A deletion and point mutation study of the human papillomavirus type 16 major capsid gene

Varsani, Arvind; Williamson, Anna‐Lise; Jaffer, Mohamed A.; Rybicki, Edward P.

doi:10.1016/j.virusres.2006.07.012

Cited by 32 publications

(25 citation statements)

References 45 publications

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“…In addition, although there was no genetic change in the primary lesion, we found point mutations in the base sequences of the E6 and E7 genes of HPV in the metastatic lesions, as well as a difference in the amino acid sequence in the E6 protein. There have been some reports that point mutations in HPV genes have been detected in various tumor cells and that these point mutations contribute to the occurrence of malignancy 10–12 . Although we were unable to identify the roles played by the point mutations of these genes in carcinogenesis, this is the first report of findings of point mutations of HPV DNA in metastatic lesions but not in the primary lesion of Bowen’s carcinoma.…”

Section: Discussionmentioning

confidence: 55%

“…There have been some reports that point mutations in HPV genes have been detected in various tumor cells and that these point mutations contribute to the occurrence of malignancy. [10][11][12] Although we were unable to identify the roles played by the point mutations of these genes in carcino-(a) (b) Figure 4 In situ hybridization in both (a) primary and (b) metastatic lesions revealed HPV DNA indicated by small blue dots inside the nuclei of tumor cells. Some cells contained only one dot, but these were all identical in shape; other cells contained groups of several smaller dots genesis, this is the first report of findings of point mutations of HPV DNA in metastatic lesions but not in the primary lesion of Bowen's carcinoma.…”

Section: Discussionmentioning

confidence: 99%

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Detection of human papillomavirus type 16 in Bowen’s carcinoma of the toe

et al. 2012

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Section: Discussionmentioning

confidence: 55%

Section: Discussionmentioning

confidence: 99%

Detection of human papillomavirus type 16 in Bowen’s carcinoma of the toe

et al. 2012

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“…Moreover, the deletion of 22 amino acids in HPV 16 L1 protein did not have any effect on the assembly of T=7 VLPs. Most of the C-terminal-deleted L1 variant formed T=7 VLPs (Varsani et al [2006]). Bian et al reported that HPV 16 L1 ΔC34 (deleted 34 amino acids at its C-terminus) fused with an N-terminal domain (1–70 amino acids) of HPV E7 formed 11–12 nm of capsomeres, but not as large as VLPs (Bian et al [2008]).…”

Section: Resultsmentioning

confidence: 99%

Expression of human papillomavirus 6b L1 protein in silkworm larvae and enhanced green fluorescent protein displaying on its virus-like particles

2012

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Human papillomavirus (HPV) 6b L1 capsid protein was expressed using the Bombyx mori nucleopolyhedrovirus (BmNPV) bacmid expression system in silkworm larvae. Two constructs, full-length L1 (500 a.a) and C-terminal-deleted short L1 (479 a.a), and three PCR-manipulated antigenic loops at amino acids 55–56, 174–175, and 348–349 regions were incorporated with whole enhanced green fluorescent protein (EGFP). Expressed in full, short L1 proteins and variants were purified in heparin affinity column chromatography and confirmed by SDS-PAGE and western blot. The presence of self-assembled virus-like particles (VLPs) and EGFP incorporation on the surface of VLPs were confirmed by the observation of transmission electron and immunoelectron microscopies, respectively. HPV 6b L1 major capsid protein was successfully expressed in silkworm, and effective manipulation on the antigenic regions showed the path to versatile vaccine development based on HPV L1-VLPs.

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“…Polymorphism within these loops is likely to result in the generation of neutralizing antibodies of different binding affinities due to the presence of different HPV types displaying distinct features on their surfaces [14]. Given that the prevalence of cervical cancer varies in different regions and countries, a number of studies have addressed the possible association of E6 based HPV16 variant status with different risks for progression to malignancy and suggested that HPV variants can influence the viral persistence and development of cervical cancer [15][16][17][18].…”

Section: Introductionmentioning

confidence: 99%

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2017

Bioinformation

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Abstract:HPV L1 protein is a corner stone in HPV structure, it's involved in the formation of the viral capsid; widely used as a systematic material and considered as the main component in vaccines development and production. The present study aims to characterize genetic variation of L1 gene of HPV 16 specimens and to evaluate in silico the impact of major variants on the epitope change affecting its conformational structure. A fragment of L1 gene from 35 HPV 16 confirmed specimens were amplified by PCR and sequenced. Overall, five amino acids residues changes were reported: T390P in 16 specimens, M425I and M431I in 2 cases, insertion of Serine at 460 and aspartic acid deletion at position 477 in all analyzed cases. The 3D generated model showed that T389P amino acid substitution is located in the H-I loop; the two substitutions M424I and M430I are both located in the H2 helice. The Serine insertion and aspartic acid deletion are located in the H4 helice and B-C loop, respectively. Superimposition of sequences' structures showed that they share a very similar conformation highlighting that the reported amino acids variations don't affect the structure of the L1 protein. However T389P, located in the H-I loop identified as an immunogenetic region of L1 capsid, was reported in 51.4% of cases could interact with vaccines induced monoclonal antibodies suggesting a potential impact on the efficacy of available anti-HPV vaccines.Keywords: HPV 16, L1 protein, genetic variation, in silico prediction, vaccine Background:Worldwide, Cervical cancer is the fourth most common cancer in women, with an estimated 528,000 new cases in 2012, and more than 85% of the global burden occurs in developing countries, where it accounts for 13% of all female cancer [1]. There's evidence that persistent infection with high risk Human papillomavirus (HPV) is the main etiological factor in the development of cervical cancer [2]. Of these high-risk types, HPV-16 and HPV-18 are responsible for about 70% of cervical cancers [3]. Human papillomavirus (HPV) genomes are circular dsDNA characterized by eight open reading frames (ORFs), which are all transcribed from the same DNA strand and orientation, and yield two classes of proteins which are classified as non-structural regulatory proteins (E1-E7) and structural proteins L1 and L2 based on their temporal expression. Infectious HPV is primarily composed of 72 pentameric capsomeres of

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A deletion and point mutation study of the human papillomavirus type 16 major capsid gene

Cited by 32 publications

References 45 publications

Detection of human papillomavirus type 16 in Bowen’s carcinoma of the toe

Detection of human papillomavirus type 16 in Bowen’s carcinoma of the toe

Expression of human papillomavirus 6b L1 protein in silkworm larvae and enhanced green fluorescent protein displaying on its virus-like particles

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