Reviews in Medical Virology最新文献

{"title":"USP10 Dysregulation in Oncogenic Virus-Driven Tumourigenesis and Immune Evasion.","authors":"Zike Li, Dongjing Zhang, Siqi Chen, Xin Zhang, Zhihong Wang, Changsheng Huang, Qi Wu, Anyi Liu, Kangdi Li, Ziran Wei, Junbo Hu","doi":"10.1002/rmv.70145","DOIUrl":"10.1002/rmv.70145","url":null,"abstract":"<p><p>Ubiquitination is a critical post-translational modification that regulates protein stability, signalling pathways, and cellular homoeostasis. Increasing evidence shows that oncogenic viruses exploit the host ubiquitin system to promote viral persistence, immune evasion, and malignant transformation. Among the various host factors targeted, deubiquitinating enzymes (DUBs) play a pivotal role because they reverse ubiquitination, thereby regulating the stability, localization, and activity of key signalling proteins. Ubiquitin-specific peptidase 10 (USP10) has emerged as a particularly critical DUB in the context of viral tumourigenesis, functioning as a molecular rheostat that balances tumour suppression and oncogenic progression. The dysregulation of USP10 by viral oncoproteins facilitates a dual assault on the host: the subversion of innate immune sensors, specifically the RIG-I, MAVS, and cGAS-STING pathways, and the evasion of adaptive immune surveillance through the stabilisation of immune checkpoints, such as PD-L1, and the disruption of MHC-I antigen presentation. This comprehensive analysis explores the biochemical architecture of USP10, its paradoxical roles in cancer, and the specific mechanisms through which oncogenic viruses exploit this enzyme to drive malignancy and immune escape.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70145"},"PeriodicalIF":5.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147699644","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Vertical Transmission of Type B Coxsackieviruses: A Systematic Review Emphasising Clinical Evidence and Seriousness of a Neglected Issue.","authors":"Aymen Halouani, Hela Jaidane","doi":"10.1002/rmv.70144","DOIUrl":"10.1002/rmv.70144","url":null,"abstract":"<p><p>Group B Coxsackieviruses (CV-B), like other enteroviruses, are essentially transmitted from person to person through the faecal-oral route. However, vertical transmission from mother to infant, through transplacental passage or inhalation of contaminated cervical swabs during delivery, can also occur. This underestimated route of CV-B transmission has been associated with serious consequences, mainly abortion, stillbirth, congenital malformations, as well as serious morbidity and mortality in the newborns. Based on a systematic review of clinical observations, this paper explains the mechanisms of CV-B vertical transmission and its diverse consequences, with a special focus on associated diseases. Preventive measures, therapeutic strategies, and recommendations are also addressed.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70144"},"PeriodicalIF":5.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147616572","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A Comprehensive Review of Vaccine Technologies for Pandemic Preparedness Against Highly Pathogenic Avian Influenza.","authors":"Muzamil Ahmad Rather, Muttahir Aman, Amreena Hassan, Parvaiz A Koul, Varsha Potdar, Nazir Ahmad Ganai, Nadeem Shabir","doi":"10.1002/rmv.70161","DOIUrl":"10.1002/rmv.70161","url":null,"abstract":"<p><p>Highly Pathogenic Avian Influenza Virus (HPAIV) poses a serious threat to the poultry industry and public health due to its global spread to avian and non-avian hosts. To combat the spread of HPAIVs in poultry and reduce the risk of zoonotic transmission, the World Health Organization underscores the importance of strategic surveillance and advancements in vaccination strategies. For the prevention of avian influenza outbreaks in poultry and their transmission to humans and cattle, vaccination would be a critical tool. We critically review the limitations of current vaccine platforms and highlight innovative vaccine strategies against HPAIV that are essential for addressing future pandemic threats. The aim is to clarify the progress and challenges in AIV vaccine development and offer insights into recent technological advancements shaping future vaccination strategies.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70161"},"PeriodicalIF":5.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147820278","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Congenital CMV and Hearing Loss-How Does it Happen and How to Prevent it.","authors":"Karen B Fowler","doi":"10.1002/rmv.70156","DOIUrl":"10.1002/rmv.70156","url":null,"abstract":"<p><p>Congenital cytomegalovirus (cCMV) is found worldwide and significantly contributes to permanent childhood hearing loss. CMV has been known to cause sensorineural hearing loss (SNHL) for more than half a century, and CMV-related hearing loss has consistently been present in all childhood populations where infants with cCMV have been identified and followed in the first years of life. CMV-related hearing loss has a variable onset, with some cases of hearing loss occurring at birth and others developing within the first 5 years of life. Further deterioration of hearing loss may occur in children with CMV-related hearing loss. In contrast, other children experience improvements or fluctuating hearing loss. SNHL due to CMV is likely to involve both direct viral-mediated damage that occurs when the virus infects cells within the cochlea and immune or inflammatory responses in the inner ear. The studies in animal models and human temporal bones support that virus infection and host inflammatory responses may lead to both virus-mediated and virus and host-derived damage to the auditory system. As more children are being tested for CMV by newborn screening, SNHL is being identified more often. Current recommendations are for valganciclovir treatment in children with cCMV infection and SNHL; however, research gaps exist regarding the long-term effectiveness of valganciclovir. Without a licenced CMV vaccine, CMV behavioural preventative measures that minimise maternal saliva and urine exposures from young children is the only primary intervention available to reduce CMV infections and, therefore, CMV-related SNHL. Lack of CMV awareness and knowledge of the CMV disease burden in the population limits this approach, and more CMV education is needed. Data gaps exist in estimating the public health burden and lifetime economic burden of CMV. Without this data, it is not possible to accurately evaluate the cost-effectiveness of any CMV intervention or prevention strategy. Even after decades of attempting to identify which children with cCMV will have SNHL, further progression of loss, or late-onset loss, the need remains to identify the children with cCMV at increased risk of SNHL to provide timely detection and intervention for possible hearing loss.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70156"},"PeriodicalIF":5.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13110109/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147779794","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Oncovirus-Driven Endothelial Plasticity: Endothelial-to-Mesenchymal Transition as a Hijacked Pathway in Oncoviral Cardiovascular Pathogenesis.","authors":"Ming Li, Zhibo Li, Zhuo Zhao, Ziyuan Guo","doi":"10.1002/rmv.70143","DOIUrl":"10.1002/rmv.70143","url":null,"abstract":"<p><p>Oncoviruses utilise various molecular strategies to modulate host cells and induce microenvironments that favour viral persistence, immune evasion, and disease progression. Endothelial-to-mesenchymal transition (EndMT) has recently emerged as a critical, yet underrecognized, pathway hijacked by oncoviral pathogens to modulate endothelial plasticity within the cardiovascular system. Accumulating evidence indicates that Oncogenic and non-oncogenic viruses, including Kaposi's sarcoma-associated herpesvirus (KSHV/HHV-8), severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), human immunodeficiency virus (HIV), and other endothelial-tropic viruses, directly manipulate host signalling networks, such as TGF-β, Wnt/β-catenin, Notch, and NF-κB, to induce partial or complete EndMT. This virus-driven EndMT contributes to vascular remodelling, chronic inflammation, aberrant angiogenesis, and the development of oncoviral-associated cardiovascular pathology and vascular tumours. The present review integrates current virological and mechanistic insights into EndMT as a hijacked host process, highlighting its role at the virus-host interface and discussing emerging antiviral and pathway-targeted strategies aimed at limiting oncovirus-mediated endothelial dysfunction.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70143"},"PeriodicalIF":5.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147663085","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Post-Infectious Fatigue and Depression Following Dengue: A Systematic Review and Meta-Analysis of Associated Factors.","authors":"Anna Condé, Olivier Maillard, Chaturaka Rodrigo, Antoine Bertolotti, Carolina X Sandler, Andrew R Lloyd, Patrick Gérardin","doi":"10.1002/rmv.70164","DOIUrl":"10.1002/rmv.70164","url":null,"abstract":"<p><p>Post-dengue fatigue syndrome is a debilitating long-term condition that affects daily activities, quality of life, and productivity. Its underlying mechanisms remain unclear, but clinical similarities with post-dengue depression complicate differentiation. Therefore, we conducted a systematic review and meta-analysis to identify and compare factors associated with post-dengue fatigue and post-dengue depression. We searched PubMed, Science Direct, Web of Science and Google Scholar databases until 6 June 2025, with an update performed on 31 December 2025. This systematic review was conducted according to PRISMA guidelines. Meta-analyses were conducted to assess associations of demographic, biological, clinical, medical or psychosocial factors with post-dengue fatigue and post-dengue depression using pooled odds ratios (OR). The study protocol was registered in PROSPERO (CRD420250655004). Nine studies (2006-2023) covering 1470 patients were included. The systematic review identified 13 factors eligible for meta-analysis: twelve factors for post-dengue fatigue and one for post-dengue depression. Among these factors, female sex (OR 1.69, 95% CI: 1.33-2.14), myalgia (OR 3.45, 95% CI: 2.10-5.69), and severe dengue (OR 4.02, 95% CI: 1.45-11.13), particularly dengue haemorrhagic fever (OR 1.53, 95% CI: 1.04-2.24), were associated with post-dengue fatigue. No factor was associated with post-dengue depression in the meta-analysis. However, narrative synthesis revealed thrombocytopaenia as a shared factor of both outcomes. This study highlights risk profiles for post-dengue fatigue syndrome and depression, with female sex, myalgia, and dengue severity specifically associated with fatigue, while thrombocytopaenia might indicate a shared pathway. These findings support targeted surveillance and management strategies for at-risk patients and highlight the need for further research into post-dengue depression mechanisms.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70164"},"PeriodicalIF":5.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147982986","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Human Polyomaviruses of Clinical Relevance: Modes of Transmission and Associated Pathologies.","authors":"Joana M Oliveira, Cristina Luxo, Ana M Matos","doi":"10.1002/rmv.70166","DOIUrl":"10.1002/rmv.70166","url":null,"abstract":"<p><p>Polyomaviruses are non-enveloped viruses with double-stranded circular DNA genome. Currently, 13 members of the Polyomaviridae family have been classified as human polyomavirus (HPyVs). Despite high seroprevalence values have been reported for the majority of the HPyVs worldwide, the main mode of transmission remains to be elucidated, and simple and common routes, such as faecal-oral and respiratory have been suggested. In general, HPyVs are responsible for asymptomatic primary infection, followed by asymptomatic lifelong persistent infection. In situations of severe immunosuppression, viral reactivation of some HPyVs may occur and result in the development of associated clinical manifestations. JCPyV is the causative agent of Progressive Multifocal Leukoencephalopathy, BKPyV is associated with nephropathy among kidney transplant recipients, MCPyV with Merkel Cell Carcinoma and TSPyV with Trichodysplasia spinulosa. The association of certain HPyVs with severe diseases, in addition to the high seroprevalence of the majority of HPyVs, emphasises the need to address various knowledge gaps that still exists in the natural history of these viruses, including the transmission routes and the pathogenic mechanisms. The present review summarises current information on HPyV transmission routes and associated diseases, including diagnosis and available treatment options, highlighting the need for further studies.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70166"},"PeriodicalIF":5.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148006442","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HTLV-1-Driven Clonal Evolution and Immune Escape in Adult T-Cell Leukaemia: From Viral Persistence to Therapeutic Failure.","authors":"Zuhair M Mohammedsaleh, Abdullah F Shater","doi":"10.1002/rmv.70162","DOIUrl":"10.1002/rmv.70162","url":null,"abstract":"<p><p>Adult T-cell leukaemia/lymphoma (ATL) is an aggressive CD4 +T-cell malignancy caused by the human T-cell leukaemia virus type 1 (HTLV-1). Approximately 3%-5% of infected individuals develop ATL after a prolonged latency of 30-50 years, during which a complex interplay between viral oncoproteins and host genomic alterations drives the transition from viral persistence to overt malignancy. This transformation is orchestrated by the viral transactivator Tax, which initiates cellular transformation, and the HTLV-1 basic leucine zipper factor (HBZ), which maintains the malignant phenotype and promotes survival through immune evasion. Genomic profiling has revealed that over 90% of ATL cases harbour activating mutations in the T-cell receptor (TCR)-NF-κB signalling pathway, enabling the malignant clone to bypass viral dependency. Furthermore, ATL cells survive host immunosurveillance through sophisticated escape mechanisms, including the loss of MHC class I presentation and programed death-ligand 1 (PD-L1) overexpression via 3'-untranslated region (UTR) disruption. Despite the use of antiviral therapies and targeted monoclonal antibodies, therapeutic failure is common due to genomic instability-specifically TP53 mutations compromising Zidovudine/Interferon efficacy and CCR4 antigenic variations leading to mogamulizumab resistance. This review delineates the multi-step journey of HTLV-1-driven clonal evolution and evaluates the molecular barriers to effective clinical management.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70162"},"PeriodicalIF":6.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147820262","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Natural History of Human Papillomavirus (HPV) Infection in Males: Global Evidence From a Systematic Review and Meta-Analysis.","authors":"Jiaxing Qi, Haibin Wu, Rui Yan, Wenkai Zhou, Fang Shen, Juping Chen, Xingxing Zhang, Rui Bian, Changtai Zhu, Shigui Yang","doi":"10.1002/rmv.70168","DOIUrl":"10.1002/rmv.70168","url":null,"abstract":"<p><p>This systematic review provides a comprehensive global synthesis of male-specific infection patterns and determinants, aiming to inform targeted prevention and control strategies in public health. A systematic review and meta-analysis were conducted in accordance with the PRISMA 2020 statement. We systematically searched PubMed, Embase, Wanfang, and CNKI for studies on the natural history of HPV infection in males published between January 1, 2003, and March 10, 2025. Meta-analyses were conducted to estimate pooled rates of HPV clearance, persistence, recurrence, progression and transmission. A total of 89 studies involving 68,477 males were included. The overall pooled clearance rate of any HPV in males was 71.04 per 1000 person-months (95% CI: 56.55-87.17). Clearance rates varied by anatomical site, with the lowest rate observed in the oral region (38.79 per 1000 person-months, 95% CI: 10.43-85.13), followed by the anal (65.14 per 1000 person-months, 95% CI: 49.04-83.52) and genital sites (89.40 per 1000 person-months, 95% CI: 66.52-116.99). Clearance rates were lower among men who have sex with men and people living with HIV (PLWH) compared with heterosexual men and those living without HIV, respectively. The pooled progression rate within 12-24 months was 20.75% (95% CI: 6.44%-40.28%). Female-to-male HPV transmission rates were higher than male-to-female transmission rates. The overall recurrence rate of anogenital warts was 50.00% (95% CI: 39.00%-60.00%). Risk factors associated with persistent infection included age over 30 years, current smoking, having male sexual partners, and CD4+ cell counts below 200 cells/mm³. The natural history of HPV infection in males exhibits considerable heterogeneity across behavioural, immunological, anatomical, and virological factors. These findings highlight the importance of including males, particularly high-risk populations, in HPV vaccination, surveillance, and prevention strategies to better inform clinical practice and public health policy.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70168"},"PeriodicalIF":6.6,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148034469","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The Management of Congenital Cytomegalovirus Infection in an Era of Universal Newborn CMV Screening.","authors":"Emily R Harrison, W Charles Huskins, Mark R Schleiss","doi":"10.1002/rmv.70132","DOIUrl":"10.1002/rmv.70132","url":null,"abstract":"<p><p>The most common infectious disease responsible for paediatric developmental disability is congenital infection with human cytomegalovirus (cCMV). Many serious sequelae are caused by cCMV, including microcephaly, intracranial calcifications, neuronal migration defects, seizure disorders, developmental delay, and sensorineural hearing loss (SNHL). Although long-term neurodevelopmental impairment is clearly more common in newborns with clinically apparent disease at birth, more knowledge is needed about management in the era of universal cCMV screening, since screening identifies infants that, in the past, would not have been discovered during routine newborn care-infants that we reference in this review as having clinically inapparent cCMV (CICMV) infections. For newborns identified with CICMV infections by universal cCMV screening, longitudinal audiologic assessment is needed, but other necessary laboratory and neuroimaging studies, as well as indications for antiviral therapy, are uncertain. This review summarises current concepts about the approach to cCMV infections identified by universal screening, with emphasis on the CICMV infant. We identify areas for future research that should inform and direct future evaluation and management of these infants.</p>","PeriodicalId":21180,"journal":{"name":"Reviews in Medical Virology","volume":"36 3","pages":"e70132"},"PeriodicalIF":5.5,"publicationDate":"2026-05-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13036300/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147582313","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":2,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}