| Virus Name | Human papillomavirus type 16 |
| Virus Short Name | HPV16 |
| Order | Unassigned |
| Virus Family | Papillomaviridae |
| Virus Subfamily | N.A. |
| Genus | Alphapapillomavirus |
| Species | Human papillomavirus 16 |
| Host | Human, monkeys |
| Cell Tropism | Epithelial cells of skin, mucous membranes |
| Associated Disease | Malignant tumours |
| Mode of Transmission | Sexual, indirect and direct contact, auto-inoculation |
| VIPR DB link | N.A. |
| ICTV DB link | https://talk.ictvonline.org/ictv-reports/ictv_9th_report/dsdna-viruses-2011/w/dsdna_viruses/121/papillomaviridae |
| Virus Host DB link | http://www.genome.jp/virushostdb/view/?virus_lineage=Papillomaviridae |
| Paper Title | TGF-beta1 and IL-4 downregulate human papillomavirus-16 oncogene expression but have differential effects on the malignant phenotype of cervical carcinoma cells |
| Author's Name | Manuela Donalisio, Maura Cornaglia, Santo Landolfo, David Lembo |
| Journal Name | Virus Research |
| Pubmed ID | 18206261 |
| Abstract | Host immune response to human papillomavirus (HPV) is a crucial factor in viral clearance and control of persistent infections. The existence of an intercellular control mechanism mediated by cytokines to suppress HPV-gene transcription and to prevent malignant conversion of HPV-infected cells, has been postulated. In a previous study, we demonstrated the inhibitory activity of several cytokines on the HPV-16 long control region (LCR)-driven transcription among these, IL-4 was reported as a LCR inhibitor for the first time and proposed as a candidate for further studies. Here, we addressed the question of whether IL-4 represses HPV-16 oncogene transcription and exerts antitumor activity in HPV-16 positive cervical carcinoma cell lines. Results indicated that downregulation of E6 and E7 levels by IL-4 in CaSki cells is weaker than that exerted by TGF-beta1, a known LCR inhibitor, although both cytokines are equally active in suppressing LCR-driven transcriptional activity in a reporter cell line. Moreover, only TGF-beta rescued p53 expression, Rb response pathway, and induced cellular senescence. SiHa cells were unresponsive to both cytokines. These findings suggest that the two cytokines may play a role in the control of HPV infections, however, cervical carcinoma cells developed a partial or a total resistance to their inhibitory activity. |
| Used Model | CaSki and SiHa cells |
| DOI | 10.1016/j.virusres.2007.12.003 |
