Journal of NeuroVirology最新文献

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Suppression of HIV-TAT and cocaine-induced neurotoxicity and inflammation by cell penetrable itaconate esters. 可穿透细胞的衣康酸酯可抑制 HIV-TAT 和可卡因诱发的神经毒性和炎症。
IF 2.3 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-17 DOI: 10.1007/s13365-024-01216-9
B Celia Cui, Marina Aksenova, Aliaksandra Sikirzhytskaya, Diana Odhiambo, Elizaveta Korunova, Vitali Sikirzhytski, Hao Ji, Diego Altomare, Eugenia Broude, Norma Frizzell, Rosemarie Booze, Michael D Wyatt, Michael Shtutman
{"title":"Suppression of HIV-TAT and cocaine-induced neurotoxicity and inflammation by cell penetrable itaconate esters.","authors":"B Celia Cui, Marina Aksenova, Aliaksandra Sikirzhytskaya, Diana Odhiambo, Elizaveta Korunova, Vitali Sikirzhytski, Hao Ji, Diego Altomare, Eugenia Broude, Norma Frizzell, Rosemarie Booze, Michael D Wyatt, Michael Shtutman","doi":"10.1007/s13365-024-01216-9","DOIUrl":"10.1007/s13365-024-01216-9","url":null,"abstract":"<p><p>HIV-associated neurological disorder (HAND) is a serious complication of HIV infection marked by neurotoxicity induced by viral proteins like Tat. Substance abuse exacerbates neurocognitive impairment in people living with HIV. There is an urgent need for therapeutic strategies to combat HAND comorbid with Cocaine Use Disorder (CUD). Our analysis of HIV and cocaine-induced transcriptomes in primary cortical cultures revealed significant overexpression of the macrophage-specific gene aconitate decarboxylase 1 (Acod1). The ACOD1 protein converts the tricarboxylic acid intermediate cis-aconitate into itaconate during the activation of inflammation. Itaconate then facilitates cytokine production and activates anti-inflammatory transcription factors, shielding macrophages from infection-induced cell death. However, the immunometabolic function of itaconate was unexplored in HIV and cocaine-exposed microglia. We assessed the potential of 4-octyl-itaconate (4OI), a cell-penetrable ester form of itaconate known for its anti-inflammatory properties. When primary cortical cultures exposed to Tat and cocaine were treated with 4OI, microglial cell number increased and the morphological altercations induced by Tat and cocaine were reversed. Microglial cells also appeared more ramified, resembling the quiescent microglia. 4OI treatment inhibited secretion of the proinflammatory cytokines IL-1α, IL-1β, IL-6, and MIP1-α induced by Tat and cocaine. Transcriptome profiling determined that Nrf2 target genes were significantly activated in Tat and 4OI treated cultures relative to Tat alone. Further, genes associated with cytoskeleton dynamics in inflammatory microglia were downregulated by 4OI treatment. Together, the results strongly suggest 4-octyl-itaconate holds promise as a potential candidate for therapeutic development to treat HAND coupled with CUD comorbidities.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-06-17","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141331137","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}
引用次数: 0
CD4 nadir and neurocognitive trajectories in people living with HIV. 艾滋病毒感染者的 CD4 最低点和神经认知轨迹。
IF 3.2 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-10 DOI: 10.1007/s13365-024-01217-8
Razmig Garabet, Will Dampier, Shinika Tillman, Kim Malone, Zsofia Szep, Amy Althoff, Vanessa Pirrone, Michael R Nonnemacher, Brian Wigdahl, Maria Schultheis, Kathryn N Devlin
{"title":"CD4 nadir and neurocognitive trajectories in people living with HIV.","authors":"Razmig Garabet, Will Dampier, Shinika Tillman, Kim Malone, Zsofia Szep, Amy Althoff, Vanessa Pirrone, Michael R Nonnemacher, Brian Wigdahl, Maria Schultheis, Kathryn N Devlin","doi":"10.1007/s13365-024-01217-8","DOIUrl":"https://doi.org/10.1007/s13365-024-01217-8","url":null,"abstract":"<p><p>Human immunodeficiency virus-associated neurocognitive disorders persist in the combination antiretroviral therapy era. CD4 nadir is a well-established predictor of cognition cross-sectionally, but its impact on longitudinal neurocognitive (NC) trajectories is unclear. The few studies on this topic examined trajectories of global cognition, rather than specific NC domains. The current study examined CD4 nadir in relation to domain-specific NC decline. 132 HIV + adults from the Temple/Drexel Comprehensive NeuroHIV Center, Clinical and Translational Research Support Core Cohort were administered comprehensive NC assessments longitudinally, with last visit occurring an average of 12 years after CD4 nadir. Linear mixed models were used to examine CD4 nadir in relation to longitudinal NC trajectories in three empirically identified NC domains: speed/executive function (S/EF), visuospatial memory (VM), and verbal fluency (VF). CD4 nadir was associated with change in VF (p = 0.020), but not with S/EF or VM. Specifically, those with CD4 nadir < 200 demonstrated increasing VF over time (p = .002), whereas those with CD4 nadir > 200 demonstrated stable VF (p = .568), though these differing trajectories may partly reflect regression to the mean or differential practice effect. CD4 dynamics over time were analyzed as potential mechanisms for the identified associations, with mixed findings. While low CD4 nadir has been associated with weaker neurocognition among people living with HIV, the results of this study suggest that low CD4 nadir is not associated with ongoing decline a decade later. Nadir-related deficits in VF may be stable or even improve over time, possibly reflecting the beneficial cognitive effects of long-term treatment and immune reconstitution.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":3.2,"publicationDate":"2024-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141296223","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}
引用次数: 0
Induced expression of rabies glycoprotein in the dorsal hippocampus enhances hippocampal dependent memory in a rat model of Alzheimer's disease. 在阿尔茨海默病大鼠模型中,诱导海马背侧表达狂犬病糖蛋白可增强海马依赖性记忆。
IF 2.3 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-01 Epub Date: 2024-06-28 DOI: 10.1007/s13365-024-01221-y
Shayan Aliakbari, Leila Hasanzadeh, Mohammad Sayyah, Niloufar Amini, Hamid Gholami Pourbadie
{"title":"Induced expression of rabies glycoprotein in the dorsal hippocampus enhances hippocampal dependent memory in a rat model of Alzheimer's disease.","authors":"Shayan Aliakbari, Leila Hasanzadeh, Mohammad Sayyah, Niloufar Amini, Hamid Gholami Pourbadie","doi":"10.1007/s13365-024-01221-y","DOIUrl":"10.1007/s13365-024-01221-y","url":null,"abstract":"<p><p>The Rabies virus is a neurotropic virus that manipulates the natural cell death processes of its host to ensure its own survival and replication. Studies have shown that the anti-apoptotic effect of the virus is mediated by one of its protein named, rabies glycoprotein (RVG). Alzheimer's disease (AD) is characterized by the loss of neural cells and memory impairment. We aim to examine whether expression of RVG in the hippocampal cells can shield the detrimental effects induced by Aβ. Oligomeric form of Aβ (oAβ) or vehicle was bilaterally microinjected into the dorsal hippocampus of male Wistar rats. One week later, two μl (10<sup>8</sup> T.U. /ml) of the lentiviral vector carrying RVG gene was injected into their dorsal hippocampus (post-treatment). In another experiment, the lentiviral vector was microinjected one week before Aβ injection (pre-treatment). One week later, the rat's brain was sliced into cross-sections, and the presence of RVG-expressing neuronal cells was confirmed using fluorescent microscopy. Rats were subjected to assessments of spatial learning and memory as well as passive avoidance using the Morris water maze (MWM) and the Shuttle box apparatuses, respectively. Protein expression of AMPA receptor subunit (GluA1) was determined using western blotting technique. In MWM, Aβ treated rats showed decelerated acquisition of the task and impairment of reference memory. RVG expression in the hippocampus prevented and restored the deficits in both pre- and post- treatment conditions, respectively. It also improved inhibitory memory in the oAβ treated rats. RVG increased the expression level of GluA1 level in the hippocampus. Based on our findings, the expression of RVG in the hippocampus has the potential to enhance both inhibitory and spatial learning abilities, ultimately improving memory performance in an AD rat model. This beneficial effect is likely attributed, at least in part, to the increased expression of GluA1-containing AMPA receptors.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468753","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}
引用次数: 0
Limited HIV-associated neuropathologies and lack of immune activation in sub-saharan African individuals with late-stage subtype C HIV-1 infection. 撒哈拉以南非洲晚期 C 亚型 HIV-1 感染者中与 HIV 相关的神经病理变化有限且缺乏免疫激活。
IF 2.3 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-01 Epub Date: 2024-06-28 DOI: 10.1007/s13365-024-01219-6
Zhou Liu, Peter Julius, Victor Mudenda, Guobin Kang, Luis Del Valle, John T West, Charles Wood
{"title":"Limited HIV-associated neuropathologies and lack of immune activation in sub-saharan African individuals with late-stage subtype C HIV-1 infection.","authors":"Zhou Liu, Peter Julius, Victor Mudenda, Guobin Kang, Luis Del Valle, John T West, Charles Wood","doi":"10.1007/s13365-024-01219-6","DOIUrl":"10.1007/s13365-024-01219-6","url":null,"abstract":"<p><p>Although previous studies have suggested that subtype B HIV-1 proviruses in the brain are associated with physiological changes and immune activation accompanied with microgliosis and astrogliosis, and indicated that both HIV-1 subtype variation and geographical location might influence the neuropathogenicity of HIV-1 in the brain. The natural course of neuropathogenesis of the most widespread subtype C HIV-1 has not been adequately investigated, especially for people living with HIV (PLWH) in sub-Saharan Africa. To characterize the natural neuropathology of subtype C HIV-1, postmortem frontal lobe and basal ganglia tissues were collected from nine ART-naïve individuals who died of late-stage AIDS with subtype C HIV-1 infection, and eight uninfected deceased individuals as controls. Histological staining was performed on all brain tissues to assess brain pathologies. Immunohistochemistry (IHC) against CD4, p24, Iba-1, GFAP, and CD8 in all brain tissues was conducted to evaluate potential viral production and immune activation. Histological results showed mild perivascular cuffs of lymphocytes only in a minority of the infected individuals. Viral capsid p24 protein was only detected in circulating immune cells of one infected individual, suggesting a lack of productive HIV-1 infection of the brain even at the late-stage of AIDS. Notably, similar levels of Iba-1 or GFAP between HIV + and HIV- brain tissues indicated a lack of microgliosis and astrogliosis, respectively. Similar levels of CD8 + cytotoxic T lymphocyte (CTL) infiltration between HIV + and HIV- brain tissues indicated CTL were not likely to be involved within subtype C HIV-1 infected participants of this cohort. Results from this subtype C HIV-1 study suggest that there is a lack of productive infection and limited neuropathogenesis by subtype C HIV-1 even at late-stage disease, which is in contrast to what was reported for subtype B HIV-1 by other investigators.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141468816","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}
引用次数: 0
A viral attack on brain tumors: the potential of oncolytic virus therapy. 病毒攻击脑肿瘤:溶瘤病毒疗法的潜力。
IF 2.3 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-01 Epub Date: 2024-05-28 DOI: 10.1007/s13365-024-01209-8
Kasra Mokhtarpour, Milad Akbarzadehmoallemkolaei, Nima Rezaei
{"title":"A viral attack on brain tumors: the potential of oncolytic virus therapy.","authors":"Kasra Mokhtarpour, Milad Akbarzadehmoallemkolaei, Nima Rezaei","doi":"10.1007/s13365-024-01209-8","DOIUrl":"10.1007/s13365-024-01209-8","url":null,"abstract":"<p><p>Managing malignant brain tumors remains a significant therapeutic hurdle that necessitates further research to comprehend their treatment potential fully. Oncolytic viruses (OVs) offer many opportunities for predicting and combating tumors through several mechanisms, with both preclinical and clinical studies demonstrating potential. OV therapy has emerged as a potent and effective method with a dual mechanism. Developing innovative and effective strategies for virus transduction, coupled with immune checkpoint inhibitors or chemotherapy drugs, strengthens this new technique. Furthermore, the discovery and creation of new OVs that can seamlessly integrate gene therapy strategies, such as cytotoxic, anti-angiogenic, and immunostimulatory, are promising advancements. This review presents an overview of the latest advancements in OVs transduction for brain cancer, focusing on the safety and effectiveness of G207, G47Δ, M032, rQNestin34.5v.2, C134, DNX-2401, Ad-TD-nsIL12, NSC-CRAd-S-p7, TG6002, and PVSRIPO. These are evaluated in both preclinical and clinical models of various brain tumors.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141161635","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}
引用次数: 0
Caffeine upregulates SIRT3 expression to ameliorate astrocytes-mediated HIV-1 Tat neurotoxicity via suppression of EGR1 signaling pathway. 咖啡因通过抑制EGR1信号通路上调SIRT3的表达,从而改善星形胶质细胞介导的HIV-1 Tat神经毒性
IF 2.3 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-01 Epub Date: 2024-06-26 DOI: 10.1007/s13365-024-01222-x
Lin Gao, Weixi Sun, Lei Zhang, Caixia Liang, Dongmei Zhang
{"title":"Caffeine upregulates SIRT3 expression to ameliorate astrocytes-mediated HIV-1 Tat neurotoxicity via suppression of EGR1 signaling pathway.","authors":"Lin Gao, Weixi Sun, Lei Zhang, Caixia Liang, Dongmei Zhang","doi":"10.1007/s13365-024-01222-x","DOIUrl":"10.1007/s13365-024-01222-x","url":null,"abstract":"<p><p>Caffeine is one of the most popular consumed psychostimulants that mitigates several neurodegenerative diseases. Nevertheless, the roles and molecular mechanisms of caffeine in HIV-associated neurocognitive disorders (HAND) remain largely unclear. Transactivator of transcription (Tat) is a major contributor to the neuropathogenesis of HAND in the central nervous system. In the present study, we determined that caffeine (100 µM) treatment significantly ameliorated Tat-induced decreased astrocytic viability, oxidative stress, inflammatory response and excessive glutamate and ATP release, thereby protecting neurons from apoptosis. Subsequently, SIRT3 was demonstrated to display neuroprotective effects against Tat during caffeine treatment. In addition, Tat downregulated SIRT3 expression via activation of EGR1 signaling, which was reversed by caffeine treatment in astrocytes. Overexpression of EGR1 entirely abolished the neuroprotective effects of caffeine against Tat. Furthermore, counteracting Tat or caffeine-induced differential expression of SIRT3 abrogated the neuroprotection of caffeine against Tat-triggered astrocytic dysfunction and neuronal apoptosis. Taken together, our study establishes that caffeine ameliorates astrocytes-mediated Tat neurotoxicity by targeting EGR1/SIRT3 signaling pathway. Our findings highlight the beneficial effects of caffeine on Tat-induced astrocytic dysfunction and neuronal death and propose that caffeine might be a novel therapeutic drug for relief of HAND.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141457514","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}
引用次数: 0
Role of inflammatory cytokine burst in neuro-invasion of Japanese Encephalitis virus infection: an immunotherapeutic approaches. 炎性细胞因子爆发在日本脑炎病毒感染的神经入侵中的作用:一种免疫治疗方法。
IF 2.3 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-01 Epub Date: 2024-06-06 DOI: 10.1007/s13365-024-01212-z
Firoz Ahmad, Shad Ahmad, Adil Husain, Niharika Pandey, Mohd Khubaib, Rolee Sharma
{"title":"Role of inflammatory cytokine burst in neuro-invasion of Japanese Encephalitis virus infection: an immunotherapeutic approaches.","authors":"Firoz Ahmad, Shad Ahmad, Adil Husain, Niharika Pandey, Mohd Khubaib, Rolee Sharma","doi":"10.1007/s13365-024-01212-z","DOIUrl":"10.1007/s13365-024-01212-z","url":null,"abstract":"<p><p>Japanese Encephalitis remains a significant global health concern, contributing to millions of deaths annually worldwide. Microglial cells, as key innate immune cells within the central nervous system (CNS), exhibit intricate cellular structures and possess molecular phenotypic plasticity, playing pivotal roles in immune responses during CNS viral infections. Particularly under viral inflammatory conditions, microglial cells orchestrate innate and adaptive immune responses to mitigate viral invasion and dampen inflammatory reactions. This review article comprehensively summarizes the pathophysiology of viral invasion into the CNS and the cellular interactions involved, elucidating the roles of various immune mediators, including pro-inflammatory cytokines, in neuroinflammation. Leveraging this knowledge, strategies for modulating inflammatory responses and attenuating hyperactivation of glial cells to mitigate viral replication within the brain are discussed. Furthermore, current chemotherapeutic and antiviral drugs are examined, elucidating their mechanisms of action against viral replication. This review aims to provide insights into therapeutic interventions for Japanese Encephalitis and related viral infections, ultimately contributing to improved outcomes for affected individuals.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141260473","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}
引用次数: 0
Diagnostic value of anti-VZV IgG in neurological diseases among varicella unvaccinated individuals. 抗 VZV IgG 对未接种水痘疫苗者神经系统疾病的诊断价值。
IF 2.3 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-01 Epub Date: 2024-07-31 DOI: 10.1007/s13365-024-01224-9
Ilakkiya Arumugam, Sivacchandran Subbarayan Rajasekaran, Krithika Gopalakrishnan, Sivasubramaniyan Gnanaskandan, Seetha N Jeganathan, Jayasri Athi, Ranjana Shanmugaraj, Rithivik Ramesh, V Shankar, Kaveri Krishnasamy, Lakshmi Narasimhan Ranganathan, Umamaheswari Balakrishnan, Ravi Mahalingam, Andrew N Bubak, Maria Acena Nagel, Padma Srikanth
{"title":"Diagnostic value of anti-VZV IgG in neurological diseases among varicella unvaccinated individuals.","authors":"Ilakkiya Arumugam, Sivacchandran Subbarayan Rajasekaran, Krithika Gopalakrishnan, Sivasubramaniyan Gnanaskandan, Seetha N Jeganathan, Jayasri Athi, Ranjana Shanmugaraj, Rithivik Ramesh, V Shankar, Kaveri Krishnasamy, Lakshmi Narasimhan Ranganathan, Umamaheswari Balakrishnan, Ravi Mahalingam, Andrew N Bubak, Maria Acena Nagel, Padma Srikanth","doi":"10.1007/s13365-024-01224-9","DOIUrl":"10.1007/s13365-024-01224-9","url":null,"abstract":"<p><p>Varicella zoster virus (VZV) is a neurotropic alphaherpesvirus that causes neurological manifestations either as a complication of primary infection or reactivation. VZV induced neurological diseases have a good prognosis when confirmed early and treated with anti-viral therapy. Myelitis, encephalitis, ventriculitis or meningitis can occur without a telltale rash in immunocompetent and immunocompromised individuals making the diagnosis difficult. We analyzed CSF and serum samples from 30 unvaccinated study participants (17 male and 13 female) to determine the presence of VZV DNA by PCR in CSF and to estimate serum and CSF anti-VZV IgG and albumin levels in participants with neurological manifestations with/without rash. Anti-VZV IgG was detected in CSF (n = 22, [73%]) and serum (n = 29, [97%]) of pediatric and adult participants. Anti-VZV IgG were detected in CSF of participants with varied clinical presentation altered sensorium (n = 8, [36%]), meningitis (n = 4, [18%]), acute febrile illness (n = 3, [14%], encephalopathy/meningoencephalitis (n = 2, [9%]), irritability (n = 2, [9%]) and each patient from cerebrovascular stroke, demyelinating disorder and febrile seizure (n = 1, [4.5%]). VZV DNA was detected from one participant and CSF serum albumin levels were elevated in 53% of study participants. VZV DNA is present up to 1-2 weeks post onset of disease, after which anti-VZV antibody may be the only indicator of disease and therefore both VZV DNA and anti-VZV IgG need to be tested for in CSF. As VZV DNA and VZV IgG antibody are both good indicators of VZV reactivation, routine testing would result in reduced morbidity and mortality by early detection of disease and antiviral treatment.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141860071","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}
引用次数: 0
Differential expression of cellular prion protein (PrPC) in mouse hepatitis virus induced neuroinflammation. 细胞朊病毒蛋白(PrPC)在小鼠肝炎病毒诱导的神经炎症中的差异表达。
IF 2.3 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-01 Epub Date: 2024-06-26 DOI: 10.1007/s13365-024-01215-w
Satavisha Ghosh, Rishika Jana, Soumen Jana, Rahul Basu, Madhurima Chatterjee, Nishtha Ranawat, Jayasri Das Sarma
{"title":"Differential expression of cellular prion protein (PrP<sup>C</sup>) in mouse hepatitis virus induced neuroinflammation.","authors":"Satavisha Ghosh, Rishika Jana, Soumen Jana, Rahul Basu, Madhurima Chatterjee, Nishtha Ranawat, Jayasri Das Sarma","doi":"10.1007/s13365-024-01215-w","DOIUrl":"10.1007/s13365-024-01215-w","url":null,"abstract":"<p><p>The cellular prion protein (PrP<sup>C</sup>) is an extracellular cell membrane protein. Due to its diversified roles, a definite role of PrP<sup>C</sup> has been difficult to establish. During viral infection, PrP<sup>C</sup> has been reported to play a pleiotropic role. Here, we have attempted to envision the function of PrP<sup>C</sup> in the neurotropic m-CoV-MHV-RSA59-induced model of neuroinflammation in C57BL/6 mice. A significant upregulation of PrP<sup>C</sup> at protein and mRNA levels was evident in infected mouse brains during the acute phase of neuroinflammation. Furthermore, investigation of the effect of MHV-RSA59 infection on PrP<sup>C</sup> expression in specific neuronal, microglial, and astrocytoma cell lines, revealed a differential expression of prion protein during neuroinflammation. Additionally, siRNA-mediated downregulation of prnp transcripts reduced the expression of viral antigen and viral infectivity in these cell lines. Cumulatively, our results suggest that PrP<sup>C</sup> expression significantly increases during acute MHV-RSA59 infection and that PrP<sup>C</sup> also assists in viral infectivity and viral replication.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141450665","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}
引用次数: 0
Serum mir-142-3p release in children with viral encephalitis and its relationship with nerve injury and inflammatory response. 病毒性脑炎患儿血清 mir-142-3p 的释放及其与神经损伤和炎症反应的关系。
IF 2.3 4区 医学
Journal of NeuroVirology Pub Date : 2024-06-01 Epub Date: 2024-06-11 DOI: 10.1007/s13365-024-01214-x
Yanjiang Liu, ZhenFang Wang, Xiaoli Liu, Qinghua Yang, Zhuoling Tian, Junmei Liu
{"title":"Serum mir-142-3p release in children with viral encephalitis and its relationship with nerve injury and inflammatory response.","authors":"Yanjiang Liu, ZhenFang Wang, Xiaoli Liu, Qinghua Yang, Zhuoling Tian, Junmei Liu","doi":"10.1007/s13365-024-01214-x","DOIUrl":"10.1007/s13365-024-01214-x","url":null,"abstract":"<p><strong>Background: </strong>Viral encephalitis (VE) is a common infectious disease of the central nervous system in children. Children with severe disease may have progressive neurological damage and even lead to death.</p><p><strong>Aims: </strong>To assess the serum miR-142-3p levels in children with VE and the correlation between miR-142-3p and the severity and prognosis of VE. Besides, its relationship with nerve injury and inflammatory response was assessed.</p><p><strong>Methods: </strong>Children with VE were regarded as a case group and healthy children served as control. The content of serum miR-142-3p was determined using real-time quantitative PCR. The risk factors associated with severity and prognosis of cases were evaluated using logistic analysis. The discrepancy in miR-142-3p levels, nerve injury-related indicators, and inflammatory cytokines were contrasted among groups. The ROC curve was conducted to assess the diagnostic performance of serum miR-142-3p in predicting prognosis of children with VE.</p><p><strong>Results: </strong>The altered expression of miR-142-3p in serum of children with VE was enhanced in contrast to healthy control. Serum nerve injury indicators MBP, β-EP, and NSE levels and serum inflammatory cytokines IL-6, IL-18, and IFN-γ were high in children with VE in contrast to healthy control, and had positive relevance with serum miR-142-3p. Besides, serum miR-142-3p was a risk factor associated with the severity and prognosis of children with VE. Serum miR-142-3p had diagnostic performance in predicting the prognosis of children with VE.</p><p><strong>Conclusion: </strong>Serum miR-142-3p content is high in children with VE and maybe a diagnosis marker for predicting prognosis. The specific miR-142-3p expression may be directly related to the severity of nerve injury and inflammatory response for VE.</p>","PeriodicalId":16665,"journal":{"name":"Journal of NeuroVirology","volume":null,"pages":null},"PeriodicalIF":2.3,"publicationDate":"2024-06-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141300808","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}
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