Journal of NeuroVirology最新文献

{"title":"Diagnostic challenges in HIV-associated Burkitt lymphoma initially presenting with multifocal neurological symptoms.","authors":"Motohiro Okumura, Kenichi Sakuta, Yui Shiozawa, Yuichiro Muraoka, Yuri Mizuno-Shojima, Shota Nakagawa, Ai Iwauchi, Hideki Uryu, Yasuyuki Iguchi","doi":"10.1007/s13365-026-01330-w","DOIUrl":"10.1007/s13365-026-01330-w","url":null,"abstract":"<p><p>A 46-year-old male initially presented with multifocal neurological symptoms including leptomeningeal involvement, multiple cranial nerve palsies, myeloradiculopathy, myelopathy, and cauda equina syndrome. On admission, the patient tested positive for the human immunodeficiency virus (HIV). Based on the initial physical examination, which suggested Guillain-Barré syndrome, plasma exchange was initiated; however, clinical improvement was limited. Further evaluation, including histopathological analysis of the ileocecal mass and flow cytometry of the cerebrospinal fluid, revealed Burkitt lymphoma with widespread involvement of the central and peripheral nervous systems. Despite the early initiation of chemotherapy, the patient died. This case illustrates the diagnostic complexity of neurological presentations in patients with HIV infection and suggests that Burkitt lymphoma may be included in the differential diagnosis of rapidly progressive multifocal neurological symptoms.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620461","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Association between graded short-term lymphocyte count decline and epilepsy risk in HIV-positive patients: a retrospective cohort study.","authors":"Khalid Mohamed, Chimezie Amaefuna, Huda Al-Bana, Ronak Bhatia, Aman Shahzad, Faiza Chowdhury, Anand Deonarine, Nicholas Azinge, Mekdem Bisrat, Elizabeth Beyene, Miriam Michael","doi":"10.1007/s13365-026-01329-3","DOIUrl":"10.1007/s13365-026-01329-3","url":null,"abstract":"<p><p>To evaluate whether varying degrees of lymphocyte count decline in HIV-positive adults are associated with increased short-term incidence of epilepsy or convulsions. A retrospective cohort study was conducted using the TriNetX global research network. HIV-positive patients with a lymphocyte count ≥ 1.2 × 10³/µL were categorized based on subsequent decline within 3 months: mild (1.01-1.19), moderate (0.81-1.0), or significant (0.61-0.8). Risk analysis and Kaplan-Meier survival analysis were performed and patients with prior diagnosis of epilepsy (G40) or convulsions (R56.9) were excluded. The risk of developing epilepsy or convulsions increased with greater lymphocyte decline. Compared to patients with stable counts, the odds ratios were 1.073 for the mild group, 2.222 for the moderate group, and 3.189 for the significant drop group. Hazard ratios followed a similar trend, reaching 3.24 in the 0.61-0.8 group. Only the mild drop group did not show a statistically significant difference in risk or survival curves. Kaplan-Meier analysis at 1 year showed significant separation between survival curves for all groups except the mild group (p = 0.6973). Among HIV-positive adults, greater short-term lymphocyte count decline is associated with a higher short-term risk of epilepsy or convulsions. These findings suggest that lymphocyte trends may serve as an early signal for neurologic vulnerability. Further investigation is warranted to clarify the underlying mechanisms and clinical implications.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-29","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148620307","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Retraction Note: Neurotoxic effects of the HCV core protein are mediated by sustained activation of ERK via TLR2 signaling.","authors":"Amy D Paulino, Kiren Ubhi, Edward Rockenstein, Anthony Adame, Leslie Crews, Scott Letendre, Ronald Ellis, Ian P Everall, Igor Grant, Eliezer Masliah","doi":"10.1007/s13365-026-01332-8","DOIUrl":"10.1007/s13365-026-01332-8","url":null,"abstract":"","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148603934","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"The emerging role of circular RNAs in neurodegenerative diseases and viral infections.","authors":"Finley Medina, Anna Bellizzi","doi":"10.1007/s13365-026-01324-8","DOIUrl":"10.1007/s13365-026-01324-8","url":null,"abstract":"<p><p>Circular RNAs (circRNAs) represent a class of highly stable, covalently closed RNA molecules increasingly recognized as important regulators of brain aging and neurodegenerative disease. Growing evidence also implies circRNAs in viral infection, suggesting a potential intersection between viral neuropathogenesis and neurodegeneration. However, no studies have yet directly integrated circRNAs, neurotropic viral infections, and neurodegenerative disorders within a single mechanistic framework. To date, specific circRNAs have been linked to the progression of Alzheimer's disease and Parkinson's disease, where they regulate central pathological processes including amyloid-β clearance, neuroinflammation, synaptic plasticity, neuronal apoptosis, and oxidative stress. Moreover, it has been established that both host cells and viruses produce circRNAs during infection. Virus-derived circRNAs can enhance viral replication, promote immune evasion, and support latency. In contrast, host circRNAs contribute to antiviral defense by acting as microRNA sponges, interacting with viral proteins, or encoding peptides with antiviral activity, mechanisms particularly explored in viral oncogenesis. In this review, we will evaluate the most updated research evidence on the role of circRNAs in major neurodegenerative diseases and neurotropic viral infections. Considering the growing concern regarding the long-term neurological consequences of viral infections, including chronic neuroinflammation, viral reactivation, and post-viral syndromes, dysregulated circRNAs may represent a mechanistic link between viral infection and associated neurodegenerative processes. Finally, we will discuss future directions for identifying circRNAs-based biomarkers and developing circRNAs-targeted therapeutic strategies for age-related and virus-associated neurological disorders.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13350144/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148421273","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HSV-1 and VZV co-reactivation: implications for worsening neurological and neurodegenerative diseases.","authors":"Christy S Niemeyer, Maria A Nagel, Diego Restrepo, Andrew N Bubak","doi":"10.1007/s13365-026-01323-9","DOIUrl":"10.1007/s13365-026-01323-9","url":null,"abstract":"<p><p>Herpes simplex virus type 1 (HSV-1) and varicella zoster virus (VZV) are neurotropic human alphaherpesviruses that establish lifelong latency in peripheral ganglia. While traditionally studied in isolation, increasing evidence indicates that co-reactivation of these viruses may be clinically significant, especially in the context of aging and immunosuppression, and underdiagnosed. Recent studies show that both viruses can reside in the same trigeminal ganglion (TG) and interact synergistically to potentiate and exacerbate neurological and neurodegenerative disease. This review summarizes emerging insights into the clinical, immunological, and neuropathological implications of HSV-1 and VZV co-reactivation, with a particular emphasis on VZV-derived extracellular vesicles (EVs) as mediators of immune suppression and enhancers of secondary HSV-1 infection.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13346214/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148405267","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Plasma suPAR and domain-specific cognitive performance in virologically suppressed women with HIV.","authors":"Hemil Gonzalez, K Ridgeway, Eran F Shorer, Raha Dastgheyb, Rohan Rajagopal, Yanxia Cao, Ralph Morack, Eunsil Hahm, Kathleen M Weber, Leah H Rubin, Audrey L French","doi":"10.1007/s13365-026-01321-x","DOIUrl":"10.1007/s13365-026-01321-x","url":null,"abstract":"<p><p>Cognitive impairment remains common among people living with HIV despite effective antiretroviral therapy, with women disproportionately affected. Identifying stable and scalable inflammatory biomarkers that reflect domain-specific vulnerability is important for improving risk assessment in this population. Soluble urokinase plasminogen activator receptor (suPAR) is a circulating marker of immune activation with established analytical stability and prognostic value across multiple inflammatory conditions, including HIV. However, its relationship to cognitive performance in virologically suppressed women living with HIV (WLWH) is not well characterized. We conducted a cross-sectional study of 200 virologically suppressed WLWH enrolled at the Chicago-Cook County site of the MWCCS. Plasma suPAR was measured using the suPARnostic® AUTO Flex ELISA. Cognitive performance was assessed using demographically adjusted T-scores across executive function, psychomotor speed, motor function, memory, attention/working memory, verbal fluency, and learning. Multivariable linear regression models examined associations between log-transformed suPAR and continuous cognitive scores, adjusting for menopause status and suPAR storage duration. Relationships between log-suPAR and odds of impairment (T-score ≤ 40) were examined in adjusted logistic regression models. A same-visit subset was analyzed to account for timing differences between blood collection and cognitive testing. Higher log-suPAR was associated with lower psychomotor speed, lower motor function, and lower global average cognition. Odds of impairment in psychomotor speed, and motor function were higher with increasing log-suPAR. Sensitivity analyses showed consistent effect directions and magnitudes. These findings suggest that elevated suPAR reflects inflammation-related, domain-specific cognitive vulnerability in virologically suppressed WLWH and warrants further evaluation in longitudinal studies; clinical translation will require validation in larger, more demographically diverse cohorts, with concurrent assessment of menopausal and vascular risk profiles.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-08","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13346328/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148405275","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"HTLV-1 infection in patients with neurological manifestations in Northeast Brazil.","authors":"Artur Fernando Soares da Silva, Yan Charles da Silva Bastos, Juliana Tiemi Oikawa, Ana Eliza Vargas Eskinazi Sant'Anna, Gabriel Galindo Cunha, Clarice Neuenschwander Lins de Morais, Elisa de Almeida Neves Azevedo, Maria Rosângela Cunha Duarte Coêlho","doi":"10.1007/s13365-026-01322-w","DOIUrl":"10.1007/s13365-026-01322-w","url":null,"abstract":"<p><p>Human T-lymphotropic virus type 1 (HTLV-1) infection is associated with a broad spectrum of neurological manifestations, including conditions that may precede the development of HTLV-1-associated myelopathy/tropical spastic paraparesis (HAM/TSP). This analytical, descriptive cross-sectional study aimed to estimate the prevalence of HTLV-1 infection and describe associated sociodemographic, socioeconomic, behavioral, and clinical characteristics among patients with neurological disorders followed at a tertiary public hospital in Northeast Brazil between 2024 and 2025. A total of 300 patients underwent serological screening using an enzyme-linked immunosorbent assay (ELISA) with a commercial kit (DiaSorin Murex HTLV-1 + 2). Samples with positive or indeterminate results underwent DNA extraction and molecular confirmation by polymerase chain reaction (PCR) to differentiate viral types. Three patients tested positive for HTLV-1, resulting in an overall prevalence of 1.0%. All HTLV-1-positive individuals were women aged 43 to 72 years with low educational attainment and income. Univariate analyses identified significant associations with injection drug use, history of blood transfusion, and family history of HTLV-1 infection. Clinically, HTLV-1-positive patients presented heterogeneous neurological manifestations, ranging from urinary dysfunction and lower limb sensory and motor impairment to musculoskeletal and inflammatory symptoms. These findings highlight the broad spectrum of neurological involvement associated with HTLV-1 infection. Early identification of HTLV-1 may contribute to improved clinical management and inform public health strategies.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13337575/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390985","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Circadian-guided oncolytic virotherapy for glioblastoma.","authors":"Alexandro Guterres","doi":"10.1007/s13365-026-01325-7","DOIUrl":"10.1007/s13365-026-01325-7","url":null,"abstract":"<p><p>Glioblastoma (GBM) remains one of the most aggressive and lethal malignancies, with clinical outcomes under the standard-of-care Stupp protocol remaining suboptimal. While oncolytic virus (OV) therapy has emerged as a mechanistically distinct and promising approach, its clinical success is frequently hindered by profound intratumoral heterogeneity and emerging resistance. This critical review proposes that the efficacy of virotherapy may be meaningfully enhanced by integrating circadian biology into treatment schedules; a paradigm termed \"Oncolytic Chronovirotherapy.\" Recent evidence demonstrates that the infection cycle of neurotropic viruses, which serve as the scaffold for many OVs, is not a static process but is inherently regulated by the host's circadian clock. Fundamental studies reveal that the expression of essential viral entry receptors, such as Nectin-1 (for HSV-1) and p75NTR, exhibits robust circadian oscillations directly coordinated by the core molecular clock, specifically the BMAL1/CLOCK complex. Furthermore, the tumor immune microenvironment and cellular vulnerability to adjuvant chemotherapy (temozolomide) show synchronized peaks of activity, typically concentrated during the morning window, which often coincides with the nadir of DNA repair enzymes like MGMT. We argue that synchronizing OV administration with these windows of maximal receptor density and robust immune surveillance may maximize tumor lysis and facilitate the conversion of \"cold\" tumors into \"hot,\" immune-responsive environments. The utilization of personalized circadian biomarkers and mathematical modeling to guide therapy delivery will be essential for the next generation of precision neuro-oncology.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-07-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13337691/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148390996","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Hantavirus infection: Neurologic manifestations should not be overlooked.","authors":"Annarita Botta, Christian Messina","doi":"10.1007/s13365-026-01320-y","DOIUrl":"10.1007/s13365-026-01320-y","url":null,"abstract":"<p><p>Hantavirus infection is primarily associated with hemorrhagic fever with renal syndrome (HFRS) and hantavirus cardiopulmonary syndrome (HCPS), with predominant renal and pulmonary involvement. However, neurological manifestations affecting both the central nervous system (CNS) and peripheral nervous system (PNS) are increasingly recognized. We conducted a narrative review of the literature to summarize the current evidence regarding hantavirus-associated neurological involvement. Reported CNS manifestations included encephalitis, encephalopathy, seizures, meningitis, neurocognitive alterations, posterior reversible encephalopathy syndrome, transverse myelitis, and cerebral hemorrhage. PNS involvement appeared less frequent and included Guillain-Barré syndrome, cranial nerve palsies, neuropathic pain, and sensory disturbances. Neuroimaging findings were heterogeneous, while cerebrospinal fluid analysis often demonstrated nonspecific inflammatory changes. Advanced molecular techniques such as metagenomic next-generation sequencing may improve diagnostic sensitivity, particularly in immunocompromised patients. Current evidence suggests that neurological involvement may result from endothelial dysfunction, neuroinflammation, immune-mediated injury, blood-brain barrier disruption, and, in selected cases, direct viral neuroinvasion. Greater clinical awareness is needed to improve recognition of neurological complications during hantavirus infection. Further prospective studies are required to better define the epidemiology, pathogenesis, and optimal diagnostic approaches of hantavirus-associated neurological disease.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148330508","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Zika virus infection in the brains of lymphocyte-deficient mice does not lead to neurological symptoms despite sustained high viral load.","authors":"Amelia Montemarano, Elizabeth Balint, Ali A Ashkar","doi":"10.1007/s13365-026-01319-5","DOIUrl":"10.1007/s13365-026-01319-5","url":null,"abstract":"<p><p>Zika virus (ZIKV) infections have been linked to severe neurological disorders, including microcephaly and Guillain-Barré syndrome in humans as well as mouse models of ZIKV infection. Despite the association, the mechanisms underlying ZIKV-induced neuropathology remain incompletely understood. We have recently shown that antigen independent CD8⁺ T cells mediate neurological disease in ZIKV-infected mice independent of the amount of infectious virus in the CNS. To further investigate the role of brain viral load and lymphocytes in ZIKV infection we studied the viral kinetics, pathology, and immune responses of ZIKV-infected NOD-Rag1^-/-Il2rg^-/- mice, which are deficient in lymphoid cells. Despite prolonged high viral titers in the brain, NOD-Rag1^-/-IL2rg^-/- mice did not develop neurological symptoms following ZIKV infection, contrasting with the infection outcomes of Ifnar1^-/- mice which exhibit paralysis despite lower viral load. Notably, we observed significant differences in brain myeloid cells in the presence or absence of lymphoid cells. While Ifnar1^-/- mice showed robust infiltration of CD45^hiCD11b⁺ cells in the brain, lymphocyte-deficient NOD-Rag1^-/-IL2rg^-/- mice exhibited reduced recruitment and activation of these cells. Additionally, we found that CD45^hiCD11b⁺ cells displayed a more inflammatory phenotype in Ifnar1^-/- mice compared to NOD-Rag1^-/-IL2rg^-/- mice. Our study highlights the complex interplay between the immune system and viral infection in ZIKV-induced neuropathology and underscores the importance of considering immune responses in the development of therapeutic interventions for ZIKV.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148302015","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}