Tumour Virus Research最新文献

{"title":"Provider preferences for anal cancer prevention screening: Results of the International Anal Neoplasia Society survey","authors":"Rosalyn E. Plotzker ,&nbsp;Gregory M. Barnell ,&nbsp;Dorothy J. Wiley ,&nbsp;Elizabeth A. Stier ,&nbsp;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 &lt; 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 &lt; 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}

{"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 ,&nbsp;Ihsane Laâbi ,&nbsp;Birgit H.B. van Benthem ,&nbsp;Renske D.M. Steenbergen ,&nbsp;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 &lt; 0.0001 to p &lt; 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 &lt; 0.0001 to p &lt; 0.001). Vaccinated women had significantly less infections with HPV16/18 vaccine-types (2.8% vs 13.7%, p &lt; 0.0001) and HPV31/35/45 cross-protective types (7.4% vs 21.1%, p &lt; 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}

{"title":"Oral human papillomavirus prevalence, persistence, and risk-factors in HIV-positive and HIV-negative adults","authors":"James Riddell IV ,&nbsp;Andrew F. Brouwer ,&nbsp;Heather M. Walline ,&nbsp;Lora P. Campredon ,&nbsp;Rafael Meza ,&nbsp;Marisa C. Eisenberg ,&nbsp;Emily C. Andrus ,&nbsp;Rachel L. Delinger ,&nbsp;Monica L. Yost ,&nbsp;Jodi K. McCloskey ,&nbsp;Trey B. Thomas ,&nbsp;Suiyuan Huang ,&nbsp;Robert L. Ferris ,&nbsp;Dong Moon Shin ,&nbsp;Carole Fakhry ,&nbsp;Thomas Ow ,&nbsp;Daniel Li ,&nbsp;Ashley Berlot ,&nbsp;Thomas E. Carey ,&nbsp;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 &lt; 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 &lt; 0.001). Among 8 HIV + participants with CD4 counts &lt;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":"Editorial board member","authors":"","doi":"10.1016/S2666-6790(22)00007-6","DOIUrl":"https://doi.org/10.1016/S2666-6790(22)00007-6","url":null,"abstract":"","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"13 ","pages":"Article 200241"},"PeriodicalIF":4.3,"publicationDate":"2022-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666679022000076/pdfft?md5=53e5e1f8b159f719782c04dfc237add3&pid=1-s2.0-S2666679022000076-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"137411893","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,&nbsp;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}

{"title":"HPV16 and HPV18 type-specific APOBEC3 and integration profiles in different diagnostic categories of cervical samples","authors":"Sonja Lagström ,&nbsp;Alexander Hesselberg Løvestad ,&nbsp;Sinan Uğur Umu ,&nbsp;Ole Herman Ambur ,&nbsp;Mari Nygård ,&nbsp;Trine B. Rounge ,&nbsp;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}

{"title":"Potential entry receptors for human γ-herpesvirus into epithelial cells: A plausible therapeutic target for viral infections","authors":"Annu Rani ,&nbsp;Shweta Jakhmola ,&nbsp;Srikanth Karnati ,&nbsp;Hamendra Singh Parmar ,&nbsp;Hem Chandra Jha","doi":"10.1016/j.tvr.2021.200227","DOIUrl":"10.1016/j.tvr.2021.200227","url":null,"abstract":"<div><p>Herpesviruses are ubiquitous viruses, specifically the Epstein Barr virus (EBV). EBV and Kaposi's sarcoma-associated herpesvirus (KSHV) establish their latency for a long period in B-cells and their reactivation instigates dreadful diseases from cancer to neurological modalities. The envelope glycoprotein of these viruses makes an attachment with several host receptors. For instance; glycoprotein 350/220, gp42, gHgL and gB of EBV establish an attachment with CD21, HLA-DR, Ephs, and other receptor molecules to hijack the B- and epithelial cell machinery. Ephs are reported recently as potent receptors for EBV entry into epithelial cells. Eph receptors play a role in the maintenance and control of various cellular processes including morphology, adhesion, proliferation, survival and differentiation. Alterations in the structure and expression of Eph and ephrin (Eph ligands) molecules is entangled with various pathologies including tumours and neurological complications. Along with Eph, integrins, NRP, NMHC are also key players in viral infections as they are possibly involved in viral transmission, replication and persistence. Contrarily, KSHV gH is known to interact with EphA2 and -A4 molecules, whereas in the case of EBV only EphA2 receptors are being reported to date. The ELEFN region of KSHV gH was involved in the interaction with EphA2, however, the interacting region of EBV gH is elusive. Further, the gHgL of KSHV and EBV form a complex with the EphA2 ligand-binding domain (LBD). Primarily by using gL both KSHV and EBV gHgL bind to the peripheral regions of LBD. In addition to γ-herpesviruses, several other viruses like Nipah virus, Cedar virus, Hepatitis C virus and Rhesus macaque rhadinovirus (RRV) also access the host cells via Eph receptors. Therefore, we summarise the possible roles of Eph and ephrins in virus-mediated infection and these molecules could serve as potential therapeutic targets.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"12 ","pages":"Article 200227"},"PeriodicalIF":4.3,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://ftp.ncbi.nlm.nih.gov/pub/pmc/oa_pdf/cc/76/main.PMC8628264.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39751836","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":"Editorial board member","authors":"","doi":"10.1016/S2666-6790(21)00018-5","DOIUrl":"10.1016/S2666-6790(21)00018-5","url":null,"abstract":"","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"12 ","pages":"Article 200228"},"PeriodicalIF":4.3,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.sciencedirect.com/science/article/pii/S2666679021000185/pdfft?md5=445b6fd00383ec30671edc83a68780ad&pid=1-s2.0-S2666679021000185-main.pdf","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"48849002","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":"Comparison of Alinity m HPV and cobas HPV assays on cervical specimens in diverse storage media","authors":"Dan Jang ,&nbsp;Sam Ratnam ,&nbsp;Marek Smieja ,&nbsp;David J. Speicher ,&nbsp;Manuel Arias ,&nbsp;Avery Clavio ,&nbsp;Dustin Costescu ,&nbsp;Laurie Elit ,&nbsp;Shihai Huang ,&nbsp;Erika Herrero-Garcia ,&nbsp;Ajith M. Joseph ,&nbsp;Hao Jiang ,&nbsp;Robert Needle ,&nbsp;Max Chernesky","doi":"10.1016/j.tvr.2021.200224","DOIUrl":"10.1016/j.tvr.2021.200224","url":null,"abstract":"<div><h3>Objective</h3><p>To assess the concordance of high-risk HPV (HR-HPV) testing with the Alinity assay on cervical samples collected with diverse collection/storage protocols (ThinPrep, SurePath, Cervicollect) and to assess inter-assay concordance of HR-HPV testing of cervical cell specimens with Alinity m HR HPV assay (Alinity) vs cobas® 4800 HPV assay (cobas).</p></div><div><h3>Methods</h3><p>Specimens were obtained from 560 women attending a Women's Health clinic. Two specimens were obtained from each woman with combinations of two of the three collection devices and aliquots were tested by the two assays.</p></div><div><h3>Results</h3><p>Alinity showed an agreement of 93.9%, Kappa = 0.89 (263/280) between ThinPrep and SurePath specimens; 97.5%, Kappa = 0.95 (347/356) and 92.9%, Kappa = 0.85 (104/112) between ThinPrep and SurePath aliquots taken before or after cytology processing, respectively. Cervi-Collect specimens showed an agreement of 94.6%, Kappa = 0.89 (265/280) with ThinPrep specimens. Compared to cobas, Alinity showed agreements of 94.3%, Kappa = 0.88 (395/419) and 91.8%, Kappa = 0.82 (257/280) between ThinPrep and SurePath specimens, respectively. Alinity and cobas detected genotypes 16/18 and other high-risk HPV types at similar rates and showed similar correlations with cytology grades.</p></div><div><h3>Conclusions</h3><p>Compared to cobas, Alinity performed equally well for detecting HPV in cervical specimens obtained with ThinPrep and SurePath. The Cervi-Collect device compared well to the other collection methods. Alinity is a reliable assay for simultaneous detection of HPV-16/18 and other high-risk genotypes in cervical specimens.</p></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"12 ","pages":"Article 200224"},"PeriodicalIF":4.3,"publicationDate":"2021-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://sci-hub-pdf.com/10.1016/j.tvr.2021.200224","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"39168834","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}