Summary
Varicella-zoster virus, a herpesvirus, causes varicella (chickenpox) and, after endogenous reactivation, herpes zoster (shingles). Varicella, which is recognised by a characteristic vesicular rash, arises mainly in young children, although older individuals can be affected. In immunocompetent patients, symptoms are usually mild to moderate, but an uncomplicated severe case can have more than 1000 lesions and severe constitutional symptoms. Serious complications'including central nervous system involvement, pneumonia, secondary bacterial infections, and death'are sometimes seen. Varicella can be prevented by vaccination. Vaccine is about 80–85% effective against all disease and highly (more than 95%) effective in prevention of severe disease. In the USA, a routine childhood immunisation programme has reduced disease incidence, complications, hospital admissions, and deaths in children and in the general population, indicating strong herd immunity. Similar immunisation programmes have been adopted by some other countries, including Uruguay, Germany, Taiwan, Canada, and Australia, and are expected to be implemented more widely in future.
Varicella-zoster virus is the causal agent of varicella (chickenpox) and herpes zoster (shingles). 1–3 Varicella, the primary varicella-zoster virus infection, is predominantly a childhood disease in non-vaccinated populations. 4–9 It is characterised by a vesicular exanthem (figure 1 ), which is frequently accompanied by fever and malaise. Although varicella usually results in mild to moderate illness in immunocompetent patients, serious complications (such as central nervous system involvement, pneumonia, secondary bacterial infections, and death) can arise. 10–15 Varicella is highly infectious, with attack rates in susceptible contacts ranging from 61% to 100%. 4,16–18 The disease occurs worldwide and is endemic in most populations. The disease causes a sizeable societal burden for patients and their caregivers, and can necessitate school absenteeism and work loss. 19–22
After primary infection, the virus persists in sensory nerve ganglia of the dorsal root and establishes latent infection in neuronal cells. 23 The virus can reactivate years or decades later and spread unilaterally along a dermatome to cause herpes zoster (shingles), a painful, localised vesicular rash. 24–26 Varicella can be prevented by vaccination. A new vaccine to prevent or modify herpes zoster and its complications in adults aged 60 years or older was licensed in the USA in 2006. 27,28 In this Seminar, we focus on primary varicella infection.