Control of papillomavirus DNA replication and transcription.
Hallmarks of HPV infection include a restricted tropism for human epithelial cells and a viral life cycle tightly linked to the differentiation program of the host keratinocyte. This particular viral cycle has hampered the study of the HPV vegetative life cycle for decades, due to the lack of suitable in-vitro culture conditions. The tissue and differentiation dependence seems to be dictated by viral transcription rather than viral DNA replication. Indeed, viral transcription is restricted to epithelial cells of human origin, more specifically to keratinocytes. In contrast, HPV genomes can replicate in various undifferentiated cell lines regardless of their natural permissiveness to infection, as long as the viral replication proteins E1 and E2 are expressed.
Desaintes
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Département des Biotechnologies URA 1644 du CNRS, Institut Pasteur, Paris, France.
Demeret
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D004261:DNA Replication; D004279:DNA, Viral / Q000235:genetics*; D006801:Humans; D009369:Neoplasms / Q000235:genetics; D015513:Oncogene Proteins / Q000502:physiology; D009856:Oncogene Proteins, Viral / Q000502:physiology; D027383:Papillomaviridae / Q000235:genetics*; D011230:Precancerous Conditions / Q000235:genetics; D014158:Transcription, Genetic
D004279:DNA, Viral; C093478:E1 protein, Human papillomavirus 16; D015513:Oncogene Proteins; D009856:Oncogene Proteins, Viral; C069102:oncogene protein E2, Human papillomavirus type 18