Tumour Virus Research最新文献

{"title":"Transcriptomic profile of the immune genes, oncogenes, and tumor suppressor genes in HPV associated Cervical Intraepithelial Neoplasia 3 (CIN 3) and Cervical Squamous Cell Carcinoma (CSCC): Comparable expressions indicative of invasive potential.","authors":"Maaweya Awadalla, Halah Z Al Rawi, Reham M Alahmadi, Osamah T Khojah, Samia T Al-Shouli, Mansour I Almansour, Bandar Alosaimi","doi":"10.1016/j.tvr.2025.200327","DOIUrl":"10.1016/j.tvr.2025.200327","url":null,"abstract":"<p><p>Cervical cancer is the fourth most common cancer among women globally, with a woman dying every 2 min. Despite the need to understand the tumor microenvironment (TME) transcriptome of cervical squamous cell carcinoma (CSCC) and cervical intraepithelial neoplasia grade 3 (CIN 3), studies remain limited. This study compares the TME transcriptome of HPV-positive CSCC and CIN 3, analyzing 168 genes involved in tumor cell interactions with inflammatory and immune mediators, transcription, signal transduction, oncogenesis, tumor suppression, angiogenesis, and apoptosis. Co-expressed genes identified in HPV + CSCC and CIN 3 were analyzed using computational biology. Gene Ontology and KEGG enrichment identified relevant biological pathways and cancer hallmarks. Fifty-five co-expressed genes were linked to cancer pathways, inflammatory responses, cell migration, and development. KEGG enrichment highlighted viral protein interactions involving cytokines, IL-17 signaling, and chemokine receptor interactions. These genes were associated with cancer hallmark pathways, including angiogenesis, inflammation, proliferation, genomic instability, invasion, and metastasis. Their similar expression in CSCC and CIN 3 suggests a potential prognostic value and that CIN 3 progression may involve changes in gene expression. We propose the term \"CSCC-like carcinoma,\" indicating CIN 3's increased invasive potential at the molecular level.</p>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":" ","pages":"200327"},"PeriodicalIF":8.1,"publicationDate":"2025-08-05","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12354963/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769304","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":"Dysregulation of histone methylation in SV40 chromosomes during replication results in aberrant transcription and chromatin structure.","authors":"Barry Milavetz, Ranna Dawlaty, Jacob Haugen","doi":"10.1016/j.tvr.2025.200326","DOIUrl":"10.1016/j.tvr.2025.200326","url":null,"abstract":"<p><p>Since early and late transcription are both regulated from the same central regulatory region in SV40 chromatin, the location of nucleosomes carrying histone modifications may contribute to controlling the direction of transcription from the regulatory region. This could occur through the generation of active chromatin in the direction of transcription and repressive chromatin in the opposite direction. In order to test this hypothesis, we have characterized the products of SV40 transcription and location of nucleosomes carrying histone modifications in SV40 chromatin following treatment of infected cells with inhibitors of histone methylation metabolism. The inhibitors used included GSK-LSD1 to inhibit demethylation of H3K4me1 and H3K9me1, A366 to inhibit the introduction of H3K9me1, and UNC1999 to inhibit the introduction of H3K27me3. The results are consistent with a regulatory model in which nucleosomes carrying H3K9me1 and H3K27me3 located at the ends of the SV40 regulatory region act to regulate transcription.</p>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":" ","pages":"200326"},"PeriodicalIF":8.1,"publicationDate":"2025-07-31","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC12354966/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144769303","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":"Precise identification of viral–host integration events in HPV-positive cervical cancers by targeted long-read sequencing","authors":"Preetiparna Parida ,&nbsp;Nivedita Mukherjee ,&nbsp;Agastya Singh ,&nbsp;Shirley Lewis ,&nbsp;Krishna Sharan ,&nbsp;Sandeep Mallya ,&nbsp;Ashima Singh ,&nbsp;Surya Sarathi Das ,&nbsp;Mahadev Rao ,&nbsp;Daniel S. Higginson ,&nbsp;Radhakrishnan Sabarinathan ,&nbsp;Rama Rao Damerla","doi":"10.1016/j.tvr.2025.200325","DOIUrl":"10.1016/j.tvr.2025.200325","url":null,"abstract":"<div><div>Human papillomaviral (HPV) integrations into host human genome, a frequently observed event in HPV associated cervical cancer, are currently mapped through expensive Whole Genome sequencing (WGS) or RNA sequencing (RNA-seq) methodologies. This study aims to develop a targeted sequencing assay to determine HPV integrations in cervical tumors without the need for WGS or RNA-seq. We employed a library preparation strategy using tiled single primers that bind to HPV genome as a template and possibly extend HPV sequences into adjacent host human genomic sequences resulting in HPV and human chimeric sequences. Using this strategy, we sequenced known HPV integrations in HPV18 positive HeLa and HPV16 positive SiHa cell lines. We further used this method to detect HPV integration sites in four HPV-positive cervical cancer patients and confirmed these integration breakpoints by WGS and Sanger sequencing. Functional impact of HPV integrations was explored through differentially expressed genes within or near topologically associating domain (TAD) boundaries, possibly disrupted by respective integration events in these patients. We found <em>ZFP36L1, CPA3, CPB1</em> and <em>CXCL8</em> as some of the differentially expressed genes within disrupted TADs, which are known cancer associated genes. Our approach also reduced the cost of HPV integration detection by 90 % compared to WGS while also minimizing sequencing data volume. We believe that this method captures HPV integrations at significantly reduced costs and lesser sequencing data volume leading to better understanding of disease progression and monitoring cancer treatment.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"20 ","pages":"Article 200325"},"PeriodicalIF":4.7,"publicationDate":"2025-07-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668997","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}

{"title":"Recurrent integration of domestic cat hepatitis B virus DNA near feline CCNE1 supports an oncogenic role in hepatocellular carcinoma in cats","authors":"João P. Cavasin ,&nbsp;Min-Chun Chen ,&nbsp;Harout Ajoyan ,&nbsp;Melanie J. Dobromylskyj ,&nbsp;Wei-Hsiang Huang ,&nbsp;Mason Jager ,&nbsp;Kate Van Brussel ,&nbsp;Rebecca Rockett ,&nbsp;Omid Nekouei ,&nbsp;Penny Watson ,&nbsp;Jason Bestwick ,&nbsp;Yan Ru Choi ,&nbsp;Jonathan A. Lidbury ,&nbsp;John M. Cullen ,&nbsp;Edward Holmes ,&nbsp;Jörg M. Steiner ,&nbsp;Thomas Tu ,&nbsp;Julia A. Beatty","doi":"10.1016/j.tvr.2025.200324","DOIUrl":"10.1016/j.tvr.2025.200324","url":null,"abstract":"<div><div>Hepatitis B virus (HBV) is the major cause of hepatocellular carcinoma (HCC) in humans. Domestic cat hepatitis B virus (DCHBV) naturally infects cats worldwide, but the oncogenic potential of this hepadnavirus is unclear. We investigated whether DCHBV contributes to feline HCC. Feline liver biopsies diagnosed with HCC (cases) and lymphocytic cholangitis (controls) were tested for DCHBV DNA by PCR. DCHBV-positive HCCs were further characterised by <em>in situ</em> hybridisation (ISH), whole-genome sequencing (WGS) and phylogenetic analysis. Targeted capture sequencing was used to identify and map viral DNA integrations. DCHBV DNA was detected in 17/71 (23.9 %) HCCs versus 0/88 controls (P &lt; 0.001). ISH confirmed hepatocyte-specific viral localization. Phylogenetic analysis placed six viruses in genotype A, and a seventh divergent virus in genotype B virus. Virus-host chimeric sequences, consistent with integration sites, were identified in 11/16 PCR-positive HCCs. Eight of the 11 integration sites were independently confirmed with WGS. Viral termini in integrated DCHBV sequences corresponded to double-stranded linear DNA, the substrate for HBV integration. Five unique DCHBV integrations fell within, or were adjacent to, the promoter of the feline homologue of proto-oncogene <em>CCNE1</em>, a recurrent target for HBV integration in human HCC. Our findings reveal a compelling association between DCHBV detection and HCC in cats. Critically, virus integration in DCHBV-associated HCC is described for the first time, supporting that, like HBV, DCHBV can promote hepatocarcinogenesis by insertional mutagenesis. Clarification of fundamental DCHBV virology <em>in vitro,</em> and the consequences of natural infection could advance disease-prevention strategies for feline and human patients.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"20 ","pages":"Article 200324"},"PeriodicalIF":8.1,"publicationDate":"2025-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144668998","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}

{"title":"The immunological heterogeneity of squamous cell carcinoma and adenocarcinoma of the uterine cervix: a systematic review","authors":"Marije Adriana Strikwerda ,&nbsp;Sabrina Anouck Weerstand ,&nbsp;George Louis Burchell ,&nbsp;Jacqueline Maria Tromp ,&nbsp;Constantijne Helene Mom ,&nbsp;Tanja Denise de Gruijl","doi":"10.1016/j.tvr.2025.200323","DOIUrl":"10.1016/j.tvr.2025.200323","url":null,"abstract":"<div><h3>Background</h3><div>Cervical cancer is the fourth most common malignancy in women worldwide and generally driven by persistent infection with high-risk human papillomavirus. Squamous cell carcinoma (SCC) and adenocarcinoma (AC) are the two most common histological subtypes, with a relative increase in adenocarcinomas in the last decades. The immunological differences between cervical squamous cell carcinoma and adenocarcinoma remain largely unexplored. Understanding these distinctions is crucial for developing tailored therapies that can improve treatment outcomes for patients with cervical cancer. This systematic review provides an overview of the immunological features of squamous cell carcinoma and adenocarcinoma of the uterine cervix.</div></div><div><h3>Methods</h3><div>A systematic search was performed in PubMed, Embase.com, Web of Science, and Cochrane Library. All articles addressing immunological features of squamous cell carcinoma and adenocarcinoma of the uterine cervix were reviewed and included based on predefined inclusion and exclusion criteria.</div></div><div><h3>Results</h3><div>In total, 3207 articles were screened, of which 43 were included. Studies show that cervical squamous cell carcinomas are characterised by a more inflamed tumour microenvironment, but also contain more regulatory T cells and immune checkpoints. In contrast, adenocarcinomas are characterised by lower immune cell infiltration, contributing to its poorer prognosis and more limited response to treatment.</div></div><div><h3>Conclusion</h3><div>The observed differences emphasize the need for further research into subtype-specific differences and distinct therapeutic strategies. For squamous cell carcinomas, future research should focus on combinatorial immune checkpoint blockade, including regulatory T cell-depleting strategies. For adenocarcinomas, oncolytic virotherapy, therapeutic vaccination, and oncogenic signalling interference should be explored.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"20 ","pages":"Article 200323"},"PeriodicalIF":4.7,"publicationDate":"2025-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144596442","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}

{"title":"Human cytomegalovirus UL82 promotes colorectal cancer cell proliferation through inhibiting the ubiquitination of OGDH via ANGPT2","authors":"Lanni Wang ,&nbsp;Ruini Li ,&nbsp;Haitao Ren ,&nbsp;Chaoyi Jiang ,&nbsp;Ye Shi ,&nbsp;Bing Wang ,&nbsp;Wenyu Jin ,&nbsp;Jiaxue Wang ,&nbsp;Linhua Lan ,&nbsp;Feng Xu ,&nbsp;Guangxin Xiang ,&nbsp;Xiaoqun Zheng","doi":"10.1016/j.tvr.2025.200322","DOIUrl":"10.1016/j.tvr.2025.200322","url":null,"abstract":"<div><div>Human cytomegalovirus (HCMV) infection and its association with tumorigenesis and tumor progression have garnered increasing attention. Previous research results have indicated that the detection rate of HCMV <em>UL82</em> is higher in colorectal cancer (CRC) tissues and is correlated with poor prognosis in patients, yet the underlying mechanisms remain unclear. In this study, a cell model transfected with UL82 was established. Through <em>in vitro</em> and <em>in vivo</em> experiments, it was found that UL82 promoted the proliferation of CRC cells. Transcriptomic and metabolomic analyses revealed that UL82 could influence CRC glucose metabolism and cell proliferation by upregulating the key TCA cycle enzyme OGDH. Additionally, UL82 also affected CRC cell proliferation by upregulating the expression of ANGPT2, and silencing ANGPT2 resulted in a reduction in OGDH protein levels. Finally, through the investigation of the ubiquitin-mediated degradation pathway of OGDH, it was demonstrated that ANGPT2 inhibited the protein degradation of OGDH via deubiquitination, thereby maintaining its stability. In summary, UL82 promotes CRC cell proliferation by upregulating ANGPT2, which inhibits the ubiquitin-mediated degradation of OGDH, suggesting that targeting the UL82/ANGPT2/OGDH axis may offer a potential clinical strategy for the diagnosis of CRC.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"20 ","pages":"Article 200322"},"PeriodicalIF":4.7,"publicationDate":"2025-06-24","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144470582","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}

{"title":"Editorial board member","authors":"","doi":"10.1016/S2666-6790(25)00008-4","DOIUrl":"10.1016/S2666-6790(25)00008-4","url":null,"abstract":"","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200320"},"PeriodicalIF":4.7,"publicationDate":"2025-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144271982","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}

{"title":"Clinical performance of the SureX PCR HPV test versus hybrid capture assays (DH2/careHPV) in primary cervical cancer screening","authors":"Yumei Ouyang ,&nbsp;Guzhanuer Abuduxikuer ,&nbsp;Tangnuer Abulimiti ,&nbsp;Guligeina Abudurexiti ,&nbsp;Qian Zhuo ,&nbsp;Wenyun Li ,&nbsp;Kadeliya Muhetaer ,&nbsp;Shaliya Abuduwufu ,&nbsp;Gulixian Tuerxun ,&nbsp;Remila Rezhake ,&nbsp;Guzhalinuer Abulizi","doi":"10.1016/j.tvr.2025.200319","DOIUrl":"10.1016/j.tvr.2025.200319","url":null,"abstract":"<div><h3>Background</h3><div>Evaluating novel human papillomavirus (HPV) tests in well-designed, population-based screening studies is essential for ensuring the benefits of cervical cancer screening.</div></div><div><h3>Methods</h3><div>8638 women aged over 25 years from China underwent HPV screening using a PCR-based full genotyping HPV assay (SureX HPV), alongside hybrid-capture HPV tests (DH2/careHPV) and cytology. Any abnormal results triggered colposcopy and biopsy if indicated. Screening performance was evaluated for detecting cervical intraepithelial neoplasia grade 2 or worse (CIN2+) and CIN3+.</div></div><div><h3>Results</h3><div>The high-risk HPV (hrHPV) positive rate by SureX HPV was significantly higher than by careHPV (11.0 % vs. 8.2 %, <em>P</em> &lt;0.01) but similar to DH2 HPV (12.0 % vs. 11.5 %, <em>P</em> =0.34). The overall agreement rates between SureX HPV and careHPV/DH2 HPV were 93.5 % (Kappa=0.63) and 94.0 % (Kappa=0.71). For CIN2+ detection, SureX HPV showed not-significantly higher sensitivity than careHPV (91.2 % vs 82.5 %, <em>P</em> =0.18) but lower specificity (91.2 % vs. 93.1 %, <em>P</em> &lt;0.01). Compared to DH2, SureX HPV demonstrated comparable sensitivity (95.7 % for both, <em>P</em> =1.0) and specificity (89.5 % vs. 90.2 %, <em>P</em> =0.21). Similar patterns were observed for CIN3+ detection. The area under the receiver operating characteristic curve (AUC) for the SureX HPV was similar to hybrid-capture HPV tests (<em>P</em> &gt;0.05 for both) and significantly higher than the cytology (ASC-US+) test for CIN2+/CIN3+ detection (<em>P</em> &lt;0.05 for both).</div></div><div><h3>Conclusions</h3><div>The PCR-based SureX HPV test demonstrated good concordance with well-validated hybrid-capture HPV tests in detecting hrHPV and CIN2+/CIN3+. Despite its slightly suboptimal specificity, SureX HPV could be an alternative in primary screening due to its full genotyping capability.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200319"},"PeriodicalIF":4.7,"publicationDate":"2025-05-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"144086923","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}

{"title":"Evaluating the performance of the Xpert HPV assay in detecting HPV positive cases in Morocco","authors":"Said Ali Yerim ,&nbsp;Youssef Chami Khazraji ,&nbsp;Rachid Bekkali ,&nbsp;Maria Bennai ,&nbsp;Nassiba Bahra ,&nbsp;Imane Chaoui ,&nbsp;Fatima Zahra Chellat ,&nbsp;Zineb Gaizi ,&nbsp;Nabil Tachfouti ,&nbsp;Anas Benabdellah ,&nbsp;Bouchra Belkadi ,&nbsp;Mohammed Attaleb ,&nbsp;Mohamed Amine Berraho ,&nbsp;Mohammed El Mzibri","doi":"10.1016/j.tvr.2025.200318","DOIUrl":"10.1016/j.tvr.2025.200318","url":null,"abstract":"<div><div>Recently, the World Health Organization recommended integrating HPV testing into cervical cancer screening programs globally. This study aimed to compare the GeneXpert assay with PCR-sequencing for HPV detection and genotyping to assess the feasibility of incorporating HPV molecular testing into cervical cancer screening. A total of 1000 women aged 30 or 40 from rural and urban areas across four regions in Morocco with high sexually transmitted infection prevalence were recruited. After excluding 21 invalid tests, DNA testing on the remaining 979 samples showed an HPV prevalence of 4.0 % (39/979) by PCR and 5.0 % (49/979) by Xpert, with an overall prevalence of 5.7 % (56/979) when combining both techniques. The concordance rate between the tests was 97.5 %. Notably, the Xpert HPV assay was highly efficient in detecting HPV, with nearly all identified HPVs being high-risk oncogenic types, predominantly HPV16, 18, 31, 35, and 45.</div><div>The Xpert HPV assay has demonstrated excellent analytical performance, making it a reliable option for HPV detection in vaginal and cervical swabs. Its integration into primary cervical cancer screening programs could significantly enhance the early detection of HPV-positive cases, thereby strengthening the screening framework and potentially reducing both the incidence and mortality of cervical cancer. Future studies should focus on confirming these results and exploring the utility of this method in conjunction with other diagnostic tools such as visual inspection with acetic acid (VIA) for a comprehensive assessment of its effectiveness in real-world settings.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 200318"},"PeriodicalIF":4.7,"publicationDate":"2025-04-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"143847403","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}

{"title":"Daxx and HIRA go viral – How chromatin remodeling complexes affect DNA virus infection","authors":"Julia Mai ,&nbsp;Masih Nazari ,&nbsp;Thomas Stamminger ,&nbsp;Sabrina Schreiner","doi":"10.1016/j.tvr.2025.200317","DOIUrl":"10.1016/j.tvr.2025.200317","url":null,"abstract":"<div><div>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.</div></div>","PeriodicalId":52381,"journal":{"name":"Tumour Virus Research","volume":"19 ","pages":"Article 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}