Abstract: . . .  facilitate integration of HPV genome into the host cell genome and leads to malignant transformation. This is supported by the observation that mutation in E2 ORF or its binding sites within the URR leads to an enhanced immortalization activity of HPV 16 (ref. 143). The ORF coding for E5 protein also shows transforming activity, but mostly in bovine papillomavirus (BPV) and is frequently deleted in cervical cancer 141 . The role of E4 ORF and its product is not yet clearly understood but possibly has a role in productive infection of the virus. In 1978, because of the observed genetic heterogeneity of human papillomavirus, for the nomenclature of a HPV type, a new type was designated and differed by more than 50% from a prototype HPV, when tested . . .
. . .  cancers that arise in absence of HPV infection, an alternative pathway, involving specific cellular gene mutations, is perhaps responsible. Even in HPV-infected lesions numerous additional genetic changes 186–188 including gene mutations, should occur in host cells to initiate progression. Furthermore, analysis of chromosomal abnormalities in invasive cancer cases suggest alterations in several oncogenes and tumour suppressor genes. The two HPV- transforming genes E6 and E7 can functionally interfere with cell cycle control by interacting with presumptive tumour suppressor gene products such as p53 and Rb leading to deregulation of cell cycle. Also, the chromosomal instability and aneuploidy, which are often observed in invasive cervical cancer . . .
. . .  Garcia, M., Brenes, M. M., Herrero, R., Gaitan, E., Tenorio, P., de Britton, R. C., Rawls, W. E. N., Engl . J . Med ., 1989, 320 , 1437–1441. 57. Schiffman, M. H. and Brinton, L. A., Cancer , 1995, 76 , 901– 904. 58. Wang, P. D. and Lin, R. S., Gynecol . Oncol ., 1996, 62 , 10–18. 59. Runowicz, C. D., Lynberis, S., Tobias, D., Med . Scape . Women Health , 1997, 2 , 2. 60. Southern, E. M., J . Mol . Biol ., 1975, 98 , 503–517. 61. Mullis, K. B. and Faloona, F. A., Methods Enzymol ., 1987, 155 , 335–350. 62. Vincent, S. A., deLa, R. A., Salmon, R., Validine, P., Zafrani, B. and Sastre, G. X., Mod . Pathol ., 1996, 9 , 614–620. 63. Poletti, P. A., Halfon, A. and Marti, M. C., Int . J . Colorectal Dis ., 1998, 13 , 108–111. 64. Wagner, D., Ikenberg, . . .
. . .  be used for both intranasal administration as well as delivery of therapeutic antigen vaccines. The use of plasmid DNA as a vaccine appears to be the most promising approach for induction of Th1 (T-helper cell class I) or for cell-mediated, and CTL (cytotoxic T lymphocyte) responses which are beneficial in antiviral immunity. Immunization with the plasmid expressing the L1 protein of CRPV was found to be protective upon subsequent challenge with CRPV 183 . This demonstrates that DNA vaccines can work as viable options for induction of viral protection. But before implementation of HPV vaccination, there is a need for pre-evaluation of their safety and optimization of administration protocols. One of the most important questions is selection of . . .
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