Experimental infection and immune response of guinea pigs with varicella-zoster virus

Y, Matsunaga; Yamanishi, Koichi; Takahashi, Michiaki

doi:10.1128/iai.37.2.407-412.1982

Cited by 58 publications

(20 citation statements)

References 10 publications

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“…Antibody responses to VZV were also observed in guinea pigs. In this species antibody titers were found only after inoculation of the attenuated OKA strain but not after inoculation of the nonattenuated OKA or other wild VZV strains [Matsumaga et al, 1982;Yamanishi et al, 19801. It is likely that the immunogenicity of the attenuated OKA strain in guinea pigs was due to the series of passages in embryonic guinea pig cell cultures performed in the course of attenuation [Takahashi et al, 19751. The findings taken in their sum suggest that subhuman primates and other animal species have the capability of responding in a particular way to strains of VZV which have an altered pathogenicity for humans.…”

Section: Discussionmentioning

confidence: 99%

Immunogenicity of wild and attenuated varicella‐zoster virus strains in rhesus monkeys

Asano

Albrecht

Behr

et al. 1984

Journal of Medical Virology

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Thirty susceptible rhesus monkeys were inoculated with cell-free varicella-zoster virus strain OKA or strain KMcC. Both wild and attenuated strains were used. No clinical signs characteristic of human varicella were seen in any of the animals. Virus was not isolated from throat swabs, blood, or cerebrospinal fluid. Antibodies were measured by an enhanced plaque neutralization test. The wild and attenuated OKA strains produced comparable levels of antibodies for 3 months after inoculation. Attenuated KMcC strains produced lower titers than the wild strain. On rechallenge 3 months after primary inoculation animals boostered with the attenuated OKA strain developed significantly higher antibody titers than animals receiving the wild strain. Animals primed and challenged with the attenuated KMcC strains showed significantly lower antibody titers than animals which received the wild strain. The results indicate that the immunogenicity of attenuated OKA and KMcC strains in rhesus monkeys parallels the experience obtained with these strains in humans.

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Section: Discussionmentioning

confidence: 99%

Immunogenicity of wild and attenuated varicella‐zoster virus strains in rhesus monkeys

Asano

Albrecht

Behr

et al. 1984

Journal of Medical Virology

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“…Research on the consequences of VZV infection in neurons has been hampered by the lack of a suitable animal model. Investigators have had limited success in infecting guinea pig DRG (Arvin et al 1987;Lowry et al 1992Lowry et al , 1993Matsunga et al 1982;Myers et al 1980Myers et al , 1985Myers et al , 1991Sato et al 2003) and, although latent infection of ganglia has been achieved in cotton rats (Cohen et al 2007) and rats (Rentier et al 1996), VZV has not been reactivated in either of these animals. We have furthered our own ability to analyze the life cycle of VZV by developing an in vitro model that utilizes enteric neurons isolated from the guinea pig small intestine (Chen et al 2003;Gershon et al 2008b).…”

Section: Introductionmentioning

confidence: 99%

VZV Infection of Keratinocytes: Production of Cell-Free Infectious Virions In Vivo

Gershon

2010

Current Topics in Microbiology and Immunology

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Varicella-zoster virus (VZV) is the cause of varicella (chickenpox) and zoster (shingles). Varicella is a primary infection that spreads rapidly in epidemics while zoster is a secondary infection that occurs sporadically as a result of the reactivation of previously acquired VZV. Reactivation is made possible by the establishment of latency during the initial episode of varicella. The signature lesions of both varicella and zoster are cutaneous vesicles, which are filled with a clear fluid that is rich in infectious viral particles. It has been postulated that the skin is the critical organ in which both host-to-host transmission of VZV and the infection of neurons to establish latency occur. This hypothesis is built on evidence that the large cation-independent mannose 6-phosphate receptor (MPRci) interacts with VZV in virtually all infected cells, except those of the suprabasal epidermis, in a way that prevents the release of infectious viral particles. Specifically, the virus is diverted in an MPRci-dependent manner from the secretory pathway to late endosomes where VZV is degraded. Because nonepidermal cells are thus prevented from releasing infectious VZV, a slow process, possibly involving fusion of infected cells with their neighbors, becomes the means by which VZV is disseminated. In the epidermis, however, the maturation of keratinocytes to give rise to corneocytes in the suprabasal epidermis is associated uniquely with a downregulation of the MPRci. As a result, the diversion of VZV to late endosomes does not occur in the suprabasal epidermis where vesicular lesions occur. The formation of the waterproof, chemically resistant barrier of the epidermis, however, requires that constitutive secretion outlast the downregulation of the endosomal pathway. Infectious VZV is therefore secreted by default, accounting for the presence of infectious virions in vesicular fluid. Sloughing of corneocytes, aided by scratching, then aerosolizes the virus, which can float with dust to be inhaled by susceptible hosts. Infectious virions also bathe the terminals of those sensory neurons that innervate the epidermis. These terminals become infected with VZV and provide a route, retrograde transport, which can conduct VZV to cranial nerve (CNG), dorsal root ganglia (DRG), and enteric ganglia (EG) to establish latency. Reactivation returns VZV to the skin, now via anterograde transport in axons, to cause the lesions of zoster. Evidence in support of these hypotheses includes observations of the VZV-infected human epidermis and studies of guinea pig neurons in an in vitro model system.

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“…We, therefore, sought to develop a guinea pig model, which would be accessible and relevant to infection and latency of VZV in neurons. Guinea pigs were chosen as the animals to study because of the prior limited success other investigators have had in infecting guinea pig cells [Myers et al, 1980[Myers et al, , 1985Matsunga et al, 1982;Arvin et al, 1987;Lowry et al, 1992Lowry et al, , 1993Sabella et al, 1993;Cohen et al, 1998;Sato et al, 1998] moreover, the Oka strain of VZV, which is used in the varicella vaccine, was adapted for this purpose by multiple passages in guinea pig fibroblasts [Takahashi et al, 1974;Matsunga et al, 1982;Lowry et al, 1992Lowry et al, , 1993. These observations suggested that guinea pig neurons might be infected with VZV more readily than those from other species.…”

Section: Introductionmentioning

confidence: 99%

Latent and lytic infection of isolated guinea pig enteric ganglia by varicella zoster virus

et al. 2003

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Varicella zoster virus (VZV) has been demonstrated to infect guinea pig enteric neurons in vitro. Latent infection of isolated enteric neurons is established when the cultures predominantly consist of neurons and they are exposed to cell-free VZV. Neurons harboring latent infection survive for weeks in vitro and express mRNA encoding ORFs 4, 21, 29, 40, 62, and 63, but not 14(gC) or 68 (gE) (although DNA encoding the glycoproteins is present). The expressed proteins are the same as those that are also expressed in human sensory neurons harboring latent VZV. In addition to mRNA, the immunoreactivities of ORFs 4, 21, 29, 62, and 63 can be detected. ORF 62 and 29 proteins are cytoplasmic and not intranuclear. VZV does not preferentially infect and/or become latent in intrinsic enteric primary afferent neurons indicating that the virus is latent in these neurons. Lytic infection occurs when mixed cultures of neurons and non-neuronal cells of the bowel wall are exposed to cell-free VZV or when isolated enteric neurons are exposed to cell-associated VZV. When lytic infection occurs, enteric neurons die within 48 hr. Prior to their death, neurons express VZV glycoproteins, including gE and gB, and ORF 62 and 29 proteins are intranuclear. This new animal model should facilitate studies of VZV latency and the efficacy of therapies designed to prevent VZV infection, latency, and reactivation.

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Experimental infection and immune response of guinea pigs with varicella-zoster virus

Cited by 58 publications

References 10 publications

Immunogenicity of wild and attenuated varicella‐zoster virus strains in rhesus monkeys

Immunogenicity of wild and attenuated varicella‐zoster virus strains in rhesus monkeys

VZV Infection of Keratinocytes: Production of Cell-Free Infectious Virions In Vivo

Latent and lytic infection of isolated guinea pig enteric ganglia by varicella zoster virus

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