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INTRODUCTION

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Varicella-zoster virus (VZV) is 1 of the 9 human herpesviruses, which include herpes simplex virus (HSV) types 1 and 2, cytomegalovirus, Epstein-Barr virus, and human herpesviruses 6A, 6B, 7, and 8. As with HSV-1 and HSV-2, VZV establishes latency in sensory or autonomic ganglia following primary infection, with the ability for subsequent reactivation. The primary acquisition of VZV results in the clinical disease varicella (chickenpox) with reactivation from latency resulting in zoster (shingles). Live-attenuated varicella vaccine was licensed in the United States in 1995 and, over the past 20 years, has substantially altered the epidemiology of the disease in this country, with rates of varicella and its complications plummeting.

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PATHOGENESIS AND EPIDEMIOLOGY

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Humans are the only source of infection of VZV. Transmission occurs when aerosolized virus from skin lesions comes into contact with the mucosa of the upper respiratory tract or conjunctivae of susceptible persons. Although it was long thought that the source of infection was the respiratory tract of infected individuals, very limited virus has been recovered from an infected person’s airways and probably represents a much more limited source of infection than aerosolization from skin lesions.

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The infectious period extends from up to 48 hours before the appearance of rash until all skin lesions are crusted over, usually about 5 days in normal hosts. Following infectious contact, the incubation period for varicella is 10 to 21 days and up to 28 days following a dose of varicella-zoster immunoglobin (VariZIG).

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Infection of cells within the respiratory tract or conjunctivae by inhaled virions is followed by cell-associated spread to local lymph nodes, viremia, and then the development of the vesicular rash approximately 5 days later. Virus can be detected in circulating lymphocytes and monocytes. Cell-to-cell spread of virus within the skin creates infected syncytia with a striking disruption of normal cellular architecture, and VZV-infected keratinocytes appear to elicit a vigorous type I interferon response in neighboring, uninfected cells that restrains horizontal spread of virus and thus may contribute to the topology of the rash.

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In the immunocompetent host, VZV viremia and the appearance of new skin lesions are curtailed within a few days by a vigorous cellular immune response comprising both natural killer (NK) and antigen-specific (T-cell) components. Conversely, the failure to mount antigen-specific cellular responses is associated with progressive viral replication and dissemination and a potentially fatal outcome.

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Individuals with disorders purely of humoral immunity do not suffer unusually severe or repeated episodes of varicella, indicating that cellular immunity affords sufficient protection against primary infection. However, a host humoral response is detectable within 4 days of the onset of the rash and can confer passive immunity; thus, pooled immunoglobulin derived from VZV-immune donors, known as VariZIG, can be used to protect VZV-exposed subjects at high risk of severe varicella. The presence of VZV-specific antibodies is also the best available correlate of protection ...

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