Detection of human herpes virus type 6 DNA in precancerous lesions of the uterine cervix

Tran‐Thanh, Danh; Koushik, Anita; Provencher, Diane; Drouin, P; Dubuc-Lissoir, Josée; Gauthier, Philippe; Allaire, Guy; Kornegay, Janet R.; Franco, Eduardo L.; Coutlée, François

doi:10.1002/jmv.10229

Cited by 12 publications

(10 citation statements)

References 12 publications

(20 reference statements)

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“…Among those classified with HSIL, the three most prevalent types were HPV-16 (54.0%), HPV-31 (14.2%), and HPV-18 (7.9%). Among those with confirmed cervical cancer, the highest prevalence was observed for HPV-16 (48.8% [95% CI: 34.0-63.6%]) [38,43,61], followed by HPV-18 (17.1% (95% CI: 6.4-27.9%) [38,42,43,61], and HPV-45 (7.7%, [95% CI: 2.4-13.0%]) [38,61]. …”

Section: Resultsmentioning

confidence: 99%

Canadian oncogenic human papillomavirus cervical infection prevalence: Systematic review and meta-analysis

Tricco

Gîlca

et al. 2011

BMC Infect Dis

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BackgroundOncogenic human papillomavirus (HPV) infection prevalence is required to determine optimal vaccination strategies. We systematically reviewed the prevalence of oncogenic cervical HPV infection among Canadian females prior to immunization.MethodsWe included studies reporting DNA-confirmed oncogenic HPV prevalence estimates among Canadian females identified through searching electronic databases (e.g., MEDLINE) and public health websites. Two independent reviewers screened literature results, abstracted data and appraised study quality. Prevalence estimates were meta-analyzed among routine screening populations, HPV-positive, and by cytology/histology results.ResultsThirty studies plus 21 companion reports were included after screening 837 citations and 120 full-text articles. Many of the studies did not address non-response bias (74%) or use a representative sampling strategy (53%).Age-specific prevalence was highest among females aged < 20 years and slowly declined with increasing age. Across all populations, the highest prevalence estimates from the meta-analyses were observed for HPV types 16 (routine screening populations, 8 studies: 8.6% [95% confidence interval 6.5-10.7%]; HPV-infected, 9 studies: 43.5% [28.7-58.2%]; confirmed cervical cancer, 3 studies: 48.8% [34.0-63.6%]) and 18 (routine screening populations, 8 studies: 3.3% [1.5-5.1%]; HPV-infected, 9 studies: 13.6% [6.1-21.1%], confirmed cervical cancer, 4 studies: 17.1% [6.4-27.9%].ConclusionOur results support vaccinating females < 20 years of age, along with targeted vaccination of some groups (e.g., under-screened populations). The highest prevalence occurred among HPV types 16 and 18, contributing a combined cervical cancer prevalence of 65.9%. Further cancer protection is expected from cross-protection of non-vaccine HPV types. Poor study quality and heterogeneity suggests that high-quality studies are needed.

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Section: Resultsmentioning

confidence: 99%

Canadian oncogenic human papillomavirus cervical infection prevalence: Systematic review and meta-analysis

Tricco

Gîlca

et al. 2011

BMC Infect Dis

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“…Moreover, the proteins encoded by the HHV-6 U16 gene (previously designated pZVB-70) and the genomic clone pZVH-14 (encompassing U30) transactivated HPV-transforming genes. However, as outlined in "Neoplasia" below, clinical investigations argue against an association between HHV-6 infection and HPV-induced neoplasia (59,66,342,413).…”

Section: Molecular Interactions Between Hhv-6 and Other Virusesmentioning

confidence: 99%

“…It was concluded that HHV-6 (as well as HCMV and HHV-7) are bystanders rather than cofactors in the oncogenesis of cervical cancer (59). Other groups have confirmed that a causative role of HHV-6 in cervical cancer is unlikely (342,413). A role for HHV-6 in the pathogenesis of oral carcinoma has been tentatively suggested, based upon the frequent detection of HHV-6 antigen in malignant and nonmalignant oral lesions (434), but this has not been further investigated.…”

Section: Clinical Manifestations Of Hhv-6 Infectionmentioning

confidence: 99%

Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy

2005

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Human herpesvirus 6 (HHV-6) is a betaherpesvirus that is closely related to human cytomegalovirus. It was discovered in 1986, and HHV-6 literature has expanded considerably in the past 10 years. We here present an up-to-date and complete overview of the recent developments concerning HHV-6 biological features, clinical associations, and therapeutic approaches. HHV-6 gene expression regulation and gene products have been systematically characterized, and the multiple interactions between HHV-6 and the host immune system have been explored. Moreover, the discovery of the cellular receptor for HHV-6, CD46, has shed a new light on HHV-6 cell tropism. Furthermore, the in vitro interactions between HHV-6 and other viruses, particularly human immunodeficiency virus, and their relevance for the in vivo situation are discussed, as well as the transactivating capacities of several HHV-6 proteins. The insight into the clinical spectrum of HHV-6 is still evolving and, apart from being recognized as a major pathogen in transplant recipients (as exemplified by the rising number of prospective clinical studies), its role in central nervous system disease has become increasingly apparent. Finally, we present an overview of therapeutic options for HHV-6 therapy (including modes of action and resistance mechanisms)

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“…We detected HHV-6 DNA in 48% of the tested samples. Although the amount of HHV-6 DNA in cervical swabs of Chlamydia -infected patients is comparatively high, HHV-6 or other HHVs have been frequently detected in cervical swabs earlier [17], [43], [44], [45]. We also detected HHV-6 DNA in blood cells of 59% of the patients.…”

Section: Discussionmentioning

confidence: 55%

“…Herpes simplex virus 2 (HSV-2) is associated with C. trachomatis in endometritis and acute salpingitis [16]. HHV-6 DNA is frequently detected in different grades of cervical lesions [17], [18]. C. trachomatis infection has also been separately linked to cervical cancer [19] but it is unclear, whether both these pathogens contribute to the development of cervical cancer.…”

Section: Introductionmentioning

confidence: 99%

Chlamydia trachomatis Infection Induces Replication of Latent HHV-6

et al. 2013

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Human herpesvirus-6 (HHV-6) exists in latent form either as a nuclear episome or integrated into human chromosomes in more than 90% of healthy individuals without causing clinical symptoms. Immunosuppression and stress conditions can reactivate HHV-6 replication, associated with clinical complications and even death. We have previously shown that co-infection of Chlamydia trachomatis and HHV-6 promotes chlamydial persistence and increases viral uptake in an in vitro cell culture model. Here we investigated C. trachomatis-induced HHV-6 activation in cell lines and fresh blood samples from patients having Chromosomally integrated HHV-6 (CiHHV-6). We observed activation of latent HHV-6 DNA replication in CiHHV-6 cell lines and fresh blood cells without formation of viral particles. Interestingly, we detected HHV-6 DNA in blood as well as cervical swabs from C. trachomatis-infected women. Low virus titers correlated with high C. trachomatis load and vice versa, demonstrating a potentially significant interaction of these pathogens in blood cells and in the cervix of infected patients. Our data suggest a thus far underestimated interference of HHV-6 and C. trachomatis with a likely impact on the disease outcome as consequence of co-infection.

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Detection of human herpes virus type 6 DNA in precancerous lesions of the uterine cervix

Cited by 12 publications

References 12 publications

Canadian oncogenic human papillomavirus cervical infection prevalence: Systematic review and meta-analysis

Canadian oncogenic human papillomavirus cervical infection prevalence: Systematic review and meta-analysis

Update on Human Herpesvirus 6 Biology, Clinical Features, and Therapy

Chlamydia trachomatis Infection Induces Replication of Latent HHV-6

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