Tumour Virus Research最新文献

Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.

IF 4.7

Tumour Virus Research Pub Date : 2025-03-20 DOI: 10.1016/j.tvr.2025.200317

Julia Mai, Masih Nazari, Thomas Stamminger, Sabrina Schreiner

{"title":"Daxx and HIRA go viral - How chromatin remodeling complexes affect DNA virus infection.","authors":"Julia Mai, Masih Nazari, Thomas Stamminger, Sabrina Schreiner","doi":"10.1016/j.tvr.2025.200317","DOIUrl":"https://doi.org/10.1016/j.tvr.2025.200317","url":null,"abstract":"<p><p>Daxx and HIRA are key proteins in the host response to DNA virus infections. Daxx is involved in apoptosis, transcription regulation, and stress responses. During DNA virus infections, Daxx helps modulate the immune response and viral progression. Viruses like adenoviruses and herpesviruses can exploit Daxx to evade immune detection, either by targeting it for degradation or inhibiting its function. Daxx also interacts with chromatin to regulate transcription, which viruses can manipulate to enhance their own gene expression and replication. HIRA is a histone chaperone and reported to be essential for chromatin assembly and gene regulation. It plays a critical role in maintaining chromatin structure and modulating gene accessibility. During DNA virus infection, HIRA influences chromatin remodeling, affecting both viral and host DNA accessibility, which impacts viral replication and gene expression. Additionally, the histone variant H3.3 is crucial for maintaining active chromatin states. It is incorporated into chromatin independently of DNA replication and is associated with active gene regions. During viral infections, H3.3 dynamics can be altered, affecting viral genome accessibility and replication efficiency. Overall, Daxx and HIRA are integral to orchestrating viral infection programs, maintaining latency and/or persistence, and influencing virus-induced transformation by modulating chromatin dynamics and host immune responses, making them significant targets for therapeutic strategies once fully understood. Here, we summarize various DNA viruses and their crosstalk with Daxx and HIRA.</p>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":" ","pages":"200317"},"PeriodicalIF":4.7,"publicationDate":"2025-03-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143694439","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: 0

Drosophila Model of HPV18-Induced Pathogenesis Reveals a Role for E6 Oncogene in Regulation of NF-κB and Wnt to Inhibit Apoptosis.

IF 4.7

Tumour Virus Research Pub Date : 2025-03-10 DOI: 10.1016/j.tvr.2025.200316

Mojgan Padash Barmchi, Rami N Hassan, Mehrnaz Afkhami, John P Masly, Harrison Brown, Quincy P Collins, Michael J Grunsted

{"title":"Drosophila Model of HPV18-Induced Pathogenesis Reveals a Role for E6 Oncogene in Regulation of NF-κB and Wnt to Inhibit Apoptosis.","authors":"Mojgan Padash Barmchi, Rami N Hassan, Mehrnaz Afkhami, John P Masly, Harrison Brown, Quincy P Collins, Michael J Grunsted","doi":"10.1016/j.tvr.2025.200316","DOIUrl":"https://doi.org/10.1016/j.tvr.2025.200316","url":null,"abstract":"<p><p>Cancers caused by high-risk human papillomavirus (HPV) remain a significant health threat resulting in more than 300,000 deaths, annually. Persistent expression of two HPV oncogenes, E6 and E7, are necessary for cancer development and progression. E6 has several functions contributing to tumorigenesis one of which is blocking programmed cell death, apoptosis. The detailed mechanism of anti-apoptosis function of E6 is not fully understood. Here, using a Drosophila model of HPV18E6 and the human UBE3A-induced pathogenesis, we show that anti-apoptotic function of E6 is conserved in Drosophila. We demonstrate that the Drosophila homologs of human NF-κB transcription factors, Dorsal and Dif are proapoptotic. They induce the expression of Wingless (Wg, the Drosophila homolog of human Wnt), leading to apoptosis. Our results indicate that E6 oncogene inhibits apoptosis by downregulating the expression of Wg, Dorsal, and Dif. Additionally, we find that Dorsal and Dif, not only promote apoptosis but also regulate autophagy and necrosis. Dorsal promotes autophagy while Dif counteracts it, inducing the formation of acidic vacuoles and necrosis. Interestingly, although E6 blocks the proapoptotic function of Dorsal and Dif, it lacks the ability to interfere with their role in apoptosis-independent cell death. Given the high conservation of NF-κB transcription factors our results provide new insight into potential mechanisms mediated by NF-κB to intervene with cell immortalization action of E6 oncoprotein in HPV-infected cells.</p>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":" ","pages":"200316"},"PeriodicalIF":4.7,"publicationDate":"2025-03-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143617835","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: 0

Regulation of epithelial growth factor receptors by the oncoprotein E5 during the HPV16 differentiation-dependent life cycle

IF 4.7

Tumour Virus Research Pub Date : 2025-03-07 DOI: 10.1016/j.tvr.2025.200315

Mariano A. Molina , Sneha Biswas , Omar Jiménez-Vázquez , Jason M. Bodily

{"title":"Regulation of epithelial growth factor receptors by the oncoprotein E5 during the HPV16 differentiation-dependent life cycle","authors":"Mariano A. Molina , Sneha Biswas , Omar Jiménez-Vázquez , Jason M. Bodily","doi":"10.1016/j.tvr.2025.200315","DOIUrl":"10.1016/j.tvr.2025.200315","url":null,"abstract":"<div><div>Human papillomavirus (HPV) 16 infection initiates upon viral entry into the basal cells of the epithelium. The virus manipulates signaling pathways to complete its life cycle, which depends on cellular differentiation. The virus expresses the oncoproteins E5, E6, and E7 to promote immune evasion, cell cycle progression, apoptosis inhibition, and viral replication. The least studied viral oncoprotein is E5 (16E5), which can regulate epithelial growth factor receptor (GFR) signaling pathways. GFRs such as transforming growth factor-beta receptor (TGFBR), epidermal growth factor receptor (EGFR), and keratinocyte growth factor receptor (KGFR) have essential roles in cell growth, differentiation, and proliferation. These receptors obtain their ligands from the microenvironment, and once activated, regulate cellular behavior in the epithelium. GFRs therefore represent valuable targets for the virus to establish and maintain a cellular environment supportive of infection. The ability of 16E5 to regulate proliferation and differentiation varies through the differentiating epithelium, making it necessary to adequately describe the association between 16E5 and GFRs. Here we summarize the regulation of GFR signaling pathways by 16E5, discuss the roles of stromal growth factors, and outline unresolved questions over cellular differentiation and proliferation during the HPV life cycle.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200315"},"PeriodicalIF":4.7,"publicationDate":"2025-03-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143577986","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

De-regulation of aurora kinases by oncogenic HPV; implications in cancer development and treatment

IF 4.7

Tumour Virus Research Pub Date : 2025-02-07 DOI: 10.1016/j.tvr.2025.200314

Kemi Hannah Oladipo , Joanna L. Parish

{"title":"De-regulation of aurora kinases by oncogenic HPV; implications in cancer development and treatment","authors":"Kemi Hannah Oladipo , Joanna L. Parish","doi":"10.1016/j.tvr.2025.200314","DOIUrl":"10.1016/j.tvr.2025.200314","url":null,"abstract":"<div><div>Human papillomaviruses (HPVs) cause diseases ranging from benign warts to invasive cancers. HPVs are the cause of almost all cervical cancers and a sub-set of other epithelial malignancies including head and neck cancers, specifically within the oropharynx. The oncogenic properties of HPV are largely mediated through the viral oncoproteins E6 and E7, which disrupt many cellular pathways to drive uncontrolled cell proliferation. One family of proteins targeted by HPV is the Aurora kinase family. Aurora kinases are serine/threonine kinases including Aurora kinase A (AURKA), B (AURKB), and C (AURKC) which are often dysregulated in many cancer types, including HPV driven cancers. All three family members play essential roles in mitotic regulation and accurate cell division.</div><div>The deregulation of Aurora kinases by HPV infection highlights their potential as therapeutic targets in HPV-associated malignancies. Targeting Aurora kinase activity, in combination with current HPV therapies, may provide new avenues for treating HPV-induced cancers and reducing the burden of HPV-related diseases. Combinatorial inhibition targets distinct but overlapping functions of these kinases, thereby reducing the potential for cancer cells to develop resistance. This broad impact emphasizes the capability for Aurora kinase inhibitors not only as anti-mitotic agents but also as modulators of multiple oncogenic pathways. This review explores the combinatorial effects of Aurora kinase inhibition, offering insights into novel therapeutic strategies for the treatment of HPV-driven cancers.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200314"},"PeriodicalIF":4.7,"publicationDate":"2025-02-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143383935","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

How can HPV E6 manipulate host cell differentiation process to maintain the reservoir of infection HPV E6如何操纵宿主细胞分化过程以维持感染库。

IF 4.7

Tumour Virus Research Pub Date : 2025-01-19 DOI: 10.1016/j.tvr.2025.200313

Yuwen Chen , Nagayasu Egawa , Ke Zheng , John Doorbar

引用次数: 0

Rapid-onset cancer 迅速发生癌症。

IF 4.7

Tumour Virus Research Pub Date : 2025-01-02 DOI: 10.1016/j.tvr.2024.200312

Andrea Bilger, Paul F. Lambert

引用次数: 0

Too many cooks in the kitchen: HPV driven carcinogenesis – The result of collaboration or competition? 厨房里的厨师太多：HPV驱动的致癌作用——是合作还是竞争的结果？

IF 4.7

Tumour Virus Research Pub Date : 2024-12-27 DOI: 10.1016/j.tvr.2024.200311

Weimer Kathleen

引用次数: 0

Editorial: Tumour Virus Research on Virus Host Interactions and Cell Transformation 社论：肿瘤病毒在病毒宿主相互作用和细胞转化方面的研究。

IF 4.7

Tumour Virus Research Pub Date : 2024-12-20 DOI: 10.1016/j.tvr.2024.200310

Lawrence Banks, Peter Stern

引用次数: 0

Drugs and drug targets for the treatment of HPV-positive cervical cancer 治疗hpv阳性子宫颈癌的药物和药物靶点。

IF 4.7

Tumour Virus Research Pub Date : 2024-12-19 DOI: 10.1016/j.tvr.2024.200309

Carly A. Burmeister, Saif F. Khan, Sharon Prince

{"title":"Drugs and drug targets for the treatment of HPV-positive cervical cancer","authors":"Carly A. Burmeister, Saif F. Khan, Sharon Prince","doi":"10.1016/j.tvr.2024.200309","DOIUrl":"10.1016/j.tvr.2024.200309","url":null,"abstract":"<div><div>Cervical cancer is primarily driven by persistent infection with high-risk human papillomavirus (HPV) strains and remains a significant global health challenge, particularly in low- and middle-income countries where late-stage diagnoses is common. While vaccination and screening programs have reduced incidence rates, the need for novel and more effacacious and cost-effective therapeutic options is therefore critical especially for advanced cervical cancer. This review highlights several key advances in the understanding of HPV-induced carcinogenesis and the development of therapeutic strategies over the past five years. Important areas of focus include the role of HPV oncoproteins E5, E6 and E7 in modulating signalling pathways, treatment strategies for precancerous lesions, the potential of natural compounds to target cervical cancer cells, and the emergence of immunotherapies, checkpoint inhibitors, antibody-drug conjugates, and novel drug combinations to treat cervical cancer. Additionally, lifestyle recommendations and the integration of natural supplements are discussed for their potential to enhance treatment efficacy and improve patient outcomes. The developments reported in this review underscore the evolving landscape of cervical cancer treatment and the need for continued research to validate and integrate these emerging therapies into clinical practice.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200309"},"PeriodicalIF":4.7,"publicationDate":"2024-12-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11733058/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142873371","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

Intraperitoneal delivery of cannabidiol (CBD) and Δ9-tetrahydocannabinol (THC) promotes papillomavirus infections in athymic nude mice 腹腔注射大麻二酚（CBD）和Δ9-tetrahydocannabinol （THC）促进乳突裸鼠乳头瘤病毒感染。

IF 4.7

Tumour Virus Research Pub Date : 2024-12-16 DOI: 10.1016/j.tvr.2024.200307

Sarah A. Brendle , Jingwei Li , Dongxiao Sun , Junjia Zhu , Angela N. Henderson-Redmond , Daniel J. Morgan , Karla K. Balogh , Danielle Covington , Debra A. Shearer , Jiafen Hu

{"title":"Intraperitoneal delivery of cannabidiol (CBD) and Δ9-tetrahydocannabinol (THC) promotes papillomavirus infections in athymic nude mice","authors":"Sarah A. Brendle , Jingwei Li , Dongxiao Sun , Junjia Zhu , Angela N. Henderson-Redmond , Daniel J. Morgan , Karla K. Balogh , Danielle Covington , Debra A. Shearer , Jiafen Hu","doi":"10.1016/j.tvr.2024.200307","DOIUrl":"10.1016/j.tvr.2024.200307","url":null,"abstract":"<div><div>We used our mouse papillomavirus (MmuPV1) model to test the hypothesis that two primary psychoactive ingredients of marijuana, Δ<sup>9</sup>-tetrahydrocannabinol (THC) and cannabidiol (CBD), promote papillomavirus persistence in the oral mucosa of infected mice. We conducted intraperitoneal (ip) injections of a moderate dose (3 mg/kg) of either CBD and/or THC in both male and female athymic nude mice and followed the mice up to 20 weeks post-infection. These doses are comparable to what is estimated for human conventional cannabis consumption. All mice were infected with MmuPV1 in the oral cavity at week 4 post-ip delivery of CBD, THC, or a combination of THC and CBD (T + C). THC and CBD were detected in the blood of treated mice for up to 72 h after ip injection. Significantly higher levels of viral DNA were detected in males from both CBD and T + C-treated groups compared to those in the control group at 9- 10-and 12-weeks post infection. A marginally increased viral RNA was also detected in the infected tongues of males in all tested groups compared to that in males in the vehicle control group; the opposite was observed in females. We detected significantly higher levels of dermal dendritic cells (CD205<sup>+</sup>CD11c<sup>+</sup>), granulocytes (Ly6G<sup>+</sup>), but macrophages (F4-80+) recruited to the infected tongues of CBD-treated females. Our findings suggest that CBD may play a role in promoting MmuPV1 persistence in the oral cavity.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200307"},"PeriodicalIF":4.7,"publicationDate":"2024-12-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11731512/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142856753","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