Different P105 promoter activities among natural variants of human papillomavirus type 18

Journal of Infectious Diseases

Volumn 191, Issue 5, 2005, Pages 739-742

  Sichero, Laura ^a,b   Franco, Eduardo Luis ^c   Villa, Luisa Lina ^b  

^a UNIVERSITY OF SÃO PAULO   (Brazil)

^b LUDWIG INSTITUTE FOR CANCER RESEARCH   (Brazil)

^c MCGILL UNIVERSITY   (Canada)

Author keywords

[No Author keywords available]

Indexed keywords

LUCIFERASE;

ARTICLE; CANCER RISK; CONTROLLED STUDY; GENETIC TRANSFECTION; HELA CELL; HUMAN; HUMAN CELL; HUMAN PAPILLOMAVIRUS TYPE 18; MOLECULAR CLONING; NONHUMAN; NUCLEOTIDE SEQUENCE; PHYLOGENY; PRIORITY JOURNAL; PROMOTER REGION; SEQUENCE ANALYSIS; STRAIN DIFFERENCE; UTERINE CERVIX CARCINOMA; VIRUS CARCINOGENESIS; VIRUS STRAIN;

EID: 13944270191     PISSN: 00221899     EISSN: None     Source Type: Journal    
DOI: 10.1086/427825     Document Type: Article

References (16)

1. Bosch FX, Manos MM, Muñoz N, et al. Prevalence of human papillomavirus in cervical cancer: a worldwide perspective. International biological study on cervical cancer (IBSCC) Study Group. J Natl Cancer Inst 1995; 87:796-802.
2. Ong CK, Chan SY, Campo MS, et al. Evolution of human papillomavirus type 18: an ancient phylogenetic root in Africa and intratype diversity reflect coevolution with human ethnic groups. J Virol 1993; 67: 6424-31.
3. Hildesheim A, Wang SS. Host and viral genetics and risk of cervical cancer: a review. Virus Res 2002; 89:229-40.
4. Villa LL, Sichero L, Rahal P, et al. Molecular variants of human papillomavirus type 16 and 18 preferentially associated with cervical neoplasia. J Gen Virol 2000; 81:2959-68.
5. Bernard HU. Gene expression of genital human papillomavirus and considerations on potential antiviral approaches. Antivir Ther 2002; 7: 219-37.
6. Franco E, Villa L, Rohan T, Ferenczy A, Petzl-Erler M, Matlashewski G. Designs and methods of the Ludwig-McGill longitudinal study of the natural history of human papillomavirus infection and cervical neoplasia in Brazil. Ludwig-McGill study Group. Rev Panam Salud Publica 1999; 6: 223-33.
7. Rose B, Steger G, Dong XP, et al. Point mutations in the Spl motifs in the upstream regulatory region of human papillomavirus type 18 isolates from cervical cancer increase promoter activity. J Gen Virol 1998; 79:1659-63.
8. Pirog EC, Kleter B, Olgac S, et al. Prevalence of human papillomavirus DNA in different histological subtypes of cervical adenocarcinomas. Am J Pathol 2000; 157:1055-62.
9. Villa LL, Schlegel R. Differences in transformation activity between HPV-18 and HPV-16 map to the viral LCR-E6-E7 legion. Virology 1991; 181:374-7.
10. Romanczuk H, Villa LL, Schlegel R, Howley PM. The viral transcription regulatory region upstream of the E6 and E7 genes is a major determinant of the differential immortalization activities of the human papillomavirus types 16 and 18. J Virol 1991; 65:2739-44.
11. Burk RD, Terai M, Gravitt PE, et al. Distribution of human papillomavirus types 16 and 18 variants in squamous cell carcinomas and adenocarcinomas of the cervix. Cancer Res 2003; 63:7215-20.
12. Zehbe I, Tommasino M. The biological significance of human papillomavirus type 16 variants for the development of cervical neoplasia. Papillomavirus Rep 1999; 10:105-16.
13. Hecht JL, Kadish AS, Jiang G, Burk RD. Genetic characterization of the human papillomavirus (HPV) 18 E2 gene in clinical specimens suggests the presence of a subtype with decreased oncogenic potential. Int J Cancer 1995; 60:369-76.
14. Lizano M, Berumen J, Guido MC, Casas L, Garcia-Carranca A. Association between human papillomavirus type 18 variants and histopathology of cervical cancer. J Natl Cancer Inst 1997; 89:1227-31.
15. Kämmer C, Warthorst U, Torrez-Martinez N, Wheeler CM, Pfister H. Sequence analysis of the long control region of human papillomavirus type 16 variants and functional consequences for P97 promoter activity. J Gen Virol 2000; 81:1975-81.
16. Stöppler MC, Ching K, Stöppler H, Clancy K, Schlegel R, Icenogle J. Natural variants of human papillomavirus type 16 E6 protein differ in their abilities to alter keratinocyle differentiation and to induce p53 degradation. J Virol 1996; 70:6987-93.