Chapter 51
Varicella Zoster Virus Infections
Manuraj Singh, Judith Breuer,
Judith Breuer
Great Ormond Street Hospital, UCL Division of Infection and Immunity, London, UK
Search for more papers by this authorManuraj Singh, Judith Breuer,
Judith Breuer
Great Ormond Street Hospital, UCL Division of Infection and Immunity, London, UK
Search for more papers by this authorBook Editor(s):Peter Hoeger,
Veronica Kinsler,
Albert Yan,
John Harper,
Arnold Oranje,
Christine Bodemer,
Margarita Larralde,
David Luk, Vibhu Mendiratta,
Diana Purvis,
Peter Hoeger
Search for more papers by this authorVeronica Kinsler
Search for more papers by this authorAlbert Yan
Search for more papers by this authorJohn Harper
Search for more papers by this authorArnold Oranje
Search for more papers by this authorChristine Bodemer
Search for more papers by this authorMargarita Larralde
Search for more papers by this authorVibhu Mendiratta
Search for more papers by this authorDiana Purvis
Search for more papers by this authorFirst published: 20 November 2019
Summary
Varicella zoster virus (VZV) is characterized by its tropism for epithelial tissue and persistence following primary infection in neuronal tissue. Primary infection with VZV causes varicella (chickenpox), a common childhood infection manifesting as a vesicular rash on the face and trunk. Following primary infection the virus infects sensory nerve endings to establish latency in dorsal root or cranial nerve ganglia. Reactivation of the virus causes a painful unilateral dermatomal rash known as herpes zoster or ‘shingles’. Epithelial replication is central to the natural history of VZV infection. Following reactivation, VZV initially infects the richly innervated isthmus of the hair follicle. Further spread in skin is dependent on replication within differentiating keratinocytes. Knowledge of the pathogenesis of VZV infections and latency has improved with in vitro models and xenograft studies in the severe combined immunodeficiency (SCID) mouse model. However, the exact mechanisms responsible for latency and reactivation currently remain unresolved. Therapy for VZV infections, such as aciclovir, is not indicated in uncomplicated infections in childhood but can be lifesaving in patients with significant immunosuppression. The development of effective live attenuated vaccines has been successful in reducing the incidence and complications of VZV. However, the vaccine is not currently recommended for widespread use in the childhood immunization programme within the UK.
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