Varicella-Zoster Virus Transformation of Hamster Embryo Cells

Gelb, Lawrence D.; Huang, John J.; Wellinghoff, Wanda

doi:10.1099/0022-1317-51-1-171

Cited by 23 publications

(19 citation statements)

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“…This observation is consistent with the finding that VZV-infected cells can transform mammalian cells in vitro (Gelb et al, 1980;Gelb & Dohner, 1984). VZV is the fourth human herpesvirus that has been found to be carcinogenic in this mouse model of cervical neoplasia.…”

supporting

confidence: 81%

“…This suggests that transfection may be the initiating event in neoplasia induced by HSV-2. In contrast, Gelb et al (1980) and Gelb & Dohner (1984) found that transformation of hamster cells in vitro was induced by human embryonic lung ceils infected by a recent clinical isolate of VZV but not by cell-free VZV, VZV DNA, or laboratory passaged strains of VZV. This suggests, among other possibilities, that products of infected cells may be important in VZVassociated cellular transformation.…”

mentioning

confidence: 99%

“…Transfection is thought to be the mechanism by which neoplasia is initiated in this model (Anthony et al, 1989). As VZV is a human herpesvirus that has also been shown to induce transformation of mammalian 0000-9481 © 1990 SGM cells in vitro (Gelb et al, 1980;Gelb & Dohner, 1984), it was tested in this mouse model to determine whether, under appropriate conditions, VZV can induce oncogenesis in vivo.…”

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confidence: 99%

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Induction of cervical neoplasia in the mouse by an extract of cells infected by varicella-zoster virus

Heggie¹,

Wentz²,

Sørensen³

et al. 1990

Journal of General Virology

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Since several human herpesviruses, including varicellazoster virus (VZV), have been demonstrated to transform mammalian cells in vitro, VZV was tested in a mouse model of virus-induced cervical neoplasia to determine whether it is oncogenic in vivo. Herpes simplex viruses types 1 and 2 and cytomegalovirus have been previously shown to induce cervical neoplasia in this mouse model. VZV was propagated in WI-38 cell cultures and inactivated by ultraviolet irradiation. Control material was prepared in an identical manner from uninfected cell cultures. Cotton tampons, saturated with inactivated virus or control material, were inserted into the vaginas of C57BL mice three times a week for 60 weeks. Cervical dysplasia was detected in 40 % and invasive carcinoma in 34 % of virus-exposed mice by histological examination. No lesions were detected in control animals. These observations indicate that VZV, or some product of virus-infected cells, is oncogenic in vivo for the mouse cervix.

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supporting

confidence: 81%

mentioning

confidence: 99%

mentioning

confidence: 99%

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Induction of cervical neoplasia in the mouse by an extract of cells infected by varicella-zoster virus

Heggie¹,

Wentz²,

Sørensen³

et al. 1990

Journal of General Virology

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“…The CPE consists of cell rounding and swelling, and there is a virus spread to neighbouring cells resulting in enlarging plaques in which the centrally located cells are the first to die and detach. Also multinucleated giant cells (syncytia) are formed (Gelb 1990). In the present study, the first mentioned phenomenon was captured in GMK, and the second one in A 549 cell cultures.…”

Section: Discussionsupporting

confidence: 54%

Morphology of epithelial keratitis in herpes zoster ophthalmicus

Tabery¹

2000

Acta Ophthalmologica Scandinavica

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ABSTRACT.Purpose: To investigate the in vivo morphology of epithelial changes in acute herpes zoster keratitis. Methods: 10 patients with acute disease. In 7, systemic acyclovir treatment was started at presentation, in 2 р24 hours before, 1 was not treated. The corneae were examined with the slit lamp, followed intermittently for 3-30 days, and photographed at intervals ranging between 1 to 7 days. Results: All but one patient had epithelial changes at presentation; all developed new ones. The smallest discernible entities were abnormal cells of about 10-15 mm in diameter, singular or grouped. Larger foci measured about 100-200 mm. 2 patients showed pseudodendrites at presentation, and further 3/9 observed Ø2 weeks developed them. Some lesions showed white surface plaques. No ulcerations were observed. Healing occurred AE10-22 days after the onset of symptoms. Conclusions:The study seemed to have followed the natural course of the disease.The rapidly changing morphology in the absence of ulcerative features indicated successive damage counteracted by reparative forces.

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“…Both herpes simplex viruses (HSV-1 and HSV-2) (1, 2), cytomegalovirus (CMV) (3), and varicella zoster virus (VZV) (4) can alter the growth properties of rodent cells in culture, usually to a tumorigenic phenotype. Attempts to identify the viral genes that are responsible for HSV-mediated morphological transformation gave surprising results.…”

mentioning

confidence: 99%