Varicella zoster virus (VZV), also known as human herpesvirus 3 (HHV-3, HHV3), is one of nine known herpes viruses that can infect humans. It causes chickenpox (varicella), commonly affecting children and young adults, and shingles (herpes zoster) in adults but rarely in children. As a late complication of VZV infection, Ramsay Hunt syndrome type 2 may develop in rare cases. VZV infections are species-specific to humans. The virus can survive in external environments for a few hours. VZV multiplies in the tonsils, and causes a wide variety of symptoms. Similar to the herpes simplex viruses, after primary infection with VZV (chickenpox), the virus lies dormant in neurons, including the cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia. Many years after the person has recovered from initial chickenpox infection, VZV can reactivate to cause shingles.
Epidemiology
Chickenpox
Primary varicella zoster virus infection results in chickenpox (varicella), which may result in complications including encephalitis, pneumonia (either direct viral pneumonia or secondary bacterial pneumonia), or bronchitis (either viral bronchitis or secondary bacterial bronchitis). Even when clinical symptoms of chickenpox have resolved, VZV remains dormant in the nervous system of the infected person (virus latency), in the trigeminal and dorsal root ganglia. VZV enters through the respiratory system and has an incubation period of 10–21 days, with an average of 14 days. Targeting the skin and peripheral nerves, the period of illness lasts about 3 to 4 days. Infected individuals are most contagious 1–2 days before the lesions appear. Signs and symptoms include vesicles that fill with pus, rupture, and scab before healing. Lesions most commonly occur on the face, throat, the lower back, the chest, and the shoulders.
Shingles In about a third of cases, VZV reactivates in later life, producing a disease known as shingles or herpes zoster. The individual lifetime risk of developing herpes zoster is thought to be between 20% and 30%, or approximately 1 in 4 people. However, for people aged 85 and over, this risk increases to 1 in 2. In a 2015 study in Sweden by Nilsson, Cassel, and Lindquist, the annual incidence of herpes zoster was estimated at 315 cases per 100,000 inhabitants across all ages and 577 cases per 100,000 among people 50 years of age or older. VZV can also infect the central nervous system (CNS), with a 2013 article in the International Journal of Infectious Diseases reporting an incidence of 1.02 CNS infections per 100,000 between January 2003 and July 2010 at a hospital in Switzerland. Shingles lesions and the associated neuropathic pain, often described as burning, tend to occur on the skin that is innervated by one or two adjacent sensory nerves, almost always on one side of the body only. The skin lesions usually subside over the course of several weeks, while the pain often persists longer. In 10–15% of cases, the pain persists more than three months, a chronic and often disabling condition known as postherpetic neuralgia. Other serious complications of varicella zoster infection include Mollaret's meningitis, zoster multiplex, inflammation of arteries in the brain leading to stroke, myelitis, herpes zoster ophthalmicus, or zoster sine herpete. In Ramsay Hunt syndrome type II, VZV affects the geniculate ganglion, leaving lesions that follow specific branches of the facial nerve. Symptoms may include painful blisters on the tongue and ear, along with one-sided facial weakness and hearing loss. After infection during the initial stages of pregnancy, the fetus can be severely injured. Reye's syndrome can happen after initial infection, causing continuous vomiting and signs of brain dysfunction such as extreme drowsiness or combative behavior. In some cases, death or coma can follow. Reye's syndrome mostly affects children and teenagers; using aspirin during infection can increase this risk.
Morphology VZV is closely related to the herpes simplex viruses (HSV), sharing much genome homology. The known envelope glycoproteins (gB, gC, gE, gH, gI, gK, gL) correspond with those in HSV; however, there is no equivalent of the HSV gD protein. VZV also fails to produce the LAT (latency-associated transcripts) that play an important role in establishing HSV latency (herpes simplex virus). VZV virions are spherical and 180–200 nm in diameter. Their lipid envelope encloses the 100 nm nucleocapsid of 162 hexameric and pentameric capsomeres arranged in an icosahedral form. Its DNA is a single, linear, double-stranded molecule, 125,000 nt long. The capsid is surrounded by loosely associated proteins known collectively as the tegument; many of these proteins play critical roles in initiating the process of virus reproduction in the infected cell. The tegument is in turn covered by a lipid envelope studded with glycoproteins that are displayed on the exterior of the virion, each approximately 8 nm long.
Genomes
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 predominant isomers, depending on the orientation of the S segment, P (prototype) and IS (inverted S) which are present with equal frequency for a total frequency of 90–95%. The L segment can also be inverted resulting in a total of four linear isomers (IL and ILS). This is distinct from HSV's equiprobable distribution, and the discriminatory mechanism is not known. A small percentage of isolated molecules are circular genomes, about which little is known. (It is known that HSV circularizes on infection.) There are at least 70 open reading frames in the genome.
Evolution
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