Electron micrograph of Human Papilloma Viruses Most mucosal squamous cell head and neck<unk> s, including<unk><unk>  (OPC), have historically been attributed to tobacco and alcohol use. However this pattern has changed considerably since the 1980s. It was realised that some<unk> s occur in the absence of these risk factors and an association between human papilloma virus <unk>  and various squamous cell<unk> s, including OPC, was first described in 1983. Since then both molecular and epidemiological evidence has been accumulating, with the International Agency for Research on<unk>  (IARC) stating that high-risk<unk>  types 16 and 18 are carcinogenic in humans, in 1995, and In 2007 that<unk>  was a cause for oral<unk> s. Human papillomavirus <unk><unk><unk>  <unk> +OPC) incidence has been increasing while<unk> -negative <unk> -OPC)<unk>  incidence is declining, a trend that is estimated to increase further in coming years. Since there are marked differences in clinical presentation and treatment relative to<unk>  status,<unk> +OPC is now viewed as a distinct biologic and clinical condition. Human<unk>  has long been implicated in the pathogenesis of several anogenital<unk> s including those of the anus, vulva, vagina, cervix, and penis. In 2007 it was also implicated by both molecular and epidemiological evidence in<unk> s arising outside of the anogenital tract, namely oral<unk> s.<unk>  infection is common among healthy individuals, and is acquired through oral sex. Although less data is available, prevalence of<unk>  infection is at least as common among men as among women, with 2004 estimates of about 27% among US women aged 14–59.<unk>  oral infection precedes the development of<unk> +OPC. Slight injuries in the mucous membrane serve as an entry gate for<unk> , which thus works into the basal layer of the epithelium. People testing<unk>  for<unk>  type 16 virus <unk> 16) oral infection have a 14 times increased risk of developing<unk> +OPC. Immunosuppression seems to be an increased risk factor for<unk> +OPC. Individuals with TGF-β1 genetic variations, specially T869C, are more likely to have<unk> 16+OPC. TGF-β1 plays an important role in controlling the immune system. In 1993 it was noted that patients with human papillomavirus <unk> -associated anogenital<unk> s had a 4-fold increased risk of tonsillar squamous-cell carcinoma. Although evidence suggests that<unk> 16 is the main cause of OPC in humans not exposed to smoking and alcohol, the degree to which tobacco and/or alcohol use may contribute to increase the risk of<unk> +OPC has not always been clear but it appears that both smoking and<unk>  infection are independent and additive risk factors for developing OPC. The connection between<unk> -infection and<unk><unk>  is stronger in regions of lymphoepithelial tissue (base of tongue and palatine tonsils) than in regions of stratified squamous epithelium (soft palate and uvula). Human herpesvirus-8 infection can potentiate the effects of<unk> -16.
HPV-positive oropharyngeal cancer
Tobacco
Hepatitis C and HIV coinfection
Branchial cleft cyst
Circumcision and HIV
Oral florid papillomatosis
Hormone receptor positive breast tumor
Human papillomavirus infection