Infection with varicella zoster virus (VZV) causes varicella (chickenpox), which can be severe in immunocompromised individuals, infants and adults. Primary infection is followed by latency in ganglionic neurons. During this period, no virus particles are produced and no obvious neuronal damage occurs. Reactivation of the virus leads to virus replication, which causes zoster (shingles) in tissues innervated by the involved neurons, inflammation and cell death — a process that can lead to persistent radicular pain (postherpetic neuralgia). The pathogenesis of postherpetic neuralgia is unknown and it is difficult to treat. Furthermore, other zoster complications can develop, including myelitis, cranial nerve palsies, meningitis, stroke (vasculopathy), retinitis, and gastroenterological infections such as ulcers, pancreatitis and hepatitis. VZV is the only human herpesvirus for which highly effective vaccines are available. After varicella or vaccination, both wild-type and vaccine-type VZV establish latency, and long-term immunity to varicella develops. However, immunity does not protect against reactivation. Thus, two vaccines are used: one to prevent varicella and one to prevent zoster. In this Primer we discuss the pathogenesis, diagnosis, treatment, and prevention of VZV infections, with an emphasis on the molecular events that regulate these diseases. For an illustrated summary of this Primer, visit: http://go.nature.com/14×VI1
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.
Despite a high coverage rate with two doses of mumps-containing vaccine, a large mumps outbreak occurred, characterized by two-dose vaccine failure, particularly among midwestern college-age adults who probably received the second dose as schoolchildren. A more effective mumps vaccine or changes in vaccine policy may be needed to avert future outbreaks and achieve the elimination of mumps.
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