Quote:
Originally Posted by AKA_Monet
Yeah, post the abstract with the full reference. I didn't say inconceivable, I said highly unlikely... It doesn't mean never, it means every now and then...
It also sounds like the virus mutated again as people got "creative"...  |
I doubt it's a seperate mutation of HPV it appears that it's the same strains that cause cervical cancer. It's probably a quality of the virus and the infection that causes the cells in either mouth or cervix to mutate. The same strains can cause penile cancer as well which only supports that. (I'm not a virologist but if the same strain is doing this to multiple targets, I say it's the strain not the target)
Quote:
ABSTRACT
Background Substantial molecular evidence suggests a role for human papillomavirus (HPV) in the pathogenesis of oropharyngeal squamous-cell carcinoma, but epidemiologic data have been inconsistent.
Methods We performed a hospital-based, case–control study of 100 patients with newly diagnosed oropharyngeal cancer and 200 control patients without cancer to evaluate associations between HPV infection and oropharyngeal cancer. Multivariate logistic-regression models were used for case–control comparisons.
Results A high lifetime number of vaginal-sex partners (26 or more) was associated with oropharyngeal cancer (odds ratio, 3.1; 95% confidence interval [CI], 1.5 to 6.5), as was a high lifetime number of oral-sex partners (6 or more) (odds ratio, 3.4; 95% CI, 1.3 to 8.8). The degree of association increased with the number of vaginal-sex and oral-sex partners (P values for trend, 0.002 and 0.009, respectively). Oropharyngeal cancer was significantly associated with oral HPV type 16 (HPV-16) infection (odds ratio, 14.6; 95% CI, 6.3 to 36.6), oral infection with any of 37 types of HPV (odds ratio, 12.3; 95% CI, 5.4 to 26.4), and seropositivity for the HPV-16 L1 capsid protein (odds ratio, 32.2; 95% CI, 14.6 to 71.3). HPV-16 DNA was detected in 72% (95% CI, 62 to 81) of 100 paraffin-embedded tumor specimens, and 64% of patients with cancer were seropositive for the HPV-16 oncoprotein E6, E7, or both. HPV-16 L1 seropositivity was highly associated with oropharyngeal cancer among subjects with a history of heavy tobacco and alcohol use (odds ratio, 19.4; 95% CI, 3.3 to 113.9) and among those without such a history (odds ratio, 33.6; 95% CI, 13.3 to 84.8). The association was similarly increased among subjects with oral HPV-16 infection, regardless of their tobacco and alcohol use. By contrast, tobacco and alcohol use increased the association with oropharyngeal cancer primarily among subjects without exposure to HPV-16.
Conclusions Oral HPV infection is strongly associated with oropharyngeal cancer among subjects with or without the established risk factors of tobacco and alcohol use.
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D'Souza, Gypsyamber, Kreimer, Aimee R., Viscidi, Raphael, Pawlita, Michael, Fakhry, Carole, Koch, Wayne M., Westra, William H., Gillison, Maura L.
Case-Control Study of Human Papillomavirus and Oropharyngeal Cancer
N Engl J Med 2007 356: 1944-1956
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