.
- Ramsay Hunt syndrome type 2 may develop as a late complication of VZV infection.
- The genome was first sequenced in 1986.
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