scholarly journals Analysis of mutations in the E6/E7 oncogenes and L1 gene of human papillomavirus 16 cervical cancer isolates from China

2006 ◽  
Vol 87 (5) ◽  
pp. 1181-1188 ◽  
Author(s):  
Yuping Wu ◽  
Yulong Chen ◽  
Longyu Li ◽  
Guifang Yu ◽  
Ying He ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Patients ◽  
Hpv Infection ◽  
Typing Method ◽  
Hpv16 E6 ◽  
Human Papillomavirus 16 ◽  
Human Papillomavirus Type 16 ◽  
New Variant

Human papillomavirus type 16 (HPV16) has a number of intratypic variants; each has a different geographical distribution and some are associated with enhanced oncogenic potential. Cervical samples were collected from 223 cervical cancer patients and from 196 age-matched control subjects in China. DNA samples were amplified by using primers specific for the E6, E7 and partial L1 regions. Products were sequenced and analysed. It was found by using a PCR–sequence-based typing method that HPV infection rates in China were 92·8 % in cervical cancer patients and 15·8 % in healthy controls. HPV16 was detected in 70·4 % of cervical cancer patients and in 6·1 % of controls. In HPV16-positive cervical cancers, 23·6 % belonged to the prototype, 65·5 % were of the Asian variant, 5·5 % were of African type 1 and 3·6 % were European variants, whilst only one was a new variant that differed from any variant published so far. Prevalences of HPV16 E6 D25E and E113D variants were 67·3 and 9 %, respectively. In addition to D25E and E113D, the following E6 variations were found in this study: R129K, E89Q, S138C, H78Y, L83V and F69L. The results also showed that the prevalences of three hot spots of E7 nucleotide variation, N29S, S63F and a silent variation, nt T846C, were 70·2 % (33/47), 51·1 % (24/47) and 61·7 % (29/47), respectively. The following L1 variations were found in this study: S377A, K387E, E378D, K382E and T379P. It was also found that the average age of Asian variant-positive cervical cancer patients (42·98±10·43 years) was 7·56 years lower than that of prototype-positive patients (50·54±10·91). It is suggested that the high frequency of HPV16 Asian variants might contribute to the high incidence of cervical cancer in China.

scholarly journals Increase of human papillomavirus-16 E7-specific T helper type 1 response in peripheral blood of cervical cancer patients after radiotherapy

Immunology ◽  
2009 ◽  
Vol 126 (4) ◽  
pp. 523-534 ◽  
Author(s):  
Félix Giovanni Delgado ◽  
Elizabeth Martínez ◽  
María Angélica Céspedes ◽  
María Mercedes Bravo ◽  
María Cristina Navas ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Patients ◽  
Peripheral Blood ◽  
T Helper ◽  
Human Papillomavirus 16 ◽  
Helper Type

scholarly journals Cytotoxic T-Lymphocyte Responses to Human Papillomavirus Type 16 E5 and E7 Proteins and HLA-A*0201-Restricted T-Cell Peptides in Cervical Cancer Patients

2007 ◽  
Vol 81 (6) ◽  
pp. 2869-2879 ◽  
Author(s):  
Dai-Wei Liu ◽  
Yuh-Cheng Yang ◽  
Ho-Fan Lin ◽  
Mei-Fang Lin ◽  
Ya-Wen Cheng ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
T Cell ◽  
Cancer Patients ◽  
T Lymphocyte ◽  
Cytotoxic T Lymphocyte ◽  
Hpv 16 ◽  
Human Papillomavirus Type 16 ◽  
E5 Protein ◽  
E7 Proteins

ABSTRACT Previously, we found that human papillomavirus type 16 (HPV-16) E5 protein is a tumor rejection antigen and can induce cytotoxic T-lymphocyte (CTL) activity. Therefore, in this study, human leukocyte antigen A*0201 (HLA-A*0201)-restricted human CTL epitopes of HPV-16 E5 protein were identified using a bioinformatics approach, and the abilities of these predicted peptides to induce an immune response in HLA-A*0201 transgenic mice were confirmed by assaying E5-specific CTLs and in vitro-generated CTLs from normal peripheral blood T lymphocytes of HLA-A2-positive human donors. Second, the CTL responses to HLA-A*0201 CTL epitopes (E5 63-71 and E7 11-20) were examined in HPV-16-infected patients with HLA-A2. Third, the effect of HLA-A-type alleles on CTL activities in response to the entire E5 and E7 proteins was examined in cervical cancer patients. E5 and E7 peptides (but not the whole proteins) stimulated E5- and E7-specific CTL recall responses in HPV-16- and HLA-A2-positive cervical cancer patients, and HPV-16 E5 and E7 proteins stimulated naïve T cells in HPV-16-negative cervical cancer patients with HLA-A11 and -A24 haplotypes. In summary, this is the first demonstration that E5 63-71 is an HLA-A*0201-restricted T-cell epitope of HPV-16 E5.

scholarly journals E6^E7, a Novel Splice Isoform Protein of Human Papillomavirus 16, Stabilizes Viral E6 and E7 Oncoproteins via HSP90 and GRP78

mBio ◽  
2015 ◽  
Vol 6 (1) ◽  
Author(s):  
Masahiko Ajiro ◽  
Zhi-Ming Zheng
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Critical Role ◽  
Splice Isoforms ◽  
Hpv16 E6 ◽  
Human Papillomavirus 16 ◽  
Hpv18 E6 ◽  
Splice Isoform ◽  
E6 And E7

ABSTRACTTranscripts of human papillomavirus 16 (HPV16) E6 and E7 oncogenes undergo alternative RNA splicing to produce multiple splice isoforms. However, the importance of these splice isoforms is poorly understood. Here we report a critical role of E6^E7, a novel isoform containing the 41 N-terminal amino acid (aa) residues of E6 and the 38 C-terminal aa residues of E7, in the regulation of E6 and E7 stability. Through mass spectrometric analysis, we identified that HSP90 and GRP78, which are frequently upregulated in cervical cancer tissues, are two E6^E7-interacting proteins responsible for the stability and function of E6^E7, E6, and E7. Although GRP78 and HSP90 do not bind each other, GRP78, but not HSP90, interacts with E6 and E7. E6^E7 protein, in addition to self-binding, interacts with E6 and E7 in the presence of GRP78 and HSP90, leading to the stabilization of E6 and E7 by prolonging the half-life of each protein. Knocking down E6^E7 expression in HPV16-positive CaSki cells by a splice junction-specific small interfering RNA (siRNA) destabilizes E6 and E7 and prevents cell growth. The same is true for the cells with a GRP78 knockdown or in the presence of an HSP90 inhibitor. Moreover, mapping and alignment analyses for splicing elements in 36 alpha-HPVs (α-HPVs) suggest the possible expression of E6^E7 mostly by other oncogenic or possibly oncogenic α-HPVs (HPV18, -30, -31, -39, -42, -45, -56, -59, -70, and -73). HPV18 E6^E7 is detectable in HPV18-positive HeLa cells and HPV18-infected raft tissues. All together, our data indicate that viral E6^E7 and cellular GRP78 or HSP90 might be novel targets for cervical cancer therapy.IMPORTANCEHPV16 is the most prevalent HPV genotype, being responsible for 60% of invasive cervical cancer cases worldwide. What makes HPV16 so potent in the development of cervical cancer remains a mystery. We discovered in this study that, besides producing two well-known oncoproteins, E6 and E7, seen in other high-risk HPVs, HPV16 produces E6^E7, a novel splice isoform of E6 and E7. E6^E7, in addition to self-interacting, binds cellular chaperone proteins, HSP90 and GRP78, and viral E6 and E7 to increase the steady-state levels and half-lives of viral oncoproteins, leading to cell proliferation. The splicingciselements in the regulation of HPV16 E6^E7 production are highly conserved in 11 oncogenic or possibly oncogenic HPVs, and we confirmed the production of HPV18 E6^E7 in HPV18-infected cells. This study provides new insight into the mechanism of splicing, the interplay between different products of the polycistronic viral message, and the role of the host chaperones as they function.

scholarly journals Concordance of Human Papillomavirus Type 16 and 18 in Cervical and Oral Specimen of Cervical Cancer Patients

2019 ◽  
pp. 70
Author(s):  
Willy Akbar ◽  
Syahrul Rauf ◽  
Deviana S. Riu ◽  
St. Maisuri T. Chalid
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Oral Cavity ◽  
Cancer Patients ◽  
Oral Fluid ◽  
Cross Sectional Study ◽  
Cross Sectional ◽  
Hpv 16 ◽  
Human Papillomavirus Type 16 ◽  
Oral Hpv

Abstract Objective : To determine the conformity of HPV type 16 and 18 in cervical and oral/buccal specimens from cervical cancer patients. Methods :A cross-sectional study was conducted in March - September 2016 at several hospitals in Makassar. HPV 16 and 18 genotyping in cervical and oral fluid of 77 patients with cervical cancer performed with PCR method. Results : The prevalence of HPV type 18 infection both in the cervical and the oral fluid was higher than HPV type 16 [9(47.4%) vs 5(26.3%)]. The aggreement of HPV type 18 infection (r=0.328;p=0.000) in the cervical-oral sites was higher than HPV type 16 (r=0.194;p=0.042). Conclusion : HPV type 16 and 18 could infect both cervix and oral cavity although type-specific concordance is low. Keywords :Human papillomavirus,servix, oral cavity   Abstrak Tujuan: Mengetahui tingkat kesesuaian hasil pemeriksaan HPV tipe 16 dan 18 antara spesimen serviks dan oral/buccal pada penderita kanker serviks. Metode: Penelitian cross sectional ini dilakukan pada Maret – September 2016 pada beberapa rumah sakit di Makassar. Pemeriksaan HPV 16 dan 18 pada cairan serviks dan oral dari 77 orang penderita kanker serviks menggunakan teknik PCR. Hasil: Prevalensi infeksi bersama pada serviks dan oral HPV tipe 18 lebih tinggi dibandingkan HPV tipe 16 [9(47,4%) vs 5(26,3%)]. Tingkat kesesuaian antara HPV tipe 18 (r=0,328;p=0,000) pada serviks dan oral lebih tinggi dibandingkan tipe 16 (r=0,194;p=0,042). Kesimpulan: HPV tipe 16 dan 18 dapat menginfeksi serviks dan oral meskipun tingkat kesesuaian kedua tipe ini lemah. Kata kunci : Human papillomavirus, serviks, kavum oral

scholarly journals Phylogenetic Analysis of Human Papillomavirus 16 and 52 L1 Gene from Cervical Cancer in Bandung, Indonesia

2018 ◽  
Vol 10 (1) ◽  
pp. 40
Author(s):  
Mutia Latief ◽  
Ika Agus Rini ◽  
Gita Widya Pradini ◽  
Gatot Nyarumenteng Adhipurnawan Winarno ◽  
Edhyana Sahiratmadja ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Cancer Patients ◽  
Southwest China ◽  
Multiple Infections ◽  
Hpv 16 ◽  
Human Papillomavirus 16 ◽  
Tree Construction ◽  
High Risk Type ◽  
Cancer Multiple

BACKGROUND: Chronic infection with high-risk type of human papillomavirus (HPV) can cause cervical cancer. Previous studies showed that multiple infections of HPV are found in cervical cancer caused by multiple HPV infections and the most common are HPV-16 and HPV-52. The origin of HPV-16 circulating in Indonesia varies. The purpose of this study was to explore the origin of multiple infections of HPV-52 and HPV-16 in cervical cancer by using a phylogenetic tree.METHODS: During July-November 2010, 100 women were diagnosed with cervical cancer in the Department of Obstetrics and Gynecology, Dr. Hasan Sadikin General Hospital, Bandung, Indonesia. Only 96 patients were involved in this study. Ninety-six samples of HPV deoxyribonucleic acid (DNA) were isolated from biopsied tissue of cervical cancer. Multiple infections of HPV genotypes HPV-16 and HPV-52 were confirmed by using the linear assay for HPV genotyping test. Afterward,HPV-52L1 gene was amplified by using self-designed primer. L1 gene was also sequenced and analyzed using phylogenetic program (MEGA6.06).RESULTS: The result of phylogenetic tree construction showed that isolated HPV-52 originated from multiple infections of HPV-16 and HPV-52 from cervical cancer patients in Bandung were in a subgroup with isolates originating from EU077219 Canada (America) and KT799980 southwest China (Asia). Isolate HPV-16 in one subgroup with isolates originating from KU951191.1 (Southwest China).CONCLUSION: L1 gene sequence from multiple infections isolated from HPV-16 and HPV-52 from cervical cancer patients in Bandung refers to the variation of L1 gene reported from Canada and southwest China. This proves that Indonesia’s HPV clusters are located in the strains found in America and Asia.KEYWORDS: multiple infections, HPV-16, HPV-52, L1 gene, phylogenetic

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