Association between human papillomavirus and Epstein-Barr virus infections in human oral carcinogenesis

Moustafa, Ala‐Eddin Al; Chen, Dongfeng; Ghabreau, Lina; Akil, Nizar

doi:10.1016/j.mehy.2009.02.025

Cited by 58 publications

(66 citation statements)

References 37 publications

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“…Recent studies have examined the association between EBV and high-risk strains of HPV in the progression of human oral cancers (103,104). EBV and HPV DNA have been detected in nasopharyngeal carcinoma samples, which suggests that EBV and HPV co-infections could be involved in the neoplastic transformation of the oral epithelium (105)(106)(107).…”

Section: Ebv and Hpvmentioning

confidence: 99%

“…Although it has been established that approximately 38% of human nasopharyngeal carcinomas are associated with high-risk HPV and EBV co-infections, the mechanism of carcinogenesis is not yet understood. Some studies hypothesize that HPV oncoproteins E6/E7 cooperate with the EBNA1, LMP1, LMP2, and BARF1 EBV oncoproteins to transform the oral epithelium (103). Additional studies are needed to explore the role and pathogenesis of HPV and EBV co-infection in human nasopharyngeal carcinogenesis.…”

Section: Ebv and Hpvmentioning

confidence: 99%

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Multiple Infections and Cancer: Implications in Epidemiology

Vedham

Divi

Starks

et al. 2014

Technol Cancer Res Treat

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Approximately 18% of the global cancer burden has been attributed to infectious agents, with estimates ranging from 7% in developed countries to about 22% in developing countries.Chronic infections caused by the hepatitis B and C viruses, human papilloma viruses (HPV), and Helicobacter pylori (H. pylori) are reported to be responsible for approximately 15% of all human cancers. Interestingly, although many of the infectious agents that have been associated with cancer-such as HPV, Epstein-Barr virus (EBV), and H. pylori-are highly prevalent in the world, most infected individuals do not develop cancer but remain lifelong carriers. Malignancies associated with infectious agents may result from prolonged latency as a result of chronic infections. Pathogenic infections are necessary but are not sufficient for cancer initiation or progression. Cancer initiation may require additional cofactors, including secondary infections. Therefore, in patients with chronic infection with one agent, secondary co-infection with another agent may serve as an important co-factor that may cause cancer initiation and progression. Additionally, opportunistic co-infections could significantly inhibit response to cancer treatment and increase cancer mortality. Co-infections are relatively common in areas with a high prevalence of infectious agents, especially in developing countries. These co-infections can cause an imbalance in the host immune system by affecting persistence of and susceptibility to malignant infections. Several articles have been published that focus on infectious agents and cancer. In this article, we discuss the role of infectious agents in malignancies, highlight the role of multiple/co-infections in cancer etiology, and review implications for cancer epidemiology.

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Section: Ebv and Hpvmentioning

confidence: 99%

Section: Ebv and Hpvmentioning

confidence: 99%

Multiple Infections and Cancer: Implications in Epidemiology

Vedham

Divi

Starks

et al. 2014

Technol Cancer Res Treat

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“…Jaloluli et al (2012) detected the presence of EBV In 55% of samples from 8 different countries. A number of studies point to the co-infection by HPV and EBV in cervix cancer (Szkaradkiewicz et al, 2004) and in oral squamous cell carcinoma (Al Mustafa et al, 2009;Achayra et al, 2014;Jiang et al, 2015). Several articles indicate that co-infection by multiple oncogenic viruses may be an important risk factor in the development of OSCC (Jalouli et al, 2011;Achayra et al, 2014;Jiang et al, 2014;.…”

mentioning

confidence: 99%

Prevalence of Polyoma BK Virus (BKPyV) , Epstein-Barr Virus (EBV) and Human Papilloma Virus (HPV) in Oropharyngeal Cancer

Polz-Gruszka¹,

Morshed²,

Jarzynski³

et al. 2015

Pol J Microbiol

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A b s t r a c tThe aim of this study was to analyze the prevalence of BK virus, Human Papillomavirus and Epstein-Barr virus in oropharyngeal cancer, and to test our hypothesis that BKV/HPV/EBV co-infection plays a role in oropharyngeal squamous cell carcinoma. The correlation between viral infection, OSCC, anatomic location, pre-treatment staging, evidence of metastases to lymph nodes, and grading was also investigated. The examination samples were collected from 62 patients from paraffin tissue blocks. Males (90.3%) with, smoking (83.9%) and alcohol abuse (67.7%) problems prevailed in the studied group. G2 histological type was recognized in 80.6% cases. T4 (77.4%) and N2 (56.5%) traits occurred in the majority of patients. No cases of metastasis were observed (M0 100%). HPV -24.2%, EBV -27.4% and BKV 17.7% were detected in the studied samples. We observed co-infection EBV/BKV in 8% of cases, HPV/BKV in 4.8%, and HPV/EBV in 9% cases. Only in two cases co-infection of all three viruses was found.

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“…Furthermore, it has been suggested that normal human oral epithelial cells, especially nasopharyngeal cells, could be very susceptible to persistent HPV and EBV co-infections and that EBV and high-risk HPV co-infections may play an important role in the initiation of a neoplastic transformation of human oral epithelial cells (Al Moustafa et al 2009). To date, different degrees of associations between HPV and NPC have been described, yet no conclusive data have been obtained.…”

Section: Hpv and Npcmentioning

confidence: 99%