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].

References