Effect of herpes simplex virus on the DNA of human papillomavirus 18

Hara, Yoshihiro; Kimoto, Tatsuo; Okuno, Yoshinobu; Minekawa, Y

doi:10.1002/(sici)1096-9071(199709)53:1<4::aid-jmv2>3.0.co;2-4

Cited by 26 publications

(19 citation statements)

References 27 publications

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“…In vitro studies have shown, that HSV and HPV tolerate well each other, even enhance each other's growth and may play a synergistic role in oral carcinogenesis. 21,35,36 However, the numbers in the present study are too few to draw any further conclusions and more studies are needed. No HPV co-infections with HSV-2 or CMV were found.In our study, HPV was found in 76% in the oral cancers, which is a higher number than the recent meta-analysis have shown.…”

Section: Discussionmentioning

confidence: 99%

HPV genotypes and their prognostic significance in head and neck squamous cell carcinomas

Rautava

Kuuskoski

Syrjänen

et al. 2012

Journal of Clinical Virology

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Section: Discussionmentioning

confidence: 99%

HPV genotypes and their prognostic significance in head and neck squamous cell carcinomas

Rautava

Kuuskoski

Syrjänen

et al. 2012

Journal of Clinical Virology

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“…Oral HPV infection in individuals with and without HIV infection was associated with HSV-2 seropositivity, an accepted surrogate measurement of several sexual behaviors [27]. Recently, HSV-2 infection was demonstrated to increase the risk of an incident HPV infection [32], and it has been suggested that HSV-2 may act to promote cervical disease progression [33][34][35], even though HSV-2 sequences have not been found in tumors [36]. In the present study, however, oral HPV infection was significantly associated with seroreactivity to HSV-2 but not with HSV-1, the herpes virus that more commonly infects the oral cavity.…”

Section: Discussionmentioning

confidence: 99%

Oral Human Papillomavirus Infection in Adults Is Associated with Sexual Behavior and HIV Serostatus

et al. 2004

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The prevalence and risk factors for oral human papillomavirus (HPV) infection are unknown, despite evidence for an etiological role for HPV in oral cancers. Oral samples from human immunodeficiency virus (HIV)-seronegative (n=396) and HIV-seropositive (n=190) adults were tested for HPV DNA. High-risk HPV infections were present in 2.1% of tonsil and 6.3% of oral-rinse specimens. The prevalence of oral high-risk HPV infection was greater in HIV-seropositive individuals (13.7% vs. 4.5%; P<.001). In multiple logistic regression, odds of oral HPV infection increased with age, male sex, and herpes simplex virus (HSV)-2 seropositivity in HIV-seronegative individuals and with CD4 cell count <200 cells/mL, HSV-2 seropositivity, oral mucosal abnormalities, and >1 oral sex partner during the previous year (odds ratio, 12.8; 95% confidence interval, 3.1-52.7) among HIV-seropositive individuals. HPV type 16, which is present in most HPV-associated tonsillar cancers, was the most prevalent high-risk oral HPV infection.

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“…It seemed possible that functions of HSV-1 might be having a direct or indirect effect on activity of URR16. HSV has been reported to increase 31 or to suppress 32,33 the activities of different papillomaviruses, and cloned fragments of HSV-1 have been shown to activate the URR of HPV-16 in some cells. 34 In oral cancer cells that had been transfected with the URR-luciferase reporter plasmid, expression was increased by up to 30-fold when the cells were infected with HSV-1 ( Figure 9).…”

Section: Discussionmentioning

confidence: 99%

An oncolytic mutant of herpes simplex virus type-1 in which replication is governed by a promoter/enhancer of human papillomavirus type-16

et al. 2007

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Although herpes simplex virus type-1 (HSV-1) can be used as an oncolytic virus it has the undesirable side effect of neurotoxicity. To create a virus with improved specificity for oral cancer we used a fragment of human papillomavirus type-16, which is frequently found in oral and cervical cancers, but not elsewhere. The upstream regulatory region, URR16, was shown to have a high level of transcriptional activity in three of four oral cancer cell lines but low activity in three cell lines derived from brain cancers. URR16 was therefore placed in HSV-1, replacing the promoter of the essential gene ICP4, and the resulting virus was named HSPV-1. When cells were infected with HSPV-1, ICP4 was expressed at levels that were not associated with the level of activity of URR16. The virus replicated in each type of cell to a final titer that showed a correlation with the level of expression of ICP4, but with no correlation to either the tumor of origin or the presence of HPV sequences in the cells. To find if some function of HSV-1 was affecting the activity of URR16, oral cancer cells were transfected with a URR-reporter construct and were then infected with virus. This induced transcription, which was attributed to immediate-early viral genes other than ICP4. A promoter/enhancer from a papillomavirus therefore has the potential to regulate the functions of an oncolytic strain of HSV-1, and is affected by functions of both the host cell and of HSV-1 itself.

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Effect of herpes simplex virus on the DNA of human papillomavirus 18

Cited by 26 publications

References 27 publications

HPV genotypes and their prognostic significance in head and neck squamous cell carcinomas

HPV genotypes and their prognostic significance in head and neck squamous cell carcinomas

Oral Human Papillomavirus Infection in Adults Is Associated with Sexual Behavior and HIV Serostatus

An oncolytic mutant of herpes simplex virus type-1 in which replication is governed by a promoter/enhancer of human papillomavirus type-16

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