Tumour Virus Research最新文献_第6页

Exploring monitoring strategies for population surveillance of HPV vaccine impact using primary HPV screening 探索使用HPV初级筛查对HPV疫苗影响的人群监测策略

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2023.200255

Louiza S. Velentzis , David Hawkes , Michael Caruana , Julia ML. Brotherton , Megan A. Smith , Lara Roeske , Khurram A. Karim , Suzanne M. Garland , C. David Wrede , Jeffery Tan , Cosette Wheeler , Philip E. Castle , Marion Saville , Karen Canfell

{"title":"Exploring monitoring strategies for population surveillance of HPV vaccine impact using primary HPV screening","authors":"Louiza S. Velentzis , David Hawkes , Michael Caruana , Julia ML. Brotherton , Megan A. Smith , Lara Roeske , Khurram A. Karim , Suzanne M. Garland , C. David Wrede , Jeffery Tan , Cosette Wheeler , Philip E. Castle , Marion Saville , Karen Canfell","doi":"10.1016/j.tvr.2023.200255","DOIUrl":"10.1016/j.tvr.2023.200255","url":null,"abstract":"<div><p>Australia's cervical screening program transitioned from cytology to HPV-testing with genotyping for HPV16/18 in Dec’2017. We investigated whether program data could be used to monitor HPV vaccination program impact (commenced in 2007) on HPV16/18 prevalence and compared estimates with pre-vaccination benchmark prevalence. Pre-vaccination samples (2005–2008) (n = 1933; WHINURS), from 25 to 64-year-old women had been previously analysed with Linear Array (LA). Post-vaccination samples (2013-2014) (n = 2989; Compass pilot), from 25 to 64-year-old women, were analysed by cobas 4800 (cobas), and by LA for historical comparability. Age standardised pre-vaccination HPV16/18 prevalence was 4.85% (95%CI:3.81–5.89) by LA; post-vaccination estimates were 1.67% (95%CI:1.21–2.13%) by LA, 1.49% (95%CI:1.05–1.93%) by cobas, and 1.63% (95%CI:1.17–2.08%) for cobas and LA testing of non-16/18 cobas positives (cobas/LA). Age-standardised pre-vaccination oncogenic HPV prevalence was 15.70% (95%CI:13.79–17.60%) by LA; post-vaccination estimates were 9.06% (95%CI:8.02–10.09%) by LA, 8.47% (95%CI:7.47–9.47%) by cobas and cobas/LA. Standardised rate ratios between post-vs. pre-vaccination rates were significantly different for HPV16/18, non-16/18 HPV and oncogenic HPV: 0.34 (95%CI:0.23–0.50), 0.68 (95%CI:0.55–0.84) and 0.58 (95%CI:0.48–0.69), respectively. Additional strategies (LA for all cobas positives; combined cobas and LA results on all samples) had similar results. If a single method is applied consistently, it will provide important data on relative changes in HPV prevalence following vaccination.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"15 ","pages":"Article 200255"},"PeriodicalIF":4.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/f1/c2/main.PMC9925607.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9600309","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

Molecular dissection of the E6 PBM identifies essential residues regulating Chk1 phosphorylation and subsequent 14-3-3 recognition E6 PBM的分子解剖鉴定了调节Chk1磷酸化和随后的14-3-3识别的必要残基

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2023.200257

Arushi Vats , Jayashree V. Thatte , Lawrence Banks

{"title":"Molecular dissection of the E6 PBM identifies essential residues regulating Chk1 phosphorylation and subsequent 14-3-3 recognition","authors":"Arushi Vats , Jayashree V. Thatte , Lawrence Banks","doi":"10.1016/j.tvr.2023.200257","DOIUrl":"10.1016/j.tvr.2023.200257","url":null,"abstract":"<div><p>Previous studies have shown that the high-risk HPV E6 oncoprotein PDZ binding motifs (PBMs) can interact with PDZ proteins or members of the 14-3-3 family, depending upon the E6 phosphorylation status. However, different HPV E6 oncoproteins are subjected to phosphorylation by different cellular kinases. We have therefore been interested in determining whether we can dissect E6's PDZ and 14-3-3 interactions at the molecular level. Using HPV-18 E6, we have found that its Chk1 phosphorylation requires residues both upstream and downstream of the phospho-acceptor site, in addition to the Chk1 consensus recognition motif. Furthermore, we demonstrate that different high-risk HPV E6 types are differentially phosphorylated by Chk1 kinases, potentially due to the differences in their carboxy-terminal residues, as they are critical for kinase recognition. Moreover, differences in the E6 phosphorylation levels of different HR HPV types directly link to their ability to interact with different 14-3-3 isoforms, based on their phospho-status. Interestingly, 14-3-3 recognition appears to be less dependent upon the precise sequence constraints of the E6 carboxy terminal region, whilst minor amino acid variations have a major impact upon PDZ recognition. These results demonstrate that changes in E6 phospho-status during the life cycle or during malignant progression will modulate E6 interactions and, potentially, inversely regulate the levels of PDZ and 14-3-3 proteins.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"15 ","pages":"Article 200257"},"PeriodicalIF":4.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/cd/6c/main.PMC10009279.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9601581","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

Characterization of HPV subtypes in invasive cervical cancer in Botswana patients using a pan-pathogen microarray technology 使用泛病原体微阵列技术表征博茨瓦纳患者侵袭性宫颈癌的HPV亚型

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2023.200262

Surbhi Grover , Tyler Seckar , Le Gao , Rohini Bhatia , Xiang Lin , Nicola Zetola , Doreen Ramogola-Masire , Erle Robertson

{"title":"Characterization of HPV subtypes in invasive cervical cancer in Botswana patients using a pan-pathogen microarray technology","authors":"Surbhi Grover , Tyler Seckar , Le Gao , Rohini Bhatia , Xiang Lin , Nicola Zetola , Doreen Ramogola-Masire , Erle Robertson","doi":"10.1016/j.tvr.2023.200262","DOIUrl":"10.1016/j.tvr.2023.200262","url":null,"abstract":"<div><p>Human papillomavirus (HPV) plays a significant role in the development of cervical cancers in the setting of co-infection with HIV. Botswana has a high prevalence of HIV and cervical cancer. In this study, we investigated the distribution of HPV subtypes in cervical cancer biopsy samples from patients in Botswana using a highly sensitive pan-pathogen microarray technology, PathoChip, to detect both high- (HR-HPV) and low-risk HPV (LR-HPV) subtypes in women living with HIV (WLWH) and women living without HIV. We analyzed samples from 168 patients, of which 73% (n = 123) were WLWH with a median CD4 count of 479.5 cells/μL. Five HR-HPV subtypes were detected in the cohort: HPV 16, 18, 26, 34, and 53. The most prevalent subtypes were HPV 26 (96%) and HPV 34 (92%); 86% of WLWH (n = 106) had co-infection with four or more HR-HPV subtypes compared to 67% (n = 30) of women without HIV (p < 0.01). We detected 66 LR-HPV subtypes among all cervical cancer patients, with HPV 6b and 48 being most prevalent. Notably, signatures for LR-HPV subtypes 10, 41, 90, and 129 were only detected in WLWH. Signal intensity for HPV 18 was significantly weaker in WLWH with CD4 levels ≤200 cells/μL as compared to patients with >200 cells/μL and HIV-negative patients. Although the majority of cervical cancer specimens in this cohort were determined to have multiple HPV infections, the most prevalent HR-HPV subtypes (HPV 26 and HPV34) found in these cervical cancer samples are not covered in the current HPV vaccines. Though no conclusions can be made on the direct carcinogenicity of these subtypes the results do underlie the need for continued screening for prevention of cervical cancer.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"15 ","pages":"Article 200262"},"PeriodicalIF":4.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/1a/dc/main.PMC10239018.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9973750","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

Elevated iNOS and 3′-nitrotyrosine in Kaposi's Sarcoma tumors and mouse model 卡波西肉瘤肿瘤及小鼠模型中iNOS和3′-硝基酪氨酸升高

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2023.200259

Olga Vladimirova , Samantha Soldan , Chenhe Su , Andrew Kossenkov , Owen Ngalamika , For Yue Tso , John T. West , Charles Wood , Paul M. Lieberman

{"title":"Elevated iNOS and 3′-nitrotyrosine in Kaposi's Sarcoma tumors and mouse model","authors":"Olga Vladimirova , Samantha Soldan , Chenhe Su , Andrew Kossenkov , Owen Ngalamika , For Yue Tso , John T. West , Charles Wood , Paul M. Lieberman","doi":"10.1016/j.tvr.2023.200259","DOIUrl":"10.1016/j.tvr.2023.200259","url":null,"abstract":"<div><p>Kaposi's Sarcoma (KS) is a heterogenous, multifocal vascular malignancy caused by the human herpesvirus 8 (HHV8), also known as Kaposi's Sarcoma-Associated Herpesvirus (KSHV). Here, we show that KS lesions express iNOS/NOS2 broadly throughout KS lesions, with enrichment in LANA positive spindle cells. The iNOS byproduct 3-nitrotyrosine is also enriched in LANA positive tumor cells and colocalizes with a fraction of LANA-nuclear bodies. We show that iNOS is highly expressed in the L1T3/mSLK tumor model of KS. iNOS expression correlated with KSHV lytic cycle gene expression, which was elevated in late-stage tumors (>4 weeks) but to a lesser degree in early stage (1 week) xenografts. Further, we show that L1T3/mSLK tumor growth is sensitive to an inhibitor of nitric oxide, L-NMMA. L-NMMA treatment reduced KSHV gene expression and perturbed cellular gene pathways relating to oxidative phosphorylation and mitochondrial dysfunction. These finding suggest that iNOS is expressed in KSHV infected endothelial-transformed tumor cells in KS, that iNOS expression depends on tumor microenvironment stress conditions, and that iNOS enzymatic activity contributes to KS tumor growth.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"15 ","pages":"Article 200259"},"PeriodicalIF":4.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/42/b4/main.PMC10009278.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"10136025","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: 4

Human papillomavirus genomics: Understanding carcinogenicity 人类乳头瘤病毒基因组学:了解致癌性

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2023.200258

Chase W. Nelson , Lisa Mirabello

{"title":"Human papillomavirus genomics: Understanding carcinogenicity","authors":"Chase W. Nelson , Lisa Mirabello","doi":"10.1016/j.tvr.2023.200258","DOIUrl":"10.1016/j.tvr.2023.200258","url":null,"abstract":"<div><p>Human papillomavirus (HPV) causes virtually all cervical cancers and many cancers at other anatomical sites in both men and women. However, only 12 of 448 known HPV types are currently classified as carcinogens, and even the most carcinogenic type — HPV16 — only rarely leads to cancer. HPV is therefore necessary but insufficient for cervical cancer, with other contributing factors including host and viral genetics. Over the last decade, HPV whole genome sequencing has established that even fine-scale within-type HPV variation influences precancer/cancer risks, and that these risks vary by histology and host race/ethnicity. In this review, we place these findings in the context of the HPV life cycle and evolution at various levels of viral diversity: between-type, within-type, and within-host. We also discuss key concepts necessary for interpreting HPV genomic data, including features of the viral genome; events leading to carcinogenesis; the role of APOBEC3 in HPV infection and evolution; and methodologies that use deep (high-coverage) sequencing to characterize within-host variation, as opposed to relying on a single representative (consensus) sequence. Given the continued high burden of HPV-associated cancers, understanding HPV carcinogenicity remains important for better understanding, preventing, and treating cancers attributable to infection.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"15 ","pages":"Article 200258"},"PeriodicalIF":4.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10063409/pdf/main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9592012","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: 4

Tegument proteins of Epstein-Barr virus: Diverse functions, complex networks, and oncogenesis eb病毒被膜蛋白:多种功能、复杂网络与肿瘤发生

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2023.200260

Takayuki Murata

引用次数: 0

Unresolved issues in the management of human papillomavirus-associated mucosal high-grade pre-cancers 人乳头瘤病毒相关的粘膜高级别癌前病变治疗中尚未解决的问题

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2022.200250

Charles JN. Lacey

引用次数: 0

Association of PNPLA3 (rs738409) & TM6SF2 (rs58542926) and ATG16L1 (rs2241880) genetic variants with susceptibility to hepatocellular carcinoma in a group of Egyptian patients with HCV-induced liver cirrhosis PNPLA3 (rs738409)、TM6SF2 (rss58542926)和ATG16L1 (rs2241880)基因变异与埃及hcv诱导的肝硬化患者肝细胞癌易感性的关联

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2023.200256

Asmaa Mohamed Fteah , Ali Abdel Rahim , Afaf Ahmed AbdelHady , Hanan Shawky , Mohamed A Elrefaiy , Doaa Mamdouh Aly

引用次数: 0

The adenoviral E4orf3/4 is a regulatory polypeptide with cell transforming properties in vitro 腺病毒E4orf3/4是一种在体外具有细胞转化特性的调节多肽

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/j.tvr.2023.200254

Wing-Hang Ip, Luca D. Bertzbach, Thomas Speiseder, Thomas Dobner

{"title":"The adenoviral E4orf3/4 is a regulatory polypeptide with cell transforming properties in vitro","authors":"Wing-Hang Ip, Luca D. Bertzbach, Thomas Speiseder, Thomas Dobner","doi":"10.1016/j.tvr.2023.200254","DOIUrl":"10.1016/j.tvr.2023.200254","url":null,"abstract":"<div><p>The human adenovirus species C type 5 (HAdV-C5) early region 4 (E4) encodes several distinct polypeptides, defined as E4orf1 to E4orf6/7 according to the order and arrangement of the corresponding open reading frames (ORFs). All E4 gene products operate through a complex network of interactions with key viral and cellular regulatory proteins involved in transcription, apoptosis, cell cycle control, and DNA repair. Here, we generated a set of virus mutants carrying point mutations in the individual E4 genes. The phenotypic characterizations of these mutants revealed that mutations of these ORFs had no or only moderate effects on virus replication. Even a triple mutant that fails to produce E4orf3, E4orf4, and the yet uncharacterized alternatively spliced E4orf3/4 fusion protein, was replicating to wild type levels. The E4orf3/4 protein consists of the N-terminal 33 amino acid residues from E4orf3 and the C-terminal 28 amino acid residues from E4orf4. Intriguingly, we found that, similar to E4orf3, E4orf3/4 possesses properties that support the E1A/E1B-induced transformation of primary rodent cells. These results identify and functionally characterize E4orf3/4 and conclude that E4orf3/4 is another E4 region protein that is dispensable for virus replication but promotes the E1A/E1B-induced transformation of primary rodent cells.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"15 ","pages":"Article 200254"},"PeriodicalIF":4.3,"publicationDate":"2023-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC10258410/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"9624248","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 编委会成员

IF 4.3

Tumour Virus Research Pub Date : 2023-06-01 DOI: 10.1016/S2666-6790(23)00012-5

引用次数: 0