Sile Li, Ho Yin Luk, Chichao Xia, Zigui Chen, Paul Kay Sheung Chan, Siaw Shi Boon
{"title":"Oesophageal carcinoma: The prevalence of DNA tumour viruses and therapy","authors":"Sile Li, Ho Yin Luk, Chichao Xia, Zigui Chen, Paul Kay Sheung Chan, Siaw Shi Boon","doi":"10.1016/j.tvr.2021.200231","DOIUrl":"10.1016/j.tvr.2021.200231","url":null,"abstract":"<div><p>Oesophageal carcinoma ranks the sixth leading cause of cancer death and affected 544,000 - 604,000 people in 2020. Patients often presented with a poor cancer prognosis with a low survival rate of 15–25%. Depending upon the cell type, oesophageal carcinoma is categorised into oesophageal squamous cell carcinoma (ESCC) and oesophageal adenocarcinoma (EAC). ESCC is predominantly reported in developing countries, while EAC is more common in developed countries. Aside from the presence of exogenous co-factors, such as cigarette smoking, alcohol consumption, obesity, gastroesophageal reflux disease (GERD); infection with oncogenic viruses is suspected to be one of the major factors contributing to EC development. Oncogenic viruses, including human papillomavirus (HPV), Epstein Barr virus (EBV), Cytomegalovirus (CMV) and Herpes Simplex Virus (HSV) have been detected in various proportions of EC samples. Nonetheless, their aetiological roles in EC remain debatable. In this review, we garnered previous studies that focus on the association between oncogenic viruses and EC. Among these oncogenic viruses, HPV appears to have a stronger association with EC than the others. In addition, we also discuss the pros and cons of the treatment regimens to treat EC patients, including immunotherapy, chemo- and chemoradiotherapy, and their efficacy.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"13 ","pages":"Article 200231"},"PeriodicalIF":4.3,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/ae/14/main.PMC8717602.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39734835","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}
Darron R. Brown , Xavier Castellsagué , Daron Ferris , Suzanne M. Garland , Warner Huh , Marc Steben , Cosette M. Wheeler , Alfred Saah , Alain Luxembourg , Se Li , Christine Velicer
{"title":"Human papillomavirus seroprevalence and seroconversion following baseline detection of nine human papillomavirus types in young women","authors":"Darron R. Brown , Xavier Castellsagué , Daron Ferris , Suzanne M. Garland , Warner Huh , Marc Steben , Cosette M. Wheeler , Alfred Saah , Alain Luxembourg , Se Li , Christine Velicer","doi":"10.1016/j.tvr.2022.200236","DOIUrl":"10.1016/j.tvr.2022.200236","url":null,"abstract":"<div><h3>Background</h3><p>Estimates of the humoral immune response to incident human papillomavirus (HPV) infections are limited.</p></div><div><h3>Methods</h3><p>In this post hoc analysis of 3875 women aged 16–23 years from a 4-valent HPV vaccine trial (NCT00092482), HPV seroprevalence on day 1 was measured with a 9-valent HPV (HPV 6/11/16/18/31/33/45/52/58) competitive Luminex immunoassay and compared with cervical/external genital HPV detection by polymerase chain reaction. In the control group, among women who were HPV DNA‒negative on day 1, seroconversion following initial HPV detection was estimated using Kaplan-Meier methods.</p></div><div><h3>Results</h3><p>Type-specific HPV seropositivity among women with no day 1 cervical/external genital HPV detection was 0.6%–3.6%. Women with any 9-valent HPV (9vHPV) cervical/external genital detection (796/3875; 20.5%) had concordant seropositivity ranging from 13.4% (HPV 45) to 38.5% (HPV 6). Among women in the control group who were negative for all HPV types on day 1, seroconversion by month 30 after initial detection ranged from 29% (HPV 45) to 75% (HPV 16).</p></div><div><h3>Conclusions</h3><p>Humoral immune response to HPV is variable and dynamic, depending on type-specific exposure. This longitudinal analysis provides insight into the relationship between incident infection and seropositivity.</p><p>ClinicalTrials.gov; NCT00092482 <span>https://clinicaltrials.gov/ct2/show/NCT00092482</span><svg><path></path></svg>.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"13 ","pages":"Article 200236"},"PeriodicalIF":4.3,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666679022000027/pdfft?md5=0be29c852fae3e60322d14eb99785045&pid=1-s2.0-S2666679022000027-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49131844","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}
Sung Eun Choi , Abhishek Choudhary , Jingyi Huang , Stephen Sonis , Anna R. Giuliano , Alessandro Villa
{"title":"Increasing HPV vaccination coverage to prevent oropharyngeal cancer: A cost-effectiveness analysis","authors":"Sung Eun Choi , Abhishek Choudhary , Jingyi Huang , Stephen Sonis , Anna R. Giuliano , Alessandro Villa","doi":"10.1016/j.tvr.2021.200234","DOIUrl":"10.1016/j.tvr.2021.200234","url":null,"abstract":"<div><p>The incidence of oropharyngeal cancer (OPC) has been rising, especially among middle-aged men. While Human Papillomavirus (HPV) has been irrevocably implicated in the pathogenesis of oropharyngeal cancer (OPC), the current HPV vaccination uptake rate remains low in the US. The aim of our study was to evaluate the impact of increased HPV vaccination coverage on HPV-associated OPC incidence and costs. A decision analytic model was constructed for hypothetical cohorts of 9-year-old boys and girls. Two strategies were compared: 1) Maintaining the current vaccination uptake rates; 2) Increasing HPV vaccination uptake rates to the Healthy People 2030 target (80%) for both sexes. Increasing HPV vaccination coverage rates to 80% would be expected to prevent 5,339 OPC cases at a cost of $0.57 billion USD. Increased HPV vaccination coverage would result in 7,430 quality-adjusted life year (QALY) gains in the overall population, and it is estimated to be cost-effective for males with an incremental cost-effectiveness ratio of $86,940 per QALY gained under certain conditions. Expanding HPV vaccination rates would likely provide a cost-effective way to reduce the OPC incidence, particularly among males.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"13 ","pages":"Article 200234"},"PeriodicalIF":4.3,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/60/87/main.PMC8749055.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39777237","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}
Rosalyn E. Plotzker , Gregory M. Barnell , Dorothy J. Wiley , Elizabeth A. Stier , Naomi Jay
{"title":"Provider preferences for anal cancer prevention screening: Results of the International Anal Neoplasia Society survey","authors":"Rosalyn E. Plotzker , Gregory M. Barnell , Dorothy J. Wiley , Elizabeth A. Stier , Naomi Jay","doi":"10.1016/j.tvr.2022.200235","DOIUrl":"10.1016/j.tvr.2022.200235","url":null,"abstract":"<div><h3>Objective</h3><p>This study explores provider preferences regarding anal cancer screening indications, initiation age<strong>,</strong> tools, and referral threshold to high resolution anoscopy (HRA).</p></div><div><h3>Methods</h3><p>International Anal Neoplasia Society affiliates were invited to complete an online survey. Options for initiation age and tools were delineated by sub-groups. HRA referral thresholds separately queried recommendations by patient immune status.</p></div><div><h3>Results</h3><p>One hundred forty respondents participated. Although consensus was lacking with regard to specific screening initiation age, more respondents recommended younger initiation ages for men who have sex with men (MSM) living with HIV (LWH) compared with MSM not LWH (p < 0.01). “No age threshold” ranged 44-55% among sub-groups with lower genital tract disease. Cytology and digital anorectal exam (DARE) were the most frequently selected tools for all sub-groups (ranges 77-90% and 74-86%, respectively). HRA was recommended significantly more frequently for MSM LWH (58%) and patients with vulvar cancer (52%) compared to others (p < 0.01). “Any [test] abnormality” was more often selected as indication for HRA for immunocompromised (56%) and immunocompetent (46%) patients than a specific cytology test result (29%, 36% respectively).</p></div><div><h3>Conclusion</h3><p>Cytology and DARE were preferred screening tools; screening initiation age and HRA referral threshold showed less consensus. Evidence-based guidelines are needed and may lead to more consistent screening practices.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"13 ","pages":"Article 200235"},"PeriodicalIF":4.3,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/b5/18/main.PMC9006639.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39937485","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}
Kahren van Eer , Ihsane Laâbi , Birgit H.B. van Benthem , Renske D.M. Steenbergen , Audrey J. King
{"title":"The association between viral load and concurrent human papillomavirus infection at the genital and anal sites of young women and the impact of vaccination","authors":"Kahren van Eer , Ihsane Laâbi , Birgit H.B. van Benthem , Renske D.M. Steenbergen , Audrey J. King","doi":"10.1016/j.tvr.2021.200233","DOIUrl":"10.1016/j.tvr.2021.200233","url":null,"abstract":"<div><p>Concurrent genital-anal human papillomavirus (HPV) infections may impose an increased anal cancer risk in women with HPV-related genital lesions. High viral load may facilitate genital-anal HPV concurrence. Genital and anal HPV is reduced by a bivalent HPV16/18 vaccine, yet the effect on concurrent genital-anal HPV remains unclear.</p><p>This study analyzed viral load in concurrent genital-anal HPV infections, relative to genital-only and anal-only HPV infections and the impact of vaccination in young women. We included 1074 women, who provided both genital and anal swabs. HPV detection and genotyping was performed using the SPF10-DEIA-LiPA25. HPV copy numbers were measured with type-specific qPCRs and corrected for cellular content to obtain the viral load.</p><p>Concurrent genital-anal HPV often had significantly higher genital viral load (0.09–371 c/cell) than genital-only HPV (3.17E-04-15.9 c/cell, p < 0.0001 to p < 0.05). Moreover, nearly all concurrent genital-anal HPV types had higher genital copy numbers per PCR reaction (157-416E04 c/rxn) than anal copy numbers (0.90–884E01 c/rxn, p < 0.0001 to p < 0.001). Vaccinated women had significantly less infections with HPV16/18 vaccine-types (2.8% vs 13.7%, p < 0.0001) and HPV31/35/45 cross-protective types (7.4% vs 21.1%, p < 0.0001) than unvaccinated women.</p><p>In conclusion, particularly high genital viral load is found in concurrent genital-anal HPV infections, which are effectively reduced by vaccination.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"13 ","pages":"Article 200233"},"PeriodicalIF":4.3,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/58/91/main.PMC8732794.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39766247","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}
James Riddell IV , Andrew F. Brouwer , Heather M. Walline , Lora P. Campredon , Rafael Meza , Marisa C. Eisenberg , Emily C. Andrus , Rachel L. Delinger , Monica L. Yost , Jodi K. McCloskey , Trey B. Thomas , Suiyuan Huang , Robert L. Ferris , Dong Moon Shin , Carole Fakhry , Thomas Ow , Daniel Li , Ashley Berlot , Thomas E. Carey , Nicolas F. Schlecht
{"title":"Oral human papillomavirus prevalence, persistence, and risk-factors in HIV-positive and HIV-negative adults","authors":"James Riddell IV , Andrew F. Brouwer , Heather M. Walline , Lora P. Campredon , Rafael Meza , Marisa C. Eisenberg , Emily C. Andrus , Rachel L. Delinger , Monica L. Yost , Jodi K. McCloskey , Trey B. Thomas , Suiyuan Huang , Robert L. Ferris , Dong Moon Shin , Carole Fakhry , Thomas Ow , Daniel Li , Ashley Berlot , Thomas E. Carey , Nicolas F. Schlecht","doi":"10.1016/j.tvr.2022.200237","DOIUrl":"10.1016/j.tvr.2022.200237","url":null,"abstract":"<div><h3>Background</h3><p>HIV has been shown to increase the likelihood of oral HPV infection. In this study, we evaluated the risk of oral HPV in HIV infected patients compared with HIV-negative controls.</p></div><div><h3>Methods</h3><p>101 healthy adult volunteers (HIV-) and 245 adults living with HIV infection (HIV+) were recruited from 5 academic medical centers. Questionnaires and saliva samples were obtained every 3–8 months over a period of 2 years (2015–2017). DNA was isolated from the saliva samples and tested for 18 high- and low-risk genotypes.</p></div><div><h3>Results</h3><p>Oral HPV was detected in 23% of HIV + vs. 10% of HIV- participants (p < 0.0001). Men had a higher oral HPV prevalence than women (27% vs. 15% HIV+, p = 0.03, 16% vs. 5% HIV-, p = 0.01). Risk factors among HIV + participants included more lifetime deep kissing and oral sex partners, and history of AIDS. Persistent oral HPV was detected in 23% of HIV + vs. 5% of HIV- participants (p < 0.001). Among 8 HIV + participants with CD4 counts <200 cell/μL none had cleared their HPV infection during the study.</p></div><div><h3>Conclusions</h3><p>Risk of oral HPV infection and persistence was significantly higher in HIV + adults with a history of poorly controlled HIV, which may put them at increased risk of HPV-associated cancer.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"13 ","pages":"Article 200237"},"PeriodicalIF":4.3,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666679022000039/pdfft?md5=2bfb47919a1a953e7a6dd2904527ecb2&pid=1-s2.0-S2666679022000039-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"49345896","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}
{"title":"Merkel cell polyomavirus and associated Merkel cell carcinoma","authors":"June F. Yang, Jianxin You","doi":"10.1016/j.tvr.2021.200232","DOIUrl":"10.1016/j.tvr.2021.200232","url":null,"abstract":"<div><p>Merkel cell polyomavirus (MCPyV) is a ubiquitous skin infection that can cause Merkel cell carcinoma (MCC), a highly lethal form of skin cancer with a nearly 50% mortality rate. Since the discovery of MCPyV in 2008, great advances have been made to improve our understanding of how the viral encoded oncoproteins contribute to MCC oncogenesis. However, our knowledge of the MCPyV infectious life cycle and its oncogenic mechanisms are still incomplete. The incidence of MCC has tripled over the past two decades, but effective treatments are lacking. Only recently have there been major victories in combatting metastatic MCC with the application of PD-1 immune checkpoint blockade. Still, these immune-based therapies are not ideal for patients with a medical need to maintain systemic immune suppression. As such, a better understanding of MCPyV's oncogenic mechanisms is needed in order to develop more effective and targeted therapies against virus-associated MCC. In this review, we discuss current areas of interest for MCPyV and MCC research and the progress made in elucidating both the natural host of MCPyV infection and the cell of origin for MCC. We also highlight the remaining gaps in our knowledge on the transcriptional regulation of MCPyV, which may be key to understanding and targeting viral oncogenesis for developing future therapies.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"13 ","pages":"Article 200232"},"PeriodicalIF":4.3,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/a6/10/main.PMC8715208.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39734836","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}
{"title":"Kaposi's sarcoma-associated herpesvirus at 27","authors":"Marta Maria Gaglia","doi":"10.1016/j.tvr.2021.200223","DOIUrl":"10.1016/j.tvr.2021.200223","url":null,"abstract":"<div><p>Kaposi's sarcoma-associated herpesvirus (KSHV) was discovered 27 years ago and its link to several pathologies – Kaposi's sarcoma, primary effusion lymphoma, and the B cell variant of Multicentric Castleman disease – is now well established. However, many questions remain about how KSHV causes tumors. Here, I will review studies from the last few years (primarily 2019–2021) that report new information about KSHV biology and tumorigenesis, including new results about KSHV proteins implicated in tumorigenesis, genetic and environmental variability in KSHV-related tumor development, and potential vulnerabilities of KSHV-caused tumors that could be novel therapeutic targets.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"12 ","pages":"Article 200223"},"PeriodicalIF":4.3,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tvr.2021.200223","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39253030","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}
Sonja Lagström , Alexander Hesselberg Løvestad , Sinan Uğur Umu , Ole Herman Ambur , Mari Nygård , Trine B. Rounge , Irene Kraus Christiansen
{"title":"HPV16 and HPV18 type-specific APOBEC3 and integration profiles in different diagnostic categories of cervical samples","authors":"Sonja Lagström , Alexander Hesselberg Løvestad , Sinan Uğur Umu , Ole Herman Ambur , Mari Nygård , Trine B. Rounge , Irene Kraus Christiansen","doi":"10.1016/j.tvr.2021.200221","DOIUrl":"10.1016/j.tvr.2021.200221","url":null,"abstract":"<div><p>Human papillomavirus (HPV) 16 and 18 are the most predominant types in cervical cancer. Only a small fraction of HPV infections progress to cancer, indicating that additional factors and genomic events contribute to the carcinogenesis, such as minor nucleotide variation caused by APOBEC3 and chromosomal integration.</p><p>We analysed intra-host minor nucleotide variants (MNVs) and integration in HPV16 and HPV18 positive cervical samples with different morphology. Samples were sequenced using an HPV whole genome sequencing protocol TaME-seq. A total of 80 HPV16 and 51 HPV18 positive samples passed the sequencing depth criteria of 300× reads, showing the following distribution: non-progressive disease (HPV16 n = 21, HPV18 n = 12); cervical intraepithelial neoplasia (CIN) grade 2 (HPV16 n = 27, HPV18 n = 9); CIN3/adenocarcinoma <em>in situ</em> (AIS) (HPV16 n = 27, HPV18 n = 30); cervical cancer (HPV16 n = 5).</p><p>Similar numbers of MNVs in HPV16 and HPV18 samples were observed for most viral genes, with the exception of HPV18 E4 with higher numbers across clinical categories. APOBEC3 signatures were observed in HPV16 lesions, while similar mutation patterns were not detected for HPV18. The proportion of samples with integration was 13% for HPV16 and 59% for HPV18 positive samples, with a noticeable portion located within or close to cancer-related genes.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"12 ","pages":"Article 200221"},"PeriodicalIF":4.3,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tvr.2021.200221","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39042622","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}