Investigation of antiviral activity of 1-β-d-arabinofuranosylthymine (ara-T) and 1-β-d-arabinofuranosyl-E-5-(2-bromovinyl)uracil (BV-ara-U) in monkeys infected with simian varicella virus

Soike, Kenneth F.; Baskin, Gary B.; Cantrell, C; Gerone, Peter J.

doi:10.1016/0166-3542(84)90030-5

Cited by 33 publications

(11 citation statements)

References 21 publications

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“…SVV has been isolated during natural outbreaks in African green and Patas monkeys (Soike et al 1984a). Clinical, pathological, immunological, and virological features of SVV infection in monkeys resemble those of human VZV infection (Wenner et al 1977; Felsenfeld and Schmidt 1977, 1979; Padovan and Cantrell 1986; Myers and Connelly 1992; Dueland et al 1992).…”

Section: Simian Varicella Virusmentioning

confidence: 99%

“…During primary SVV infection, infectious virus can be recovered at the peak of viremia from blood mononuclear cells (MNCs; Clarkson et al 1967; Wolf et al 1974; Soike et al 1984a). SVV-induced rash is often hemorrhagic and disseminated (Soike 1992).…”

Section: Simian Varicella Virusmentioning

confidence: 99%

“…Unlike VZV reactivation in humans, zoster in primates often appears as a whole-body rash lasting less than 1 week, albeit obscured by fur. Although neither VZV nor SVV can be isolated from blood in otherwise healthy immunocompetent seropositive humans or primates, SVV has been isolated from skin vesicles after reactivation (Soike et al 1984a) and also during primary infection and reactivation in the same monkey (Gray and Gusick 1996). …”

Section: Simian Varicella Virusmentioning

confidence: 99%

“…At the peak of rash, SVV produces hepatitis and pneumonia. Resolution of rash correlates with the detection of virus-specific antibody by 12 dpi (Wenner et al 1977; Iltis et al 1982; Soike et al 1984a; Dueland et al 1992; Gray et al 1998; Gray 2003). During acute infection, virus antigens and nucleic acids have been found in multiple organs, including lung, liver, spleen, adrenal gland, kidney, lymph node, bone marrow, and in ganglia at all levels of the neuraxis (Wenner et al 1977; Roberts et al 1984; Padovan and Cantrell 1986; Dueland et al 1992; Gray et al 2002).…”

Section: Experimental Svv Infectionmentioning

confidence: 99%

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Simian Varicella Virus Pathogenesis

Mahalingam

Messaoudi

Gilden

2010

Current Topics in Microbiology and Immunology

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Because varicella zoster virus (VZV) is an exclusively human pathogen, the development of an animal model is necessary to study pathogenesis, latency, and reactivation. The pathological, virological, and immunological features of simian varicella virus (SVV) infection in nonhuman primates are similar to those of VZV infection in humans. Both natural infection of cynomolgus and African green monkeys as well as intrabronchial inoculation of rhesus macaques with SVV provide the most useful models to study viral and immunological aspects of latency and the host immune response. Experimental immunosuppression of monkeys latently infected with SVV results in zoster, thus providing a new model system to study how the loss of adaptive immunity modulates virus reactivation.

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Section: Simian Varicella Virusmentioning

confidence: 99%

Section: Simian Varicella Virusmentioning

confidence: 99%

Section: Simian Varicella Virusmentioning

confidence: 99%

Section: Experimental Svv Infectionmentioning

confidence: 99%

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Simian Varicella Virus Pathogenesis

Mahalingam

Messaoudi

Gilden

2010

Current Topics in Microbiology and Immunology

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“…Like human chickenpox, varicella in primates is preceded by an incubation period of one-to-two weeks, followed by fever and a papulovesicular rash of skin and mucous membranes (103). Primary SVV infection produces viremia, and infectious virus can be recovered from blood MNCs (104)(105)(106)(107). Disseminated SVV infection is frequent in monkeys after intratracheal inoculation.…”

Section: Simian Varicella Virus (Svv)mentioning

confidence: 99%

Varicella zoster virus latency, neurological disease and experimental models: an update

Randall¹

2004

Front Biosci

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Varicella zoster virus (VZV), a ubiquitous neurotropic human herpesvirus, causes chickenpox (varicella) and then remains latent for decades in cranial nerve, dorsal root and autonomic nervous system ganglia along the entire neuraxis. Virus reactivation, most often after age 60, produces shingles (zoster), characterized by pain and rash usually restricted to 1-3 dermatomes. In elderly individuals, zoster is frequently complicated by postherpetic neuralgia (PHN), pain that persists for months to years after the resolution of rash. Virus may also spread beyond ganglia to the spinal cord to cause myelitis, as well as to blood vessels of the brain, producing a unifocal or multifocal vasculopathy. The increased incidence of zoster in the elderly and immunocompromised individuals appears to be due to a VZV-specific host immunodeficiency. Recent studies indicate that PHN may be due to a chronic active VZV ganglionitis, and that VZV vasculopathy is caused by a productive virus infection in cerebral arteries. Since neurological disease produced by VZV is due to reactivation from ganglia, the physical state of viral nucleic acid and expression during latency as well as the possible mechanisms by which VZV latency is maintained and reactivates are discussed. Finally, VZV is an exclusively human herpesvirus, and experimental infection of animals with VZV does not produce disease nor does VZV reactivate from ganglia. Two varicella models in primates have proven useful: one that mimics varicella latency in humans, and one that can be used to study the efficacy of antiviral agent in driving varicella virus back to a latent state.

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Varicelloviruses

2009

Simian Virology

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Investigation of antiviral activity of 1-β-d-arabinofuranosylthymine (ara-T) and 1-β-d-arabinofuranosyl-E-5-(2-bromovinyl)uracil (BV-ara-U) in monkeys infected with simian varicella virus

Cited by 33 publications

References 21 publications

Simian Varicella Virus Pathogenesis

Simian Varicella Virus Pathogenesis

Varicella zoster virus latency, neurological disease and experimental models: an update

Varicelloviruses

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