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MeSH Review

Human papillomavirus 6

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Disease relevance of Human papillomavirus 6

  • HPV 16 and 18 E7 bound similar amounts of Rb, but HPV 6 E7 consistently bound less [1].
  • Rb binding and CK II phosphorylation were also examined for the E7 proteins of HPV 6 and HPV 18 [1].
  • The E7 oncoproteins of HPV 6, 16 and 18 each have a 17 amino acid region with striking homology to adenovirus E1a and SV40 LT [1].
  • Condylomata acuminata and low-grade squamous intraepithelial lesions with infection by low-risk HPV such as HPV-6/11 showed focal and weak immunohistochemical staining for p16 [2].
  • Extensive HPV typing by polymerase chain reaction demonstrated that a majority of screened subjects (73.7%) were infected with HPV-6 and/or HPV-11 and that a large proportion (40.1%) were infected with multiple HPV types [3].

High impact information on Human papillomavirus 6

  • No HPV-6 DNA was detected in scrapings from 18 women attending an FPC whereas scrapings from 2 of 19 STD clinic patients with normal colposcopic and cytological examination were positive-this means that DNA hybridisation detected wart virus infection where previously none was suspected [4].
  • Surprisingly, introduction of the E6 gene from HPV-6, which is rarely found in cervical cancer, or bovine papillomavirus (BPV)-1, into normal mammary cells resulted in the generation of immortal cell lines [5].
  • First, we introduced a high-affinity pRB-binding site into HPV-6 E7 (6E7G22D) and showed that, in human foreskin keratinocytes, HPV-6 E7G22D decreased the level of pRB protein but not pRB mRNA [6].
  • The low-risk HPV-6 E6 and E7 proteins did not induce such abnormalities [7].
  • High levels of p53 expression were detected in most low-grade SILs (LSILs) (83%) and HPV 6/11/42-associated lesions (86%) [8].

Chemical compound and disease context of Human papillomavirus 6

  • We have developed for formaldehyde-fixed samples a strategy that, in a homogeneous, real-time fluorescence polymerase chain reaction (PCR)-based assay, accomplishes general HPV detection by SybrGreen reporting of HPV-DNA amplicons, and genotyping of seven prevalent HPV types (HPV-6, -11, -16, -18, -31, -33, -45) by real-time molecular beacon PCR [9].
  • Thirty-five resection specimens of anal carcinoma were examined with biotin-labelled probes for HPV 6, 11, 16, and 18 DNA, using a non-isotopic in situ hybridization (ISH) technique [10].
  • We have identified three elements in the noncoding region of human papillomavirus type 6 (HPV-6) that regulate transcription when assayed in recombinant plasmids containing the bacterial gene for chloramphenicol acetyltransferase [11].
  • Two of 11 HPV-6 DNAs were identical to the prototype strain in the 6U3 region, while 9 variants had a G to A transition at nt5020, changing a valine residue to isoleucine [12].
  • On the basis of the above observations, ISIS 2105, a 20-residue phosphorothioate oligonucleotide targeted to the translation initiation of both HPV type 6 (HPV-6) and HPV-11 E2 mRNA, was designed and shown to inhibit E2-dependent transactivation by HPV-11 E2 expressed from a surrogate promoter [13].

Biological context of Human papillomavirus 6

  • The presence of this insert was confirmed by direct sequence analysis of polymerase chain reaction-amplified segments from four naturally occurring HPV-6 genomes [14].
  • In a transitory assay, the E5 ORFs from both HPV-6 and HPV-16 were mitogenic in primary human foreskin epithelial cells (keratinocytes) and acted synergistically with EGF [15].
  • These WIL were characterized by their phenotype and their specificity for E7 and L1 proteins of HPV-6 [16].
  • Thus, both YY1 and CDP appear to be negative regulators of the differentiation-induced HPV-6 E1 promoter and thereby the HPV life cycle [17].
  • The activity of the mutated E1 promoter, monitored with the reporter gene luciferase, was threefold greater than that of the wild-type promoter, suggesting that YY1 negatively regulates HPV-6 E1 promoter activity [17].

Anatomical context of Human papillomavirus 6

  • By using clones in which the coding regions of HPV-6, HPV-16, and HPV-18 E7s were preceded by identical leader sequences, we found that the ability of the E7 gene products to induce anchorage-independent growth in rodent fibroblasts correlated directly with the oncogenic association of the HPV types [18].
  • Tissues of 45 cervical cancers and paraaortic lymph nodes from the same patients were evaluated by polymerase chain reaction with L1 consensus primers and hybridization with type-specific oligomer probes of HPV-6, -11, -16, -18, -31, -33, -35, and -45 for the detection and classification of subtypes of human papillomavirus (HPV) [19].
  • Our finding of both p53 and HPV-6/11 signals in the same cell nuclei may indicate complexing of p53 and low-risk HPV's without degradation of p53 [20].
  • We evaluated antibody, cytokine (IFN-gamma, IL-5, TNF-alpha), and cytotoxic T lymphocyte (CTL) responses in chimpanzees immunized with monovalent or quadrivalent (HPV-6, -11, -16, -18) L1 virus-like particle (VLP) vaccines administered i.m. on aluminum hydroxyphosphate (alum) at weeks 0, 8 and 24 [21].
  • NIH 3T3 cells containing the HPV 6 genome and treated with MNNG did not show this potential [22].

Gene context of Human papillomavirus 6

  • In HPV 6/11 and 16/18-positive IP, significant increase of MMP-2 and 9 were observed [23].
  • Among HPV 6/11 and 16/18-positive IP, significant increase of EGFR and Ki-67 index were observed [24].
  • Sixteen of the 19 HPV-positive cases (84.2%) were p53 negative; 5 (9%) were HPV 6/11 and 11 (19%) HPV 16/18, with an inverse correlation between the presence of HPV DNA and p53 expression (P = .017, P < .05) [25].
  • Here we report yeast two-hybrid screens with HPV-6 and -11 E6 proteins that identified TRIP-Br1 as a novel cellular target [26].
  • Binding of HPV-6 E7 to p130 was necessary but not sufficient to decrease the level of p130 [6].

Analytical, diagnostic and therapeutic context of Human papillomavirus 6

  • By Southern blot analysis, it was found that C-13 harboured HPV-6 DNA but that C-1 and C-8 harboured HPV-11 DNA, indicating that the E4 proteins of HPV-6 and -11 have cross-reactive antigenicity [27].
  • These antibodies did not detect HPV-6 L1 protein after Western blotting or in HPV-6-infected tissue sections, although one did react with an HPV-18 fusion protein after Western blotting [28].
  • To evaluate the humoral immune response to human papillomavirus (HPV) in women infected with human immunodeficiency virus (HIV), serum samples of 83 HIV-positive individuals were analysed by ELISA for specific antibodies of the isotypes IgG, IgA and IgM recognizing HPV-6, -11, -16, -18 and -31 L1 virus-like particles (VLPs) [29].
  • The third peptide located on the L1 protein of HPV 6 bears a common epitope since antibodies to this peptide were detected not only in 85% of women infected by HPV 6 or 11, but also in 82% of women infected by other HPVs, and in 74% and 71% of the control groups (10-12-year-old children and adults, respectively) [30].
  • Nine patients were infected by HPV-6 alone of whom only two required a tracheotomy (P = 0.05, Fisher's Exact Test) [31].


  1. The region of the HPV E7 oncoprotein homologous to adenovirus E1a and Sv40 large T antigen contains separate domains for Rb binding and casein kinase II phosphorylation. Barbosa, M.S., Edmonds, C., Fisher, C., Schiller, J.T., Lowy, D.R., Vousden, K.H. EMBO J. (1990) [Pubmed]
  2. Expression status of p16 protein is associated with human papillomavirus oncogenic potential in cervical and genital lesions. Sano, T., Oyama, T., Kashiwabara, K., Fukuda, T., Nakajima, T. Am. J. Pathol. (1998) [Pubmed]
  3. Randomized controlled trial of an adjuvanted human papillomavirus (HPV) type 6 L2E7 vaccine: infection of external anogenital warts with multiple HPV types and failure of therapeutic vaccination. Vandepapeliere, P., Barrasso, R., Meijer, C.J., Walboomers, J.M., Wettendorff, M., Stanberry, L.R., Lacey, C.J. J. Infect. Dis. (2005) [Pubmed]
  4. Screening for wart virus infection in normal and abnormal cervices by DNA hybridisation of cervical scrapes. Wickenden, C., Steele, A., Malcolm, A.D., Coleman, D.V. Lancet (1985) [Pubmed]
  5. Enhanced degradation of p53 protein in HPV-6 and BPV-1 E6-immortalized human mammary epithelial cells. Band, V., Dalal, S., Delmolino, L., Androphy, E.J. EMBO J. (1993) [Pubmed]
  6. The E7 proteins of low- and high-risk human papillomaviruses share the ability to target the pRB family member p130 for degradation. Zhang, B., Chen, W., Roman, A. Proc. Natl. Acad. Sci. U.S.A. (2006) [Pubmed]
  7. The human papillomavirus type 16 E6 and E7 oncoproteins cooperate to induce mitotic defects and genomic instability by uncoupling centrosome duplication from the cell division cycle. Duensing, S., Lee, L.Y., Duensing, A., Basile, J., Piboonniyom, S., Gonzalez, S., Crum, C.P., Munger, K. Proc. Natl. Acad. Sci. U.S.A. (2000) [Pubmed]
  8. p53 and bcl-2 proteins as prognostic markers in human papillomavirus-associated cervical lesions. Kurvinen, K., Syrjänen, K., Syrjänen, S. J. Clin. Oncol. (1996) [Pubmed]
  9. A novel strategy for human papillomavirus detection and genotyping with SybrGreen and molecular beacon polymerase chain reaction. Szuhai, K., Sandhaus, E., Kolkman-Uljee, S.M., Lemaître, M., Truffert, J.C., Dirks, R.W., Tanke, H.J., Fleuren, G.J., Schuuring, E., Raap, A.K. Am. J. Pathol. (2001) [Pubmed]
  10. Properties of HPV-positive and HPV-negative anal carcinomas. Williams, G.R., Lu, Q.L., Love, S.B., Talbot, I.C., Northover, J.M. J. Pathol. (1996) [Pubmed]
  11. Transcriptional regulatory elements in the noncoding region of human papillomavirus type 6. Wu, T.C., Mounts, P. J. Virol. (1988) [Pubmed]
  12. Sequence and antigenic diversity in two immunodominant regions of the L2 protein of human papillomavirus types 6 and 16. Yaegashi, N., Xi, L., Batra, M., Galloway, D.A. J. Infect. Dis. (1993) [Pubmed]
  13. In vitro evaluation of phosphorothioate oligonucleotides targeted to the E2 mRNA of papillomavirus: potential treatment for genital warts. Cowsert, L.M., Fox, M.C., Zon, G., Mirabelli, C.K. Antimicrob. Agents Chemother. (1993) [Pubmed]
  14. Human papillomavirus type 6 long control region and human cellular DNA contain related sequences. Hrisomalos, T.F., Boggs, D.L., Fife, K.H. J. Virol. (1990) [Pubmed]
  15. The E5 oncoprotein of human papillomavirus type 16 transforms fibroblasts and effects the downregulation of the epidermal growth factor receptor in keratinocytes. Straight, S.W., Hinkle, P.M., Jewers, R.J., McCance, D.J. J. Virol. (1993) [Pubmed]
  16. Isolation and characterization of human papillomavirus type 6-specific T cells infiltrating genital warts. Hong, K., Greer, C.E., Ketter, N., Van Nest, G., Paliard, X. J. Virol. (1997) [Pubmed]
  17. Yin yang 1 negatively regulates the differentiation-specific E1 promoter of human papillomavirus type 6. Ai, W., Narahari, J., Roman, A. J. Virol. (2000) [Pubmed]
  18. In vitro biological activities of the E6 and E7 genes vary among human papillomaviruses of different oncogenic potential. Barbosa, M.S., Vass, W.C., Lowy, D.R., Schiller, J.T. J. Virol. (1991) [Pubmed]
  19. Human papillomavirus detection in cervical carcinoma tissues and paraaortic lymph nodes by the polymerase chain reaction. Park, J.S., Chee, Y.H., Namkoong, S.E., Han, S.K., Kim, T.E., Lee, H.Y., Kim, S.J. Gynecol. Oncol. (1994) [Pubmed]
  20. Simultaneously detected aberrant p53 tumor suppressor protein and HPV-DNA localize mostly in separate keratinocytes in anogenital and common warts. Lassus, J., Ranki, A. Exp. Dermatol. (1996) [Pubmed]
  21. Antibody, cytokine and cytotoxic T lymphocyte responses in chimpanzees immunized with human papillomavirus virus-like particles. Palker, T.J., Monteiro, J.M., Martin, M.M., Kakareka, C., Smith, J.F., Cook, J.C., Joyce, J.G., Jansen, K.U. Vaccine (2001) [Pubmed]
  22. Differential cooperation of a carcinogen with human papillomavirus type 6 and 16 DNAs in in vitro oncogenic transformation. Mitrani-Rosenbaum, S., Tsvieli, R. Intervirology (1992) [Pubmed]
  23. Increased expression of matrix metalloproteinase-2 and 9 and human papilloma virus infection are associated with malignant transformation of sinonasal inverted papilloma. Katori, H., Nozawa, A., Tsukuda, M. Journal of surgical oncology. (2006) [Pubmed]
  24. Markers of malignant transformation of sinonasal inverted papilloma. Katori, H., Nozawa, A., Tsukuda, M. European journal of surgical oncology : the journal of the European Society of Surgical Oncology and the British Association of Surgical Oncology. (2005) [Pubmed]
  25. Computer-assisted analysis of p53 and PCNA expression in oral lesions infected with human papillomavirus. Soares, C.P., Benatti Neto, C., Fregonezi, P.A., Teresa, D.B., Santos, R.T., Longatto Filho, A., Maeda, M.Y. Anal. Quant. Cytol. Histol. (2003) [Pubmed]
  26. The human papillomavirus type 11 and 16 E6 proteins modulate the cell-cycle regulator and transcription cofactor TRIP-Br1. Gupta, S., Takhar, P.P., Degenkolbe, R., Koh, C.H., Zimmermann, H., Yang, C.M., Guan Sim, K., Hsu, S.I., Bernard, H.U. Virology (2003) [Pubmed]
  27. Human papillomavirus type 6 and 11 E4 gene products in condyloma acuminata. Tomita, Y., Fuse, A., Sekine, H., Shirasawa, H., Simizu, B., Sugimoto, M., Funahashi, S. J. Gen. Virol. (1991) [Pubmed]
  28. Reactivities of polyclonal and monoclonal antibodies raised to the major capsid protein of human papillomavirus type 16. Patel, D., Shepherd, P.S., Naylor, J.A., McCance, D.J. J. Gen. Virol. (1989) [Pubmed]
  29. Specific serum IgG, IgM and IgA antibodies to human papillomavirus types 6, 11, 16, 18 and 31 virus-like particles in human immunodeficiency virus-seropositive women. Petter, A., Heim, K., Guger, M., Ciresa-Kö Nig, A., Christensen, N., Sarcletti, M., Wieland, U., Pfister, H., Zangerle, R., Höpfl, R. J. Gen. Virol. (2000) [Pubmed]
  30. Detection of antibodies to L1, L2, and E4 proteins of human papillomavirus types 6, 11, and 16 by ELISA using synthetic peptides. Le Cann, P., Chabaud, M., Leboulleux, D., Mougin, C., Mayelo, V., Legrand, M.C., Calvet, C., Afoutou, J.M., Coll-Seck, A.M., Coursaget, P. J. Med. Virol. (1995) [Pubmed]
  31. Pediatric respiratory papillomatosis: prognostic role of viral typing and cofactors. Rimell, F.L., Shoemaker, D.L., Pou, A.M., Jordan, J.A., Post, J.C., Ehrlich, G.D. Laryngoscope (1997) [Pubmed]
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