Journal of NeuroVirology最新文献

{"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}

{"title":"Cognitive and sensorimotor impairments in virally suppressed people with and without HIV in Uganda: Associations with neurofilament light chain as a biomarker of neuronal injury.","authors":"K Ridgeway, Raha M Dastgheyb, Rebecca E Easter, Eran F Shorer, Aggrey Anok, Stephen Tomusange, Julie Mannarino, Deanna Saylor, Magnus Gisslen, Henrik Zetterberg, Noeline Nakasujja, Gertrude Nakigozi, Robert Paul, Leah H Rubin","doi":"10.1007/s13365-026-01318-6","DOIUrl":"10.1007/s13365-026-01318-6","url":null,"abstract":"<p><p>Brain health disorders (BHDs) remain a concern for people with HIV (PWH) despite antiretroviral therapy access and viral suppression. The contribution of HIV to brain health is often obscured by comorbidities in high-income settings which are less prevalent in sub-Saharan Africa. Neurofilament light chain (NfL), a biomarker of axonal injury, may offer insight into underlying mechanisms. 338 virally-suppressed PWH and 250 people without HIV (PWoH) completed a Research Domain Criteria-informed battery assessing cognitive, sensorimotor, and social processing systems. Demographically-adjusted norms were derived from PWoH. Serostatus differences in impairment (≥ 1SD below the mean) were examined using multivariable logistic regression. Additional models examined associations between NfL (plasma, cerebrospinal fluid [CSF]) and task performance. PWH were similar to PWoH in age (43.9 vs. 43.5yrs), sex (female, 54 vs. 46%), and education (6.1 vs. 5.8yrs). PWH had higher odds of impairment in the cognitive control and attention (Color Trails, Symbol Digit) and sensorimotor (Grooved Pegboard) domains. Plasma NfL was associated with sensorimotor impairment in both groups. Similar trends held in CSF NfL but did not reach statistical significance, likely due to sample size (n = 85). Cognitive and sensorimotor difficulties are common in PWH in Rakai, independent of typical Western confounders. The profile of impairment differs from reports in high-income settings where declarative memory deficits are often observed. NfL was associated with sensorimotor impairment, suggesting that NfL may capture ongoing axonal injury and motor system vulnerability in PWH and PWoH. These findings suggest NfL's potential as a biomarker of sensorimotor impairment in sub-Saharan Africa.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 4","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-22","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13492402/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148301943","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":"Diffuse cerebral microhemorrhages in West Nile virus neuroinvasive disease: a case report.","authors":"Lauren M Hinkley, Alex Casella, Christina Tamargo Gaine","doi":"10.1007/s13365-026-01317-7","DOIUrl":"10.1007/s13365-026-01317-7","url":null,"abstract":"<p><p>West Nile virus neuroinvasive disease (WNND) most commonly presents as meningitis, encephalitis, or acute flaccid paralysis, with variable neuroimaging findings. While MRI abnormalities classically involve deep gray matter and brainstem structures, hemorrhagic manifestations are rarely reported. We report a 77-year-old woman who presented with rapidly progressive altered mental status following a brief febrile prodrome. Cerebrospinal fluid studies demonstrated a lymphocytic pleocytosis consistent with aseptic meningitis. Brain MRI revealed an acute lacunar infarct and diffuse cerebral microhemorrhages initially concerning for cerebral amyloid angiopathy. During hospitalization, she developed livedo reticularis-like peripheral skin changes prompting evaluation for autoimmune or vasculitic etiologies. Extensive infectious and autoimmune testing was ultimately notable for positive serum and CSF West Nile virus serologies, confirming neuroinvasive WNV infection. Despite transient neurologic improvement, her clinical course deteriorated, and she died following transition to comfort-focused care. This case highlights diffuse cerebral microhemorrhages as a potential finding in WNND, although their attribution remains uncertain. These findings may reflect underlying neurovascular inflammatory injury related to WNV or may represent coincident pathology and can mimic other small-vessel or autoimmune pathologies, complicating early diagnostic evaluation. Recognition of this expanded radiographic and clinical spectrum may aid timely diagnosis of WNND in patients with atypical presentations.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"148138499","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":"Morphine potentiates HIV infection and receptor expression in 3d brain organoids.","authors":"Michael Swingler, Doga Tasdemir, Senem Cakir, Anna Bellizzi, Martina Donadoni, Ilker K Sariyer","doi":"10.1007/s13365-026-01316-8","DOIUrl":"10.1007/s13365-026-01316-8","url":null,"abstract":"<p><p>Opioid abuse is a major comorbidity of HIV, yet its direct effects on the brain remain unclear. Using iPSC-derived 3D human cerebral organoids (hCOs), we show that morphine directly upregulates HIV receptors CD4, CCR5, and CXCR4 in the absence of peripheral immune cells or a blood-brain barrier. This receptor induction drives a significant increase in HIV viral load within the CNS, revealing a brain-intrinsic mechanisms of opioid-mediated viral enhancement. These findings establish hCOs as a unique platform to investigate neuroHIV and provide critical insight into how opioids amplify CNS infection independently of peripheral factors.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-05-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13183757/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147963749","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":"Clinical and behavioral predictors of HIV-associated neurocognitive disorder among people with HIV who use substances: a secondary analysis of the HOPE trial.","authors":"Gloria Wang, Xueying Yang, Kesheng Wang, Xiaoming Li, Zheng Dai, Shan Qiao","doi":"10.1007/s13365-026-01315-9","DOIUrl":"10.1007/s13365-026-01315-9","url":null,"abstract":"<p><p>This study examined behavioral, clinical, and hematologic factors associated with HIV-associated neurocognitive disorder (HAND) among people with HIV (PWH) using the International HIV Dementia Scale (IHDS) within a randomized clinical trial. This secondary analysis used data from the Hospital Visit as Opportunity for Prevention and Engagement for HIV-Infected Drug Users (HOPE) study, which enrolled 801 PWH who use substances from 11 U.S. hospitals. CD4 cell count, HIV-1 viral load, Global Severity Index (GSI), Global Assessment of Functioning (GAF), and Physical and Mental Component Scores (PCS, MCS) were assessed at baseline, 6 months, and 12 months. HAND was defined as an IHDS score ≤ 10. Multivariable linear and logistic regression models were used to identify baseline correlates of IHDS score and HAND, respectively. Linear mixed models were applied to evaluate the longitudinal changes in clinical outcomes. HAND prevalence was 76.3% (84.2% for females and 72.5% for males). Multivariable linear models revealed that obesity, CD4 cell counts < 200 cells/ µL, higher hemoglobin level and hematocrit, and higher GAF scores were significantly associated with IHDS score (p < 0.05). Furthermore, logistic models showed that recent alcohol use, obesity, viral suppression (≤ 200 copies/mL), hemoglobin and hematocrit levels, and GAF scores were associated with lower odds of HAND, whereas platelet count was linked to higher odds. Longitudinal analyses demonstrated significant increases in hemoglobin, hematocrit, PCS, and MCS over time, alongside decreases in platelet count and GSI. Compared with participants without HAND, those with HAND consistently exhibited lower hemoglobin, hematocrit, GAF, and GSI scores, and higher platelet counts and MCS scores across follow-up. These findings underscore the complex interplay between hematologic and mental health, substance use, and functional status in shaping neurocognitive outcomes among PWH. Targeting modifiable hematologic, behavioral, and psychosocial factors may help reduce HAND risk and improve long-term cognitive and functional outcomes. ClinicalTrials.gov ID: NCT01612169.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-05-07","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC13152875/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839335","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":"Pathogens of the human central nervous system-the major viral pathogens.","authors":"Kevin Roe","doi":"10.1007/s13365-026-01311-z","DOIUrl":"10.1007/s13365-026-01311-z","url":null,"abstract":"<p><p>Numerous pathogen infections in the human central nervous system can initiate potentially fatal neurological inflammation, including encephalitis, meningitis, meningoencephalitis and myelitis. Several bacterial, viral, fungal and protozoan parasite pathogens can initiate such neurological disorders. Pathogens of the central nervous system can achieve this either by their original active infections, or by reactivated infections after a period of latency. The original infections can be transmitted between humans by aerosols, respiratory droplets, ingestion, or physical contact. Some pathogens can also be transmitted from mother-to-child. Or the pathogens can be transmitted to humans by non-human vectors, by means of bites from mosquitoes, ticks, flies, or other insects, or by bites, contact, ingestion or proximity involving various wild or domestic animals. In summary, several viral pathogens either in their original active state or during one of their reactivations after latency, are capable of infecting the human central nervous system and initiating the most severe and dangerous types of encephalitis, meningitis, meningoencephalitis and myelitis.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":"32 3","pages":""},"PeriodicalIF":2.0,"publicationDate":"2026-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"147839290","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}