Naturally Acquired Simian Varicella Virus Infection in African Green Monkeys

Mahalingam, Ravi; Traina‐Dorge, Vicki; Wellish, Mary; Smith, J. E.; Gilden, Donald H.

doi:10.1128/jvi.76.17.8548-8550.2002

Cited by 35 publications

(35 citation statements)

References 14 publications

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“…The authors developed a model of natural SVV infection in monkeys by exposing SVV-seronegative monkeys to other monkeys that had been inoculated intratracheally with SVV [181]. These naturally infected monkeys harbor latent SVV DNA in ganglionic neurons [182] at multiple levels of the neuraxis [181], and both clinical and subclinical reactivation of SVV were induced by immunosuppression and stress [183].…”

Section: Animal Models Of Varicella Zoster Virus Infectionmentioning

confidence: 99%

“…These naturally infected monkeys harbor latent SVV DNA in ganglionic neurons [182] at multiple levels of the neuraxis [181], and both clinical and subclinical reactivation of SVV were induced by immunosuppression and stress [183]. Subclinical reactivation of latent SVV also occurs after irradiation in rhesus monkeys [184].…”

Section: Animal Models Of Varicella Zoster Virus Infectionmentioning

confidence: 99%

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Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis of Disease, and Latency

et al. 2008

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Varicella zoster virus (VZV) is an exclusively human neurotropic alpha-herpesvirus. Primary infection causes varicella (chickenpox), after which virus becomes latent in cranial nerve ganglia, dorsal root ganglia, and autonomic ganglia along the entire neuraxis. Years later, in association with a decline in cell-mediated immunity in elderly and immunocompromised individuals, VZV reactivates and causes a wide range of neurologic disease, including herpes zoster, postherpetic neuralgia, vasculopathy, myelopathy, retinal necrosis, cerebellitis and zoster sine herpete (Fig. 1). Importantly, many of these complications occur without rash. This article discusses the clinical manifestations, treatment, and prevention of VZV infection and reactivation; pathogenesis of VZV infection; and current research focusing on VZV latency, reactivation, and animal models. Clinical manifestations of primary varicella zoster virus infection VaricellaInitial infection with VZV results in chickenpox (varicella), which is typically seen in children 1 to 9 years of age [1]. Primary infection in adults is usually more severe and may be accompanied by interstitial pneumonia. Infection in immunocompromised individuals often causes severe, disseminated disease. Climate seems to affect the epidemiology of varicella. In most temperate climates, more than 90% of people are infected before adolescence [2-5] with an incidence of 13 to 16 cases per 1000 people per year [6][7][8]. In tropical climates, VZV infection occurs later in life and adults are more susceptible than children [9][10][11]. Varicella has a peak incidence in the late winter and spring [10,[12][13][14], and epidemics tend to occur every 2 to 5 years [12][13][14].Varicella is characterized by fever concurrent with a self-limiting rash on the skin and sometimes mucosa. Headache, malaise, and loss of appetite are also seen. The rash begins as macules, rapidly progresses to papules, followed by a vesicular stage and crusting of lesions. Crusts slough off after 1 to 2 weeks. VZV is highly infectious and transmission occurs by direct contact with skin lesions or by respiratory aerosols from infected individuals. Central nervous system complications include self-limiting cerebellar ataxia in 1 in 4000 cases [15], meningitis, meningoencephalitis, and vasculopathy [16]. Strokes may occur months after varicella

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Section: Animal Models Of Varicella Zoster Virus Infectionmentioning

confidence: 99%

Section: Animal Models Of Varicella Zoster Virus Infectionmentioning

confidence: 99%

Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis of Disease, and Latency

et al. 2008

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“…Hemorrhagic necrosis, inflammation and eosinophilic intranuclear inclusions are detected in skin and visceral tissues [147]. SVV establishes latent infection in neurons of multiple ganglia [148] and reactivates under stress to cause zoster [145]. VZV and SVV glycoproteins share immunologic cross-reactivity as demonstrated by the protection of SVV-infected monkeys after VZV immunization [149].…”

Section: Development Of Animal Modelsmentioning

confidence: 99%

“…SVV-seronegative monkeys are exposed to other monkeys previously inoculated intratracheally with SVV [148]. Ten to 14 days later, monkeys exposed to intratracheally inoculated monkeys develop a mild rash, and detection of SVV DNA in skin scrapings of naturally infected monkeys confirms that SVV causes the rash.…”

Section: Development Of Animal Modelsmentioning

confidence: 99%

Clinical and Molecular Aspects of Varicella Zoster Virus Infection

et al. 2008

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SummaryA declining cell-mediated immunity to varicella zoster virus (VZV) with advancing age or immunosuppression results in virus reactivation from latently infected human ganglia anywhere along the neuraxis. Virus reactivation produces zoster, often followed by chronic pain (postherpetic neuralgia or PHN) as well as vasculopathy, myelopathy, retinal necrosis and cerebellitis. VZV reactivation also produces pain without rash (zoster sine herpete). Vaccination after age 60 reduces the incidence of shingles by 51%, PHN by 66% and the burden of illness by 61%. However, even if every healthy adult over age 60 years is vaccinated, there would still be about 500,000 zoster cases annually in the United States alone, about 200,000 of whom will experience PHN. Analyses of viral nucleic acid and gene expression in latently infected human ganglia and in an animal model of varicella latency in primates are serving to determine the mechanism(s) of VZV reactivation with the aim of preventing reactivation and the clinical sequelae.

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“…A naturally transmitted infection of SVV has been shown to result in a scenario in which viral DNA is detectable only in the ganglia after 2 months [14]. We recently showed that in such naturally infected monkeys, latent virus was located exclusively in neurons in the spinal ganglia [15].…”

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confidence: 98%

The pattern of viral persistence in monkeys intra-tracheally infected with Simian varicella virus

Grinfeld

Kennedy

2007

Virus Genes

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In situ PCR (ISPCR) and in situ hybridisation (ISH) was performed on 32 tissues from 10 monkeys, intra-tracheally (IT) infected with simian varicella virus (SVV) and 5 tissues from 3 uninfected control animals. The results showed persistence of SVV DNA up to 2 years post-infection (pi) and the localisation of SVV to be confined to neurons except at time points 9 and 10 months pi where SVV positive satellite cells were also detected. There was no evidence for transcription of SVV ORFs 63 and 21 in the ganglia of the one IT infected and 2 naturally infected monkeys investigated using RNA ISH.

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Naturally Acquired Simian Varicella Virus Infection in African Green Monkeys

Cited by 35 publications

References 14 publications

Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis of Disease, and Latency

Varicella Zoster Virus Infection: Clinical Features, Molecular Pathogenesis of Disease, and Latency

Clinical and Molecular Aspects of Varicella Zoster Virus Infection

The pattern of viral persistence in monkeys intra-tracheally infected with Simian varicella virus

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