herpes simplex/nicotine

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Attenuation of the natural course of herpes simplex virus infection in human oral epithelial cell cultures by smokeless tobacco extracts suggests the possibility of a synergistic mechanism for carcinogenesis.

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High prevalence of both tobacco use and latent herpes simplex virus type 1 suggests the opportunity for synergism between these agents as cocarcinogens. In this study, postprimary human oral epithelial cell cultures were infected with herpes simplex virus type 1 pretreated with 2% extracts of either

Effect of smoked tobacco tar on the growth, cytolytic action, DNA synthesis, and gene expression of herpes simplex virus.

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Previous experiments have shown that topical application of smoked tobacco tar condensate to HSV-infected oral mucosae of mice promotes neoplastic changes. Although HSV is an oncogenic virus, the virus must be inactivated and lose its cytolytic activity to be oncogenic in vitro and in vivo.

Bupropion (Zyban, Wellbutrin) inhibits nicotine-induced viral reactivation in herpes simplex virus type 1 latent rabbits.

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We reported that nicotine applied via a transdermal patch (21 mg/day) induced viral reactivation and ocular shedding in herpes simplex virus type 1 (HSV-1) latent rabbits. One possible mechanism of action involves the release of catecholamines and other similar agents, triggering HSV reactivation.

Inhibition of herpes simplex virus replication and protein synthesis by non-smoked tobacco, tobacco alkaloids and nitrosamines.

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Inhibitory effects of snuff extract and the tobacco chemicals nicotine, anabasine, diethyl-N-nitrosamine (DEN), and the tobacco-specific nitrosamines (TSNA), N-nitrosonornicotine (NNN) and 4-(methylnitrosamino)-1-(3-pyridyl)-1-butanone (NNK) on herpes simplex virus type 1 (HSV-1) replication in

Effect of smokeless tobacco and tobacco-related chemical carcinogens on survival of ultraviolet light-inactivated herpes simplex virus.

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Low doses of ultraviolet (UV) light, x-rays, photodynamic treatment, or aflatoxins increase the survival of UV-irradiated virus in cells. This effect is postulated to occur by enhancement of the error-prone cellular repair function, which could also be associated with oncogenic cell transformation.

Synergism of herpes simplex virus and tobacco-specific N'-nitrosamines in cell transformation.

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Previous studies indicate that herpes simplex virus (HSV) enhances the carcinogenic activity of smokeless tobacco and tobacco-related chemical carcinogens in animals. Since tobacco-specific N'-nitrosamines (TSNAs) such as N'-nitrosonornicotine (NNN) and

Inhibition of herpes simplex virus replication by tobacco extracts.

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Herpes simplex virus type 1 (HSV-1) has been associated with the genesis of leukoplakias, epithelial atypia, and oral cancer. Tobacco habits, such as snuff dipping, are also definitely correlated with this type of lesion. The normal cytolytic HSV-1 infection can, after in vitro inactivation,

Variable expression of the herpes simplex virus thymidine kinase gene in Nicotiana tabacum affects negative selection.

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The potentials and limitations of negative-selection systems based on the human herpes simplex virus thymidine kinase type-1 (HSVtk) gene, which causes sensitivity to the nucleoside analog ganciclovir, were examined in tobacco as a model system. There were great differences between individual

Effect of tar condensate from smoking tobacco and water-extract of snuff on the oral mucosa of mice with latent herpes simplex virus.

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Upper lips were inoculated with virus to establish a latent infection in the trigeminal ganglia. During the latent period, tobacco smoke tar condensate or water-extract of snuff were topically applied to the primary inoculation site for two or three consecutive months. Tar condensate induced

Combined effect of herpes simplex virus and tobacco on the histopathologic changes in lips of mice.

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In the present study we have examined the combined effect of HSV-1 inoculation and tobacco application (snuff water extract or smoking tar condensate) on the histopathologic changes of mouse labial mucosa. Two months' exposure to tobacco or HSV-1 inoculation alone did not induce dysplasia in the

Effect of smokeless tobacco on the replication of herpes simplex virus in vitro and on production of viral lesions in hamster cheek pouch.

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Previous experiments have shown that combination of herpes simplex virus (HSV) infection and simulated snuff-dipping in hamster buccal pouches enhances the development of micro-invasive squamous cell carcinoma in cheek pouch epithelium. The effect has now been determined of water-extractable

[Effect of tobacco, herpes simplex virus and antioxidants on free-radical oxidation in the oral mucosa].

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Inactivation of herpes simplex virus by tobacco tar: related to viral carcinogenesis.

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Aryl hydrocarbon receptor (AhR)-mediated reporter gene expression systems in transgenic tobacco plants.

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In mammals, the aryl hydrocarbon receptor (AhR) mediates expression of certain genes, including CYP1A1, in response to exposure to dioxins and related compounds. We have constructed a mouse AhR-mediated gene expression systems for a beta-glucuronidase (GUS) reporter gene consisting of an AhR, an AhR

Recombinant aryl hydrocarbon receptors for bioassay of aryl hydrocarbon receptor ligands in transgenic tobacco plants.

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Dioxin residues widely contaminate soil and agricultural products at low concentrations and may accumulate in organisms at the top of food chains owing to their physicochemical properties. In this study, we have developed novel, dioxin-inducible, reporter gene expression systems regulated by

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