Varicella zoster virus infection

Abstract

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 and herpes zoster vaccine development: lessons learned

“…It has a distinct seasonal pattern in temperate climates where the highest incidence occurs in winter and spring [5]. Before the introduction of varicella vaccine, almost universal infection with VZV occurred, with the annual incidence of varicella in many countries corresponding approximately to the birth cohort [20].…”

“…Before the introduction of varicella vaccine, almost universal infection with VZV occurred, with the annual incidence of varicella in many countries corresponding approximately to the birth cohort [20]. There are some geographic differences, for example, infection typically occurs in early childhood in temperate settings such as the USA where more than 90% of people are infected before the age of 15 years [5,21], in contrast to tropical countries where primary VZV infection may be more common among adolescents and adults [9]. …”

“…There remains debate about the extent to which VZV-specific antibody titers can predict protection against zoster, which is largely cell mediated [5]. Nevertheless, two-dose vaccination strategies (compared to the current single-dose regimen), with doses separated by up to 12 months, seem to show little promise; there is no difference between the VZV antibody responses 4 weeks after the first or second dose [111,112].…”

“…After transmission to a susceptible host, VZV proliferates in the oropharynx [5]. During an initial viremic phase, infected T cells transport the virus to skin and possibly other organs, although the lack of suitable animal models of infection limits understanding of the precise mechanisms of VZV pathogenesis [6].…”

Issues in the Treatment of Neurological Conditions Caused by Reactivation of Varicella Zoster Virus (VZV)

“…There is supportive evidence that such individuals should be given oral aciclovir, famciclovir, or valaciclovir for 7-10 days within 72 h of the onset, which reduces the severity and duration of the acute pain [11]. Antiviral therapy does not reduce the subsequent development of postherpetic neuralgia (PHN) [11][12][13]. If the patient is immunocompromised and/or has neurological complications, then IV aciclovir should be administered for 7-10 days [12].…”