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Introduction: retroviruses, DNA viruses, and prions
Leigh Zerboni, Department of Pediatrics, Stanford University School of Medicine, Stanford, CA, USA,
Ann M. Arvin, Department of Pediatrics and Department of Microbiology & Immunology, Stanford University School of Medicine, Stanford, CA, USA
Varicella-zoster virus (VZV) is a neurotropic human herpesvirus that causes varicella, which is commonly known as chicken pox, as the primary infection in susceptible individuals. In the healthy host, varicella is usually a mild, self-limiting febrile illness characterized by a generalized, pruritic vesicular rash (Figure 12.1A). Like other alphaherpesviruses, VZV gains access to sensory ganglia of the peripheral nervous system during primary infection and establishes lifelong persistence at these sites. VZV reactivation from latency causes herpes zoster, called “shingles,” and is associated with a vesicular rash localized to one of the cutaneous dermatomes of the face, trunk, or extremities (Figure 12.1B). The dermatomal rash reflects the region of skin innervated by the cranial nerve or dorsal root ganglion where reactivation is occurring. VZV is highly contagious and is maintained in the human population by close contact with individuals who have varicella or herpes zoster. Both primary and recurrent VZV infections are more severe in immunocompromised patients because resolution requires an effective cell-mediated immune response. Antiviral drugs that inhibit VZV replication are effective in most high-risk patients with varicella or herpes zoster. VZV is the only human herpesvirus for which vaccines that prevent or modify the severity of primary and recurrent infections have been developed. These vaccines are made from the VZV/Oka strain, attenuated by passage in vitro.
While the clinical manifestations of varicella and herpes zoster are well-documented, knowledge about the mechanisms of VZV pathogenesis in the human host is limited because primary and recurrent infections are rarely fatal and VZV infection is highly species-specific for the human host.
VZV is a human alphaherpesvirus that causes varicella (chickenpox) as the primary infection and establishes latency in sensory ganglia. VZV reactivation results in herpes zoster (shingles). During the course of varicella and zoster, VZV infects differentiated human cells that exist within unique tissue microenvironments in humans. The tropism of VZV for skin is the most obvious clinical manifestation of VZV infection, producing the vesicular cutaneous lesions that are associated with varicella and zoster. The site of initial VZV infection in naïve hosts is thought to be mucosal epithelial cells of the upper respiratory tract. Entry is presumed to follow inoculation of the respiratory epithelium with infectious virus transmitted by aerosolized respiratory droplets or by contact with virus in varicella or zoster skin lesions (Arvin, 2001a; Grose, 1981). VZV in respiratory or conjunctival mucosal cells has the opportunity to interact with and infect local immune system cells and those in adjacent lymphoid tissues. Trafficking of infected peripheral blood mononuclear cells (PBMC), which appear to be predominantly T-cells, to the skin is thought to give rise to crops of cutaneous vesicles. Skin lesions contain VZV material associated with necrotic debris and, unlike virus grown in vitro, cell-free, infectious particles are detected in vesicular fluid (Williams et al., 1962). The life cycle of VZV is completed upon its transmission to a susceptible host from an individual with varicella, or it can be postponed for decades by establishing latency in neurons and transmitting to future generations during episodes of zoster.
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