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 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 Human Papillomavirus Type 16 and 18 E7-Pulsed Dendritic Cell Vaccination of Stage IB or IIA Cervical Cancer Patients: a Phase I Escalating-Dose Trial

2007 ◽  
Vol 82 (4) ◽  
pp. 1968-1979 ◽  
Author(s):  
Alessandro D. Santin ◽  
Stefania Bellone ◽  
Michela Palmieri ◽  
Alessandro Zanolini ◽  
Antonella Ravaggi ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
T Cell ◽  
Dendritic Cell ◽  
Cancer Patients ◽  
Delayed Type Hypersensitivity ◽  
Human Papillomavirus Type 16 ◽  
Stage Ib ◽  
Hpv E7 ◽  
E7 Antigen

ABSTRACT The safety and immunogenicity of the human papillomavirus type 16 (HPV16) or HPV18 (HPV16/18) E7 antigen-pulsed mature dendritic cell (DC) vaccination were evaluated for patients with stage IB or IIA cervical cancer. Escalating doses of autologous DC (5, 10, and 15 × 106 cells for injection) were pulsed with recombinant HPV16/18 E7 antigens and keyhole limpet hemocyanin (KLH; an immunological tracer molecule) and delivered in five subcutaneous injections at 21-day intervals to 10 cervical cancer patients with no evidence of disease after they underwent radical surgery. Safety, toxicity, delayed-type hypersensitivity (DTH) reaction, and induction of serological and cellular immunity against HPV16/18 E7 and KLH were monitored. DC vaccination was well tolerated, and no significant toxicities were recorded. All patients developed CD4+ T-cell and antibody responses to DC vaccination, as detected by enzyme-linked immunosorbent spot (ELISpot) and enzyme-linked immunosorbent assays (ELISA), respectively, and 8 out of 10 patients demonstrated levels of E7-specific CD8+ T-cell counts, detected by ELISpot during or immediately after immunization, that were increased compared to prevaccination baseline levels. The vaccine dose did not predict the magnitude of the antibody or T-cell response or the time to detection of HPV16/18 E7-specific immunity. DTH responses to intradermal injections of HPV E7 antigen and KLH were detected for all patients after vaccination. We conclude that HPV E7-loaded DC vaccination is safe and immunogenic for stage IB or IIA cervical cancer patients. Phase II E7-pulsed DC-based vaccination trials with cervical cancer patients harboring a limited tumor burden, or who are at significant risk of tumor recurrence, are warranted.

scholarly journals A novel CD4 T-cell epitope described from one of the cervical cancer patients vaccinated with HPV 16 or 18 E7-pulsed dendritic cells

2008 ◽  
Vol 58 (2) ◽  
pp. 309-309
Author(s):  
Xuelian Wang ◽  
Alessandro D. Santin ◽  
Stefania Bellone ◽  
Sushil Gupta ◽  
Mayumi Nakagawa
Keyword(s):  
Cervical Cancer ◽  
Dendritic Cells ◽  
T Cell ◽  
Cancer Patients ◽  
Cell Epitope ◽  
Cd4 T Cell ◽  
T Cell Epitope ◽  
Hpv 16

scholarly journals Multiple ASF/SF2 Sites in the Human Papillomavirus Type 16 (HPV-16) E4-Coding Region Promote Splicing to the Most Commonly Used 3′-Splice Site on the HPV-16 Genome

2010 ◽  
Vol 84 (16) ◽  
pp. 8219-8230 ◽  
Author(s):  
Monika Somberg ◽  
Stefan Schwartz
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Splice Site ◽  
Binding Sites ◽  
Mrna Levels ◽  
Coding Region ◽  
Cervical Lesions ◽  
Hpv 16 ◽  
Human Papillomavirus Type 16 ◽  
E6 And E7

ABSTRACT Our results presented here demonstrate that the most abundant human papillomavirus type 16 (HPV-16) mRNAs expressing the viral oncogenes E6 and E7 are regulated by cellular ASF/SF2, itself defined as a proto-oncogene and overexpressed in cervical cancer cells. We show that the most frequently used 3′-splice site on the HPV-16 genome, site SA3358, which is used to produce primarily E4, E6, and E7 mRNAs, is regulated by ASF/SF2. Splice site SA3358 is immediately followed by 15 potential binding sites for the splicing factor ASF/SF2. Recombinant ASF/SF2 binds to the cluster of ASF/SF2 sites. Mutational inactivation of all 15 sites abolished splicing to SA3358 and redirected splicing to the downstream-located, late 3′-splice site SA5639. Overexpression of a mutant ASF/SF2 protein that lacks the RS domain, also totally inhibited the usage of SA3358 and redirected splicing to the late 3′-splice site SA5639. The 15 ASF/SF2 binding sites could be replaced by an ASF/SF2-dependent, HIV-1-derived splicing enhancer named GAR. This enhancer was also inhibited by the mutant ASF/SF2 protein that lacks the RS domain. Finally, silencer RNA (siRNA)-mediated knockdown of ASF/SF2 caused a reduction in spliced HPV-16 mRNA levels. Taken together, our results demonstrate that the major HPV-16 3′-splice site SA3358 is dependent on ASF/SF2. SA3358 is used by the most abundantly expressed HPV-16 mRNAs, including those encoding E6 and E7. High levels of ASF/SF2 may therefore be a requirement for progression to cervical cancer. This is supported by our earlier findings that ASF/SF2 is overexpressed in high-grade cervical lesions and cervical cancer.

HPV16-specific cytotoxic T lymphocyte responses are detected in all HPV16-positive cervical cancer patients

2005 ◽  
Vol 96 (1) ◽  
pp. 92-102 ◽  
Author(s):  
Victor Valdespino ◽  
Clara Gorodezky ◽  
Vianney Ortiz ◽  
Andreas M. Kaufmann ◽  
Edgar Roman-Basaure ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Cancer Patients ◽  
T Lymphocyte ◽  
Cytotoxic T Lymphocyte ◽  
Lymphocyte Responses

scholarly journals Immuno-chromatographic Analysis for HPV-16 and 18 E7 Proteins as a Biomarker of Cervical Cancer Caused by Human Papillomavirus

2009 ◽  
Vol 30 (12) ◽  
pp. 2999-3005 ◽  
Author(s):  
Joo-Ho Kim ◽  
Il-Hoon Cho ◽  
Sung-Min Seo ◽  
Ji-Sook Kim ◽  
Kyu-Ha Oh ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Human Papillomavirus ◽  
Chromatographic Analysis ◽  
Hpv 16 ◽  
E7 Proteins

scholarly journals Human Papillomavirus Type 16 E7 Peptide-Directed CD8+ T Cells from Patients with Cervical Cancer Are Cross-Reactive with the Coronavirus NS2 Protein

2003 ◽  
Vol 77 (9) ◽  
pp. 5464-5474 ◽  
Author(s):  
Katja Nilges ◽  
Hanni Höhn ◽  
Henryk Pilch ◽  
Claudia Neukirch ◽  
Kirsten Freitag ◽  
...  
Keyword(s):  
Cervical Cancer ◽  
Immune Response ◽  
T Cells ◽  
Human Papillomavirus ◽  
T Cell ◽  
T Cell Responses ◽  
Cross Reactivity ◽  
Antiviral Immune Response ◽  
Human Papillomavirus Type 16 ◽  
Cell Responses

ABSTRACT Human papillomavirus type 16 (HPV16) E6 and E7 oncoproteins are required for cellular transformation and represent candidate targets for HPV-specific and major histocompatibility complex class I-restricted CD8+-T-cell responses in patients with cervical cancer. Recent evidence suggests that cross-reactivity represents the inherent nature of the T-cell repertoire. We identified HLA-A2 binding HPV16 E7 variant peptides from human, bacterial, or viral origin which are able to drive CD8+-T-cell responses directed against wild-type HPV16 E7 amino acid 11 to 19/20 (E711-19/20) epitope YMLDLQPET(T) in vitro. CD8+ T cells reacting to the HLA-A2-presented peptide from HPV16 E711-19(20) recognized also the HLA-A2 binding peptide TMLDIQPED (amino acids 52 to 60) from the human coronavirus OC43 NS2 gene product. Establishment of coronavirus NS2-specific, HLA-A2-restricted CD8+-T-cell clones and ex vivo analysis of HPV16 E7 specific T cells obtained by HLA-A2 tetramer-guided sorting from PBL or tumor-infiltrating lymphocytes obtained from patients with cervical cancer showed that cross-reactivity with HPV16 E711-19(20) and coronavirus NS252-60 represents a common feature of this antiviral immune response defined by cytokine production. Zero of 10 patients with carcinoma in situ neoplasia and 3 of 18 patients with cervical cancer showed ≥0.1% HPV16 E7-reactive T cells in CD8+ peripheral blood lymphocytes. In vivo priming with HPV16 was confirmed in patients with cervical cancer or preinvasive HPV16-positive lesions using HLA-A2 tetramer complexes loaded with the E6-derived epitope KLPQLCTEL. In contrast, we could not detect E6-reactive T cells in healthy individuals. These data imply that the measurement of the HPV16 E711-19(20) CD8+-T-cell response may reflect cross-reactivity with a common pathogen and that variant peptides may be employed to drive an effective cellular immune response against HPV.

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