Abstract: A conformationally dependent epitope for the binding of three neutralizing monoclonal antibodies (mAbs) has been mapped to residues G(131)T(132) of the L1 major capsid protein.
Abstract: The new mAbs are unlike the neutralizing mAbs previously mapped to residues G(131)T(132) in that they bind both prototype and HPV11:G131S mut
Abstract: mAbs H11.G131S.I1 and H11.G131S.K5 bind HPV6 VLPs with the 263-290 substitutions, but show little binding to HPV6 VLPs with the 346-349 substitutions.
Abstract: mAbs H11.H3 and H11.G131S.G3 bind HPV6 VLPs with substitutions derived from the 346-349 region; in addition, H11.G131S.G3 binds HPV6 VLPs with substitutions derived only from the 263-290 region.
Analysis of human papillomavirus type 16 E6 variants in relation to p53 codon 72 polymorphism genotypes in cervical carcinogenesis.
PMID: 10644829
2000
The Journal of general virology
Abstract: An initial sequence analysis of HPV-16 long control, E6 and E7 regions of 53 well-defined cervical samples containing HPV-16 revealed that a T to G transition at nucleotide position 350 within the E6 open reading frame was the most common variation, the frequency of which seemed to decrease with increasing severity of the lesion.
Absence of antibody against human papillomavirus type 16 E6 and E7 in patients with cervical cancer is independent of sequence variations.
PMID: 10783118
2000
The Journal of infectious diseases
Abstract: All E6 antigens (the prototype and the variants 350G?L83V, 131G?R10G/350G?L83V, 335T?H78Y/350G?L83V, 345G?Y81C/350G?L83V, and African 2 ?Af2) showed cross-reactivity by RIPA.
Analysis of relative binding affinity of E7-pRB of human papillomavirus 16 clinical variants using the yeast two-hybrid system.
Abstract: A T663G/C24W polymorphic change in E7 correlated with a decrease in E7-pRb relative binding affinity the significance of which remains to be clarified.
Abstract: In E7, two novel but silent polymorphic sites G663A (41.2%) and T846C (88.2%) were also prevalent in the samples analyzed.
Abstract: Particularly, a prevalent (64.7%) E6 polymorphic site A442C with an E113D amino acid substitution seems specific to Taiwanese patients.
Enhanced oncogenicity of human papillomavirus type 16 (HPV16) variants in Japanese population.
Abstract: Most of the malignant HPV16 variants contain a common mutation, L83V, in the E6 oncoprotein.
Abstract: Prototype HPV16 and its E6 variant L83V are both prevalent in preinvasive and invasive cervical lesions in Swedish women.
Abstract: The HPV16 E6 variant L83V was present in 40% of the HCIN lesions, in 54% of the invasive adenocarcinomas, in comparison to 81% of the invasive squamous carcinomas.
Abstract: These HPV16-positive cases were evaluated with analysis of the E6 gene, using a recently described PC
Intratype sequence variation among clinical isolates of the human papillomavirus type 6 L1 ORF: clustering of mutations and identification of a frequent amino acid sequence variant.
PMID: 10211973
1999
The Journal of general virology
Abstract: The R3 region contains predominantly non-silent substitutions, the most common of which is a G-to-C substitution at position 7079.
Abstract: This results in a Glu-to-Gln change at aa 431, although this change had no effect on VLP yield or stability.
Characterization of a major neutralizing epitope on human papillomavirus type 16 L1.
Abstract: Alteration of the amino acid at position 50, from L to F, completely restored H16.V5 binding and partially restored H16.E70 binding, while complete restoration of H16.E70 binding occurred with GU-2 VLPs containing both L50F and T266A alterations.
Abstract: The L50F mutant of GU-2 L1, in which the H16.V5 epitope was restored, elicited HPV-16 antibody responses comparable to those obtained with 114K VLPs.
Mutational and functional analysis of HPV-16 URR derived from Korean cervical neoplasia.
Abstract: Additionally, C-->T transition at nt 7785 (YY1-binding site 3; from 7781 to 7790) was found in 2 of 3 patients.
Abstract: Selective mutations were observed at the YY1 binding sites of HPV-16 URR in the 3 patients with invasive cervical cancer who have the episomal forms of HPV-16 DNA: A-->C transition at nt 7484 and G-->A transition at nt 7488 (YY1-binding site 2; from 7481 to 7489).
Uniform distribution of HPV 16 E6 and E7 variants in patients with normal histology, cervical intra-epithelial neoplasia and cervical cancer.
PMID: 10389753
1999
International journal of cancer
Abstract: Of all variants identified, the E6 variant 350G (L83V) and the E7 variant 822G were most frequently detected irrespective of histology and showed prevalence rates of 27% to 43% and 7% to 20%, respectively.
HPV mutation literature information.
PMID: 
2000
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