Human papillomavirus type 32 does not display in vitro transforming properties.
Human papillomavirus type 32 (HPV32) is one of the etiological agents of a benign oral condition, focal epithelial hyperplasia. However, the previously characterized properties of its E7 oncoprotein suggest a possible malignant nature for this virus. In this study we characterized the properties of HPV32 E6 and E7. Our data show that HPV32 E7, despite its high affinity for pRb, does not promote degradation of the cellular protein. In addition, HPV32 E6 does not prevent p53-mediated apoptosis and/or cell cycle arrest. Moreover, coexpression of HPV32 E6 and E7 in primary human fibroblasts or keratinocytes does not alter their proliferative state. Together, these data provide evidence of the benign nature of HPV32.
D016475:3T3 Cells; D000818:Animals; D002471:Cell Transformation, Neoplastic; D019941:Cyclin-Dependent Kinase Inhibitor p16 / Q000502:physiology; D016193:G1 Phase; D006801:Humans; D051379:Mice; D009856:Oncogene Proteins, Viral / Q000633:toxicity*; D027383:Papillomaviridae / Q000472:pathogenicity*; D016160:Retinoblastoma Protein / Q000378:metabolism; D016196:S Phase; D016159:Tumor Suppressor Protein p53 / Q000502:physiology
D019941:Cyclin-Dependent Kinase Inhibitor p16; C410917:E7 protein, Human papillomavirus type 33; D009856:Oncogene Proteins, Viral; D016160:Retinoblastoma Protein; D016159:Tumor Suppressor Protein p53