Interaction of viral oncoproteins with cellular target molecules: infection with high-risk vs low-risk human papillomaviruses.
Persistent infection by a subgroup of so-called high-risk human papillomaviruses (HPVs) that have a tropism for mucosal epithelia has been defined as the cause of more than 98% of cervical carcinomas as well as a high proportion of other cancers of the anogenital region. Infection of squamous epithelial tissues in the head and neck region by these same high-risk HPVs is also associated with a subset of cancers. Despite the general conservation of genetic structure amongst all HPV types, infection by the low-risk types, whether in genital or head and neck sites, carries a negligible risk of malignant progression, and infections have a markedly different pathology. In this review, we will examine and discuss the interactions that the principal viral oncoproteins of the high-risk mucosotrophic HPVs and their counterparts from the low-risk group make with cellular target proteins, with a view to explaining the differences in their respective pathology.
Pim
David
D
International Centre for Genetic Engineering and Biotechnology, Trieste, Italy. pim@icgeb.org <pim@icgeb.org>
Banks
Lawrence
L
D000818:Animals; D002471:Cell Transformation, Neoplastic; D006801:Humans; D009856:Oncogene Proteins, Viral / Q000502:physiology*; D027383:Papillomaviridae / Q000472:pathogenicity*; D050725:Papillomavirus E7 Proteins / Q000502:physiology*; D030361:Papillomavirus Infections / Q000821:virology*; D012097:Repressor Proteins / Q000502:physiology*; D016160:Retinoblastoma Protein / Q000502:physiology; D019098:Telomerase / Q000502:physiology; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
C068651:E6 protein, Human papillomavirus type 16; D009856:Oncogene Proteins, Viral; D050725:Papillomavirus E7 Proteins; D012097:Repressor Proteins; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53; C059731:oncogene protein E7, Human papillomavirus type 16; D019098:Telomerase