Tumour Virus Research最新文献_第5页

Epstein-Barr Virus miR-BARTs 7 and 9 modulate viral cycle, cell proliferation, and proteomic profiles in Burkitt lymphoma Epstein-Barr 病毒 miR-BARTs 7 和 9 调节伯基特淋巴瘤的病毒周期、细胞增殖和蛋白质组特征。

IF 4.3

Tumour Virus Research Pub Date : 2023-12-29 DOI: 10.1016/j.tvr.2023.200276

Brunno Felipe Ramos Caetano , Viviana Loureiro Rocha , Bruno Cesar Rossini , Lucilene Delazari Dos Santos , Deilson Elgui De Oliveira

{"title":"Epstein-Barr Virus miR-BARTs 7 and 9 modulate viral cycle, cell proliferation, and proteomic profiles in Burkitt lymphoma","authors":"Brunno Felipe Ramos Caetano , Viviana Loureiro Rocha , Bruno Cesar Rossini , Lucilene Delazari Dos Santos , Deilson Elgui De Oliveira","doi":"10.1016/j.tvr.2023.200276","DOIUrl":"10.1016/j.tvr.2023.200276","url":null,"abstract":"<div><p>The Epstein-Barr Virus (EBV) encodes viral microRNAs (miRs) that have been implicated in the pathogenesis of nasopharyngeal and gastric carcinomas, yet their potential roles in lymphomas remain to be fully elucidated. This study evaluated the impact of CRISPR/Cas9-mediated knockdown of EBV miRs BART-7 and BART-9 in EBV-positive Burkitt lymphoma cells Akata. As anticipated, the Akata cells subjected to CRISPR/Cas9-mediated knockdown of either EBV BART-7 or BART-9 exhibited a significant reduction in the expression of these viral miRs compared to cells with wild-type (wt) EBV genomes. This outcome effectively validates the experimental model employed in this study. Knocking down either BART-7 or BART-9 resulted in a notable reduction in cell viability and proliferation rates, alongside an elevation in the expression of EBV lytic genes. Global proteomic analysis revealed that the knockdown of EBV BART-7 significantly decreased the expression of ubiquitin/proteasome proteins while concurrently increasing RNA binding proteins (RBPs). Conversely, BART-9 knockdown reduced proteins associated with oxidoreductase activity, particularly those involved in fatty acid metabolism. Our findings unveil previously undiscovered EBV miRs BARTs 7 and 9 roles in cellular pathways relevant to both viral biology and lymphomagenesis.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"17 ","pages":"Article 200276"},"PeriodicalIF":4.3,"publicationDate":"2023-12-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S266667902300023X/pdfft?md5=316875d8e9bcf16995d37e8248320697&pid=1-s2.0-S266667902300023X-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"139075781","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Editorial board member 编辑委员会成员

IF 4.3

Tumour Virus Research Pub Date : 2023-12-01 DOI: 10.1016/S2666-6790(23)00020-4

引用次数: 0

Interplay between the DNA damage response and the life cycle of DNA tumor viruses DNA损伤反应与DNA肿瘤病毒生命周期之间的相互作用。

IF 4.3

Tumour Virus Research Pub Date : 2023-10-31 DOI: 10.1016/j.tvr.2023.200272

Caleb J. Studstill , Michelle Mac , Cary A. Moody

{"title":"Interplay between the DNA damage response and the life cycle of DNA tumor viruses","authors":"Caleb J. Studstill , Michelle Mac , Cary A. Moody","doi":"10.1016/j.tvr.2023.200272","DOIUrl":"10.1016/j.tvr.2023.200272","url":null,"abstract":"<div><p>Approximately 20 % of human cancers are associated with virus infection. DNA tumor viruses can induce tumor formation in host cells by disrupting the cell's DNA replication and repair mechanisms. Specifically, these viruses interfere with the host cell's DNA damage response (DDR), which is a complex network of signaling pathways that is essential for maintaining the integrity of the genome. DNA tumor viruses can disrupt these pathways by expressing oncoproteins that mimic or inhibit various DDR components, thereby promoting genomic instability and tumorigenesis. Recent studies have highlighted the molecular mechanisms by which DNA tumor viruses interact with DDR components, as well as the ways in which these interactions contribute to viral replication and tumorigenesis. Understanding the interplay between DNA tumor viruses and the DDR pathway is critical for developing effective strategies to prevent and treat virally associated cancers. In this review, we discuss the current state of knowledge regarding the mechanisms by which human papillomavirus (HPV), merkel cell polyomavirus (MCPyV), Kaposi's sarcoma-associated herpesvirus (KSHV), and Epstein-Barr virus (EBV) interfere with DDR pathways to facilitate their respective life cycles, and the consequences of such interference on genomic stability and cancer development.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"16 ","pages":"Article 200272"},"PeriodicalIF":4.3,"publicationDate":"2023-10-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666679023000198/pdfft?md5=6c6319fca79ff147cd00c76c5553053f&pid=1-s2.0-S2666679023000198-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"71429056","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Construction of a diagnostic model for hepatitis B-related hepatocellular carcinoma using machine learning and artificial neural networks and revealing the correlation by immunoassay 使用机器学习和人工神经网络构建乙型肝炎相关肝细胞癌的诊断模型，并通过免疫测定揭示相关性。

IF 4.3

Tumour Virus Research Pub Date : 2023-09-27 DOI: 10.1016/j.tvr.2023.200271

Shengke Zhang , Chenglu Jiang , Lai Jiang , Haiqing Chen , Jinbang Huang , Xinrui Gao , Zhijia Xia , Lisa Jia Tran , Jing Zhang , Hao Chi , Guanhu Yang , Gang Tian

{"title":"Construction of a diagnostic model for hepatitis B-related hepatocellular carcinoma using machine learning and artificial neural networks and revealing the correlation by immunoassay","authors":"Shengke Zhang , Chenglu Jiang , Lai Jiang , Haiqing Chen , Jinbang Huang , Xinrui Gao , Zhijia Xia , Lisa Jia Tran , Jing Zhang , Hao Chi , Guanhu Yang , Gang Tian","doi":"10.1016/j.tvr.2023.200271","DOIUrl":"10.1016/j.tvr.2023.200271","url":null,"abstract":"<div><p>HBV infection profoundly escalates hepatocellular carcinoma (HCC) susceptibility, responsible for a majority of HCC cases. HBV-driven immune-mediated hepatocyte impairment significantly fuels HCC progression. Regrettably, inconspicuous early HCC symptoms often culminate in belated diagnoses. Nevertheless, surgically treated early-stage HCC patients relish augmented five-year survival rates. In contrast, advanced HCC exhibits feeble responses to conventional interventions like radiotherapy, chemotherapy, and surgery, leading to diminished survival rates. This investigation endeavors to unearth diagnostic hallmark genes for HBV-HCC leveraging a bioinformatics framework, thus refining early HBV-HCC detection. Candidate genes were sieved via differential analysis and Weighted Gene Co-Expression Network Analysis (WGCNA). Employing three distinct machine learning algorithms unearthed three feature genes (HHIP, CXCL14, and CDHR2). Melding these genes yielded an innovative Artificial Neural Network (ANN) diagnostic blueprint, portending to alleviate patient encumbrance and elevate life quality. Immunoassay scrutiny unveiled accentuated immune damage in HBV-HCC patients relative to solitary HCC. Through consensus clustering, HBV-HCC was stratified into two subtypes (C1 and C2), the latter potentially indicating milder immune impairment. The diagnostic model grounded in these feature genes showcased robust and transferrable prognostic potentialities, introducing a novel outlook for early HBV-HCC diagnosis. This exhaustive immunological odyssey stands poised to expedite immunotherapeutic curatives' emergence for HBV-HCC.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"16 ","pages":"Article 200271"},"PeriodicalIF":4.3,"publicationDate":"2023-09-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10638043/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"41175011","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Identification and characterisation of novel potential phospho-acceptor sites in HPV-16 E7 hpv - 16e7新型潜在磷酸化受体位点的鉴定和表征

IF 4.3

Tumour Virus Research Pub Date : 2023-09-01 DOI: 10.1016/j.tvr.2023.200270

Oscar Trejo-Cerro , Justyna Broniarczyk , Nezka Kavcic , Michael Myers , Lawrence Banks

{"title":"Identification and characterisation of novel potential phospho-acceptor sites in HPV-16 E7","authors":"Oscar Trejo-Cerro , Justyna Broniarczyk , Nezka Kavcic , Michael Myers , Lawrence Banks","doi":"10.1016/j.tvr.2023.200270","DOIUrl":"10.1016/j.tvr.2023.200270","url":null,"abstract":"<div><p>Several studies have described functional regulation of high-risk human papillomaviruses (HPVs), E6 and E7 oncoproteins via posttranslational modifications (PTMs). However, how these PTMs modulate the activity of E6 and E7, particularly in their targeting of cellular proteins, is not completely understood. In this study, we show that HPV16 E7 can be phosphorylated by casein kinase I (CKI) and glycogen synthase kinase 3 (GSK3). This principal phosphorylation occurs at threonine residues 5 and 7 with a more minor role for residues 19–20 in the N-terminal region of 16 E7. Intriguingly, whilst mutational analyses suggest that residues 5 and 7 may be dispensable for the transformation of primary baby rat kidney cells by E7, intact residues 19 and 20 are required. Furthermore, negative charges at these residues (TT19-20DD) enhance the pRb-E7 interaction and cells display increased proliferation and invasion capacities. Using a proteomic approach with a phosphorylated peptide spanning the TT19-20 region of HPV16 E7, we have identified a panel of new, phospho-specific E7 interacting partners. These results shed new light on the complexity of N-terminal phosphorylation of E7 and how this can contribute towards expanding the repertoire of E7 targeted pathways.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"16 ","pages":"Article 200270"},"PeriodicalIF":4.3,"publicationDate":"2023-09-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10500460/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10258002","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

Association of two genomic variants with HPV type-specific risk of cervical cancer 两种基因组变异与宫颈癌症HPV类型特异性风险的相关性

IF 4.3

Tumour Virus Research Pub Date : 2023-07-25 DOI: 10.1016/j.tvr.2023.200269

Finja Seifert , Rieke Eisenblätter , Julia Beckmann , Peter Schürmann , Patricia Hanel , Matthias Jentschke , Gerd Böhmer , Hans-Georg Strauß , Christine Hirchenhain , Monika Schmidmayr , Florian Müller , Peter Fasching , Alexander Luyten , Norman Häfner , Matthias Dürst , Ingo B. Runnebaum , Peter Hillemanns , Thilo Dörk , Dhanya Ramachandran

{"title":"Association of two genomic variants with HPV type-specific risk of cervical cancer","authors":"Finja Seifert , Rieke Eisenblätter , Julia Beckmann , Peter Schürmann , Patricia Hanel , Matthias Jentschke , Gerd Böhmer , Hans-Georg Strauß , Christine Hirchenhain , Monika Schmidmayr , Florian Müller , Peter Fasching , Alexander Luyten , Norman Häfner , Matthias Dürst , Ingo B. Runnebaum , Peter Hillemanns , Thilo Dörk , Dhanya Ramachandran","doi":"10.1016/j.tvr.2023.200269","DOIUrl":"10.1016/j.tvr.2023.200269","url":null,"abstract":"<div><h3>Problem</h3><p>Human papillomavirus infection is integral to developing invasive cervical cancer in the majority of patients. In a recent genome-wide association study, rs9357152 and rs4243652 have been associated with seropositivity for HPV16 or HPV18, respectively. It is unknown whether these variants also associate with cervical cancer triggered by either HPV16 or HPV18.</p></div><div><h3>Methods</h3><p>We investigate whether the two HPV susceptibility variants show association with type-specific cervical cancer in a genetic case-control study with cases stratified by HPV16 or HPV18, respectively. We further tested whether rs9357152 modulates gene expression of any of 36 genes at the human leukocyte antigen locus in 256 cervical tissues.</p></div><div><h3>Results</h3><p>rs9357152 was associated with invasive HPV16-positive cervical cancer (OR 1.33, 95%CI 1.03–1.70, p = 0.03), and rs4243652 was associated with HPV18-positive adenocarcinomas (OR 2.96, 95%CI 1.18–7.41, p = 0.02). These associations remained borderline significant after testing against different sets of controls. rs9357152 was found to be an eQTL for <em>HLA-DRB1</em> in HPV-positive cervical tissues (p<sub>ANOVA</sub> = 0.0009), with the risk allele lowering mRNA levels.</p></div><div><h3>Conclusions</h3><p>We find evidence that HPV seropositivity variants at chromosome 6 and 14 may modulate type-specific cervical cancer risk. rs9357152 may exert its effect through regulating <em>HLA-DRB1</em> induction in the presence of HPV. In regard of multiple testing, these results need to be confirmed in larger studies.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"16 ","pages":"Article 200269"},"PeriodicalIF":4.3,"publicationDate":"2023-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/7c/3a/main.PMC10415783.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9986511","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0

The human Papillomavirus twilight zone – Latency, immune control and subclinical infection 人乳头瘤病毒的潜伏期、免疫控制和亚临床感染

IF 4.3

Tumour Virus Research Pub Date : 2023-06-23 DOI: 10.1016/j.tvr.2023.200268

John Doorbar

{"title":"The human Papillomavirus twilight zone – Latency, immune control and subclinical infection","authors":"John Doorbar","doi":"10.1016/j.tvr.2023.200268","DOIUrl":"10.1016/j.tvr.2023.200268","url":null,"abstract":"<div><p>The incorporation of HPV DNA testing into cervical screening programs has shown that many HPV-positive women are cytologically normal, with HPV-positivity fluctuating throughout life. Such results suggest that papillomaviruses may persist in a latent state after disease clearance, with sporadic recurrence. It appears that virus latency represents a narrow slot in a wider spectrum of subclinical and possibly productive infections. Clinical studies, and animal model infection studies, suggested a key role for host immune surveillance in maintaining such asymptomatic infections, and although infections may also be cleared, most studies have used the term ‘clearance’ to describe a situation where the presence of HPV DNA falls below the clinical detection level. Given our knowledge of papillomavirus immune evasion strategies and the restricted pattern of viral gene expression required for ‘basal cell’ persistence, the term ‘apparent clearance’ and ‘subclinical persistence’ of infection may better summarise our understanding. Subclinical infection also encompasses the lag phase, which occurs between infection and lesion development. This is dependent on infection titre, with multifocal infections developing more rapidly to disease. These concepts can usefully influence patient management where HPV-positivity occurs sometime after the onset of sexual activity, and where vertical transmission is suspected despite a lag period.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"16 ","pages":"Article 200268"},"PeriodicalIF":4.3,"publicationDate":"2023-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9754029","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 2

Is immunotherapy a potential game changer in managing human papillomavirus (HPV) infection and intraepithelial neoplasia? 免疫疗法是治疗人乳头瘤病毒(HPV)感染和上皮内瘤变的潜在改变者吗?

IF 4.3

Tumour Virus Research Pub Date : 2023-06-07 DOI: 10.1016/j.tvr.2023.200263

Peter L. Stern

引用次数: 0

Methyltransferase-independent function of enhancer of zeste homologue 2 maintains tumorigenicity induced by human oncogenic papillomavirus and polyomavirus zeste同源物2增强子不依赖甲基转移酶的功能维持人致癌乳头瘤病毒和多瘤病毒诱导的致瘤性

IF 4.3

Tumour Virus Research Pub Date : 2023-06-07 DOI: 10.1016/j.tvr.2023.200264

Michelle Khattri , Yutaka Amako , Julia R. Gibbs , Joseph L. Collura , Reety Arora , Alexis Harold , Meng Yen Li , Paul W. Harms , Elena Ezhkova , Masahiro Shuda

{"title":"Methyltransferase-independent function of enhancer of zeste homologue 2 maintains tumorigenicity induced by human oncogenic papillomavirus and polyomavirus","authors":"Michelle Khattri , Yutaka Amako , Julia R. Gibbs , Joseph L. Collura , Reety Arora , Alexis Harold , Meng Yen Li , Paul W. Harms , Elena Ezhkova , Masahiro Shuda","doi":"10.1016/j.tvr.2023.200264","DOIUrl":"10.1016/j.tvr.2023.200264","url":null,"abstract":"<div><p>Merkel cell polyomavirus (MCV) and high-risk human papillomavirus (HPV) are human tumor viruses that cause Merkel cell carcinoma (MCC) and oropharyngeal squamous cell carcinoma (OSCC), respectively. HPV E7 and MCV large T (LT) oncoproteins target the retinoblastoma tumor suppressor protein (pRb) through the conserved LxCxE motif. We identified enhancer of zeste homolog 2 (EZH2) as a common host oncoprotein activated by both viral oncoproteins through the pRb binding motif. EZH2 is a catalytic subunit of the polycomb 2 (PRC2) complex that trimethylates histone H3 at lysine 27 (H3K27me3). In MCC tissues EZH2 was highly expressed, irrespective of MCV status. Loss-of-function studies revealed that viral HPV E6/E7 and T antigen expression are required for <em>Ezh2</em> mRNA expression and that EZH2 is essential for HPV(+)OSCC and MCV(+)MCC cell growth. Furthermore, EZH2 protein degraders reduced cell viability efficiently and rapidly in HPV(+)OSCC and MCV(+)MCC cells, whereas EZH2 histone methyltransferase inhibitors did not affect cell proliferation or viability within the same treatment period. These results suggest that a methyltransferase-independent function of EZH2 contributes to tumorigenesis downstream of two viral oncoproteins, and that direct targeting of EZH2 protein expression could be a promising strategy for the inhibition of tumor growth in HPV(+)OSCC and MCV(+)MCC patients.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"16 ","pages":"Article 200264"},"PeriodicalIF":4.3,"publicationDate":"2023-06-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a3/f1/main.PMC10258072.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9679419","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 1

Diversity of cervicovaginal human papillomavirus (HPV) genotypes and naturally occurring E6/E7 DNA polymorphisms of HPV-16 in Ghana 加纳宫颈阴道人乳头瘤病毒(HPV)基因型的多样性和自然发生的HPV-16 E6/E7 DNA多态性

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2023.200261

Gladys Kaba , Andrew Stevenson , Samuel Asamoah Sakyi , Thomas Okpoti Konney , Ramya Bhatia , Nicholas A. Titiloye , Samuel A. Oppong , Francis Agyemang-Yeboah , Kate Cuschieri , Sheila V. Graham

{"title":"Diversity of cervicovaginal human papillomavirus (HPV) genotypes and naturally occurring E6/E7 DNA polymorphisms of HPV-16 in Ghana","authors":"Gladys Kaba , Andrew Stevenson , Samuel Asamoah Sakyi , Thomas Okpoti Konney , Ramya Bhatia , Nicholas A. Titiloye , Samuel A. Oppong , Francis Agyemang-Yeboah , Kate Cuschieri , Sheila V. Graham","doi":"10.1016/j.tvr.2023.200261","DOIUrl":"10.1016/j.tvr.2023.200261","url":null,"abstract":"<div><p>Human papillomavirus (HPV) E6 and E7 oncogene expression is essential for cervical carcinogenesis. Evidence exists that E6/E7 variants may have different transforming activities while the risk of HPV-16 variants (A/D) differs by race/ethnicity. We determined the type-specific diversity of HPV infection in women with high grade cervical disease or cervical cancer in Ghana and investigated naturally occurring E6/E7 DNA variants in this population. HPV genotyping was carried out on 207 cervical swab samples collected from women referred to a gynaecology clinic at two teaching hospitals in Ghana. HPV-16, HPV-18 and HPV-45 were detected in 41.9%, 23.3% and 16.3% of cases respectively. HPV-16 E6/E7 DNA sequencing was performed in 36 samples. Thirty samples contained E6/E7 variants of the HPV-16-B/C lineage. 21/36 samples were of the HPV-16C1 sublineage variant and all contained the E7 A647G(N29S) single nucleotide polymorphism (SNP). This study reveals the diversity of E6/E7 DNA and the dominance of HPV16 B/C variants in cervicovaginal HPV infection in Ghana. Type-specific HPV diversity analysis indicates that most Ghanaian cervical disease cases are vaccine preventable. The study provides an important baseline from which for the impact of vaccine and antivirals on clinically relevant HPV infection and associated disease can be measured.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"15 ","pages":"Article 200261"},"PeriodicalIF":4.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10209332/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9598854","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

引用次数: 0