The prevalence of HPV-18 and variants of E6 gene isolated from cervical cancer patients in Taiwan

Chang, Chih-Hsiung; Chen, Tze-Ho; Hsu, Reuy-Chang; Chou, Pan-Hsin; Yang, Jaw‐Ji; Hwang, Guang-Yuh

doi:10.1016/j.jcv.2004.06.011

Cited by 10 publications

(9 citation statements)

References 28 publications

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“…Furthermore, the guanine at E6 coding region nt183 is represented as HPV-18 prototype (AY262282). These results are in good agreement with a study by Chang et al [26] in Taiwan, who reported the identical nucleotide variation, and suggests that the C to G variation at nt287 may be a common mutation worldwide. Since this frequent variant is a silent mutation, it may be used as a biomarker to track and study viral transmission [26].…”

Section: Discussionsupporting

confidence: 92%

“…In this study, we described the HPV-18 intratypic diversity over a span of 7000 nucleotides among isolates from southwest China. Our data set on E1, E2, E4, E5, E6, E7, L1 and L2 sequence variations of HPV-18 complements and expands on previous descriptions of HPV-18 variants, which were based on a targeted analysis of E6, LCR-E6, E2, L1 and URR [23], [25], [26].…”

Section: Discussionmentioning

confidence: 56%

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Sequence Variation Analysis of HPV-18 Isolates in Southwest China

Shen

Ding

et al. 2013

PLoS ONE

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Intratypic variations of HPV-18 are known to differ in the persistence of the infection, frequency of carcinogenesis and the progression of precursor lesions to advanced cervical cancer. This study was designed to analyze sequence variations of HPV-18 isolates in order to discover novel HPV-18 variants and to evaluate the variations among infected women in southwest China. Cervical biopsies from 56 HPV-18-positive women with cervical neoplasia were assayed by PCR amplification and sequencing of all eight genes (E1, E2, E4, E5, E6, E7, L1, L2) of the HPV-18 genome. The most frequently observed variation was a C to G transversion at nucleotide 287 of E6, which was found in 48.2% of samples. Analysis of E7 revealed only one specimen as having sequence variations. In addition, we have identified several novel variations: A551C in E6, G6906A in L1, and C4915T and C5147A in L2. The mutations in E6 and L2 are silent, while the E7 mutation results in a single amino acid change. This study complements and expands on previous descriptions of HPV-18 variants. The sequence variation data presented here provides a foundation for future research on HPV-induced oncogenesis and may prove valuable for developing diagnostic probes and in the design of HPV vaccines for targeted populations.

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Section: Discussionsupporting

confidence: 92%

Section: Discussionmentioning

confidence: 56%

Sequence Variation Analysis of HPV-18 Isolates in Southwest China

Shen

Ding

et al. 2013

PLoS ONE

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“…This study showed that HPV 18 E6 nucleotide mutations led to 2 silent variations, nucleotide T485C and nucleotide C549A, which have been reported before in China [Wu et al, ]. Another silent variant of HPV 18 E6, C183G, was also reported in Taiwan women [Chang et al, ].…”

Section: Discussionmentioning

confidence: 94%

Prevalence of HPV and variation of HPV 16/HPV 18 E6/E7 genes in cervical cancer in women in South West China

Yang

et al. 2014

Journal of Medical Virology

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Genetic variations of High-Risk HPV E6/E7 may be associated with the development of cervical cancer in specific geographic regions. Few data have been reported about the HPV prevalence and E6/E7 variants among cervical cancer patients in Southwest China. This study was designed to investigate the prevalence of HPV and E6/E7 variants of most prevalent HPV among cervical cancer patients in Southwest China. After genotyping, E6/E7 genes of most prevalent HR HPV samples were sequenced and analyzed. Phylogenetic trees were then constructed, followed by an analysis of the diversity of secondary structure and selection pressures. HPV 16 (73.8%) and HPV 18 (16.4%) are the most prevalent infection types among cervical cancer patients, followed by HPV 58, HPV 56 and HPV 59, which is different from the high HPV 58 infection rate of outpatients in this region. Eighteen single nucleotide changes were observed in HPV 16 E6 with 13/18 non-synonymous mutations (5 in beta sheet and 2 in alpha helix). Ten single nucleotide changes were identified among HPV 16 E7 with 3/10 non-synonymous mutations. Three single nucleotide changes were observed in HPV 18 E6 with one non-synonymous mutation, and only one synonymous mutation was identified in HPV 18 E7. HPV 16 E6-D25E, E7-N29S and E7-T846C (S95S) exhibited a prevalent linkage mutation. The phylogenetic tree demonstrates that European and Asian lineages were the main patterns. This study may help understand the intrinsic geographical relatedness and oncogenic potential of HR HPV and contributes further to research of diagnostic, therapeutic and therapeutic vaccine strategy.

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Section: Introductionmentioning

confidence: 99%

“…It reacts with E6-AP and form an ubiquitin-protein ligase a process leading to degradation of the P 53 gene. 4 It also targets NFX1-9 cellular protein which normally represses reduction in telomerase (a protein that make cells to divide unlimited times) and consequently keep cell growth uncheck.5 E6 acts as a translational co-factor, specifically transcription activator when interacting with cellular transcription factor E2F/DP1. The interaction of E6 with membrane associated granulocytes kinase family (MAGUK) protein ABSTRACT Background: Epidemiological, clinical and molecular studies have established the link between genital infection with high risk human papillomavirus (HPV) and cervical cancer but there is great challenge in establishing early infection by both clinicians and the laboratories.…”

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confidence: 99%

Molecular detection of HPV 16/18 E6 genes from cervical cells

Auwal

Rogo

2015

Int J Res Med Sci

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INTRODUCTIONHuman papillomaviruses (especially types 16 and 18) are the causative agents of cervical cancer, 1 the second leading female cancer in the world; the most frequently reported cancer in most developing countries and the principal cause of mortality from cancer in general. The virus encodes for 2 oncoproteins E6 and E7 which directly contribute towards initiation and maintenance of tumour development.2 Protein products of these genes interfere with the normal function of tumour suppressor genes. E7 binds and inactivate retinoblastoma protein RB while E6 binds P 53 protein and directs its degradation leading to resistance to apoptosis, uncensored cell growth and malignant transformation. 3 E6 is of particular interest because of its multiple roles in the cell and in interacting with many other proteins. It reacts with E6-AP and form an ubiquitin-protein ligase a process leading to degradation of the P 53 gene. 4 It also targets NFX1-9 cellular protein which normally represses reduction in telomerase (a protein that make cells to divide unlimited times) and consequently keep cell growth uncheck.5 E6 acts as a translational co-factor, specifically transcription activator when interacting with cellular transcription factor E2F/DP1. The interaction of E6 with membrane associated granulocytes kinase family (MAGUK) protein ABSTRACT Background: Epidemiological, clinical and molecular studies have established the link between genital infection with high risk human papillomavirus (HPV) and cervical cancer but there is great challenge in establishing early infection by both clinicians and the laboratories. The virus cannot be grown in conventional cell cultures and serology cannot different between active and past infection. Molecular studies remain the goal standard as it detects viral nucleic acid or cellular antigens indicative of oncogenic potential in cytology or biopsy specimen. The study was aimed to molecularly determine the presence of HPV 16/18 and expression of E6 gene in squamous intraepithelial lesions. Methods: Cervical cells were collected from 18 women with positive cytology test results and 32 controls in gynaecology clinic of Murtala Muhammad Specialist Hospital, Kano Nigeria and HPV 16/18 were detected with E6 gene specific PCR primers. Results: Overall, HPV E6 gene was found in 76% of the women, 88.3% of positive cytology specimens and 71.2% controls. Conclusions: There is very high prevalence of HPV infection. The presence of HPV 16/18 E6 genes in cervical intraepithelial lesions may serve as a useful predictor of diagnosis and possible clinical outcome of the disease.

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The prevalence of HPV-18 and variants of E6 gene isolated from cervical cancer patients in Taiwan

Cited by 10 publications

References 28 publications

Sequence Variation Analysis of HPV-18 Isolates in Southwest China

Sequence Variation Analysis of HPV-18 Isolates in Southwest China

Prevalence of HPV and variation of HPV 16/HPV 18 E6/E7 genes in cervical cancer in women in South West China

Molecular detection of HPV 16/18 E6 genes from cervical cells

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