Search Results (595)

Background/Objectives: Fibromyalgia is a chronic pain condition characterized by widespread musculoskeletal pain, fatigue, sleep disturbance, cognitive dysfunction, and multisensory hypersensitivity. It is increasingly conceptualized as a heterogeneous nociplastic pain condition in which altered nociceptive processing interacts with dysfunctional pain regulation, neuroimmune mechanisms, and variable peripheral contributions. This integrative narrative review aims to synthesize current evidence on the major mechanisms underlying pain in fibromyalgia, with particular emphasis on central sensitization, descending pain modulation, neurochemical dysregulation, small-fiber pathology, neuroimmune processes, and psychobiological modulators. Methods: An integrative narrative review was conducted using iterative, mechanism-oriented searches of the biomedical literature, primarily in PubMed/MEDLINE and complemented by targeted bibliographic searches and reference tracking. Research published up to July 2026 was considered, with emphasis on human mechanistic studies, systematic reviews, meta-analyses, and landmark experimental evidence relevant to the major pathophysiological domains of fibromyalgia. Results: Central sensitization and altered nociceptive gain remain prominent mechanisms of pain amplification in fibromyalgia, but they do not fully account for the clinical phenotype. Evidence also supports impaired and heterogeneous descending pain modulation, neurochemical imbalance, neuroimmune activation, autonomic and stress-system dysregulation, and peripheral contributions, including small-fiber pathology in a substantial subgroup of patients. These mechanisms appear to interact rather than operate independently, while cognitive and emotional factors further modulate symptom severity, persistence, and functional impact. Conclusions: Fibromyalgia is best understood as a heterogeneous nociplastic pain syndrome arising from partially overlapping central, peripheral, neuroimmune, autonomic, and psychobiological mechanisms whose relative contribution varies across patients. Recognizing this mechanistic heterogeneity may improve phenotypic stratification, biomarker development, and the design of more individualized, mechanism-informed therapeutic strategies. Full article

Background: Fibromyalgia (FM) is a chronic syndrome characterized by widespread musculoskeletal pain, fatigue, sleep disturbances, and cognitive and affective symptoms. Objectives: This study aimed to examine the acute effects of Resistance Training (RT) and Pilates on pain, functional impact, flexibility, and health-related quality of life in individuals with FM. Methods: In this randomized crossover pilot study, eight adults (7 females, 1 male; mean age: 48.5 ± 8.2 years) with a clinical diagnosis of FM participated. Each participant performed both RT and Pilates sessions in a randomized order. Outcomes were assessed at baseline and 24 h post-intervention using the Fibromyalgia Impact Questionnaire (FIQ), the 36-Item Short Form Health Survey (SF-36), the Visual Analog Scale (VAS) for pain, and the Wells sit-and-reach test (WELLS). Data were analyzed using two-way repeated-measures ANOVA and paired t-tests, with effect sizes (η²p and Cohen’s d) and 95% confidence intervals (95% CI). Statistical significance was set at p < 0.05. No formal sample size calculation was performed. Results: Participants presented a mean body mass index (BMI) of 27.4 ± 4.1 kg/m² and time since diagnosis of 6.2 ± 3.1 years. Within-subject variations were observed following both interventions. FIQ scores decreased at 24 h after both RT and Pilates sessions (RT: 52.21 ± 18.61; Pilates: 45.50 ± 18.63; p = 0.038, η²p = 0.42, 95% CI [−12.5, −1.2]). Conclusions: Both Resistance Training and Pilates acutely reduced overall disease impact in individuals with fibromyalgia, with Pilates promoting superior acute gains in posterior chain flexibility. Full article

Fibromyalgia and myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) are chronic multisystem disorders characterized by persistent fatigue, pain, cognitive dysfunction, sleep disturbances, and reduced quality of life. Increasing evidence implicates mitochondrial dysfunction, oxidative and nitrosative stress, immune dysregulation, and altered redox and nicotinamide adenine dinucleotide (NAD⁺) metabolism as interconnected mechanisms contributing to fatigue, although the strength of evidence varies across these pathways. Micronutrients are essential components of mitochondrial bioenergetics, antioxidant defense, and immune–metabolic regulation. This narrative review critically examines the mechanistic and clinical evidence supporting mitochondrial-oriented micronutritional interventions in fibromyalgia and ME/CFS, including NAD⁺ precursors, B-complex vitamins, magnesium, coenzyme Q10, alpha-lipoic acid, GlyNAC, L-carnitine, pyrroloquinoline quinone, taurine, and creatine. Mechanistic plausibility is distinguished from clinical efficacy, as disease-specific randomized controlled evidence remains limited for several interventions. We further discuss biomarkers, metabolic phenotyping, and precision nutrition within a systems-based micronutrition framework. Finally, we present the rationale for a future randomized, double-blind, placebo-controlled trial in fibromyalgia patients with clinically significant fatigue, which is planned for 2027, subject to ethics approval and prospective registration, as a strategy for future clinical validation. Full article

Post-exertional malaise (PEM) and cognitive dysfunction (hereafter “cognitive dysfunction”, including the patient-reported syndrome often described as “brain fog”) are among the most disabling features of Long COVID; yet, approved disease-modifying treatments remain lacking. Emerging evidence implicates interacting disturbances in mitochondrial bioenergetics, redox regulation and neurovascular inflammation, although much of the supporting evidence remains indirect and derives from acute COVID-19, myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS), primary mitochondrial disease, inflammatory biology and mechanistic pharmacology rather than from direct Long COVID intervention trials. This hypothesis-generating narrative review develops a mechanism-based translational framework: that a pathway-targeted nutraceutical programme may modulate selected elements of these three axes, subject to prior demonstration of formulation quality, pharmacokinetic feasibility, target engagement and safety. Candidate modules comprise coenzyme Q10 and alpha-lipoic acid for bioenergetic/redox support; selenium, sulforaphane and resveratrol for Nrf2–thioredoxin-related redox regulation; and Boswellia serrata, luteolin and eicosapentaenoic acid for putative prostaglandin/resolution-pathway modulation. Sonlicromanol provides a conceptual mechanistic precedent for combined redox and prostaglandin-directed pharmacology, but it is not considered pharmacologically equivalent to an eight-agent nutraceutical combination. We summarise the mechanistic rationale, distinguish direct from indirect evidence, define qualitative evidence-grading criteria, outline safety and interaction considerations, and propose a staged translational research programme. This framework is intended to generate falsifiable hypotheses for future Long COVID studies, not to imply established clinical efficacy. Full article

Background: Post-acute sequelae of COVID-19 (PASC), commonly known as long COVID, affects an estimated 10–30% of SARS-CoV-2 non-hospitalised and 50–70% of hospitalised survivors. This condition remains clinically heterogeneous, and the specific mechanisms driving the transition from acute infection to chronic sequelae remain poorly understood. We assessed independent risk factors, tracked the evolution of clinical features, defined distinct symptom-based phenotypes, and assessed the impact of different pandemic waves on the likelihood of developing long COVID in hospitalised survivors. Methods: We conducted a single-centre, retrospective cohort study at a university hospital in London. The population comprised 627 adults hospitalised with acute COVID-19 between February 2020 and December 2022. Baseline characteristics and outcomes were compared between long COVID and resolved cases using appropriate statistical tests for continuous and categorical variables. Multivariable logistic regression identified risk factors. McNemar’s test quantified the phenotypic shift from admission to follow-up. Latent Class Analysis (LCA) identified clinical subtypes based on symptom clusters. Results: Of 627 patients, 252 (40.2%) met long COVID criteria. Comorbidity burden was the strongest predictor; patients with a single condition had a 4-fold increase in odds (aOR 4.62, 95% CI 2.36–9.04). The ORs were also significantly elevated among patients with 2 (aOR 3.26), 3 (aOR 2.68), or 4 or more (aOR 3.24) comorbidities. Older age (aOR 1.04), acute disease severity (measured by length of hospital stay) (aOR 1.27 per log-day) and elevated admission fibrinogen (aOR 1.21 per g/L) were significant predictors. Temporal analysis revealed a precipitous decline in risk from Wild-type/Alpha (>50%) to Delta/Omicron (<21%). We observed a distinct phenotypic shift: while acute respiratory inflammation resolved, systemic fatigue increased fourfold (7.0% to 32.4%), and memory difficulties emerged in the post-acute phase. LCA identified two phenotypes: fatigue-dominant and multisystem phenotypes. Conclusions: Long COVID is a multifactorial syndrome driven by host susceptibility, acute severity, and persistent coagulopathy. Clinical management should move beyond a monolithic approach and favour phenotype-specific strategies. Full article

Background: Functional somatic disorder (FSD) is prevalent, but pathological pathways have not yet been identified. Cross-sectional studies suggest an association between FSD and lipid and glucose metabolism. The aim of the present prospective study was to assess whether metabolic factors represent possible risk factors for development of FSD. Methods: A population-based cohort of 9656 men and women aged 18–76 years was established in 2011–2015, and 5738 participated in a re-examination after a median of 65 months. At both baseline and follow-up, participants answered questionnaires on lifestyle and various delimitations of FSD including bodily distress syndrome (BDS), chronic fatigue (CF), chronic widespread pain (CWP), irritable bowel (IB), and multiple chemical sensitivity (MCS). Fasting values of cholesterol, triglycerides, glucose, HbA1c, insulin, and insulin resistance were assessed at baseline and analyzed in relation to incidence of FSD using logistic regression models, adjusted for age, sex, lipid- and glucose-lowering medications, obesity, social status, lifestyle, and sleep quality. Results: Several small, although significant, effects were observed. Lower levels of cholesterol were associated with development of BDS (OR: 0.982 (95% CI: 0.971–0.993)), CF (OR: 0.980 (95% CI: 0.964–0.996)), and CWP without co-morbid FSS among men. Higher levels of triglycerides were associated with development of CF (OR: 1.022 (95% CI: 1.003–1.041)). Glucose and HbA1c levels were not associated with development of FSD. Insulin and HOMA-IR levels were associated with development of CF in a non-linear relation, being negative at lower levels and changing to a positive relation at higher levels. Conclusions: More large-scale cohort studies are necessary to explore whether metabolism could play a role in the pathological pathway of FSD as indicated in the present study. Full article

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is an idiopathic, multisystem disorder marked by debilitating fatigue, post-exertional malaise, cognitive dysfunction and neuroinflammation. Its etiology remains unclear, yet emerging evidence implicates a complex interplay between immune dysregulation, metabolic impairment, mitochondrial bioenergetics, and environmental stressors such as viral infection or low-dose ionizing radiation (LDIR). To develop treatments for ME/CFS, it is essential to identify suitable targets for therapy. In this narrative review, we discuss recent findings on the overlap of ME/CFS with LDIR effects and examine potential mechanistic links that may arise from LDIR-induced bystander effects (RIBEs). We highlight potential candidate biomarkers that bridge these domains: mitochondrial respiratory dysfunction, altered ornithine transport via SLC25A15 (ORNT1), possible roles of CD38 in the context of immunity and NAD+ depletion, cyclin D1–dependent metabolic reprogramming and modulation of gene expression, and α-synuclein as a potential neuroinflammatory damage-associated molecular pattern (DAMP). While the involvement of these biomarkers in ME/CFS is yet to be confirmed experimentally, evidence from in vitro studies of irradiated cells, exosome profiling, and patient samples suggests that RIBEs can, in theory, produce prominent cellular ME/CFS phenotypes through associated mechanisms, including those exhibiting oxidative stress, impaired ATP production, and immune modulation. We propose a hypothetical, exploratory model wherein LDIR initiates or contributes to adaptive metabolic shifts (including CD38 upregulation and cyclin D1 stabilization) that, coupled with persistent bystander signaling, could potentially culminate in chronic fatigue and neurocognitive symptoms in some reported ME/CFS cases. Finally, we outline a research agenda encompassing the establishment of standardized diagnostic criteria, multi-omics profiling of patient cohorts, exosome analysis, functional mitochondrial assays, and targeted therapeutic trials focusing on possible anti-CD38 antibodies and NAD+ precursor therapy. By integrating recent findings in low-dose radiation biology with ME/CFS pathophysiology, this review aims to promote interdisciplinary investigations that may uncover mechanistic insights and novel biomarkers for diagnosis and treatment of ME/CFS. We further review steps in a proposed model taking us from low-dose radiation exposure to a number of possible targets. Full article

Breast implant illness (BII) describes a constellation of systemic symptoms reported by some patients after breast implantation, including fatigue, cognitive dysfunction, arthralgia, myalgia, sicca symptoms, skin manifestations, and mood disturbance. Autoimmune/inflammatory syndrome induced by adjuvants (ASIA) provides a broader conceptual framework in which silicone and other biomaterials may contribute to immune dysregulation in susceptible individuals, although causality remains controversial and no validated diagnostic biomarker exists. This narrative review summarizes current evidence on BII and implant-related ASIA, focusing on epidemiology, clinical presentation, biological plausibility, diagnostic evaluation, explantation outcomes, and implant-associated complications. Proposed mechanisms include chronic foreign-body inflammation, silicone gel bleed and particulate migration, macrophage activation, inflammasome signaling, cytokine dysregulation, bacterial biofilms and biofilm-derived metabolites, adaptive immune activation, autoantibody formation, and host genetic susceptibility. The review also distinguishes BII/ASIA-like presentations from breast implant-associated anaplastic large cell lymphoma and other rare implant-associated malignancies. A practical multidisciplinary diagnostic and management algorithm is proposed to support structured assessment, red-flag triage, exclusion of alternative diagnoses, patient-centered counseling, and individualized decision-making regarding medical management and explantation. Full article

Vitamin C (L-ascorbic acid) is an essential micronutrient involved in collagen biosynthesis, redox regulation, immune function, endothelial biology, carnitine synthesis, neurotransmitter metabolism, and non-heme iron absorption. Dietary reference values are designed primarily to prevent deficiency in general populations, but vulnerability to low-vitamin C status may increase during trauma, surgery, chronic inflammation, malignancy, metabolic disease, smoking, poor intake, environmental exposure, and tissue repair. This narrative review synthesizes mechanistic, pharmacokinetic, clinical, and safety evidence on vitamin C as a stress-responsive micronutrient. Evidence is reviewed across tissue repair and wound healing, orthopedic recovery and selected complex regional pain syndrome risk contexts, fatigue, neuropsychiatric vulnerability, cancer-supportive care, vascular homeostasis, dermatologic biology, and preliminary microbiota–gut–brain axis hypotheses. The strength of evidence differs substantially across domains: biochemical functions and deficiency correction are well established, whereas benefits of supraphysiologic oral supplementation in vitamin C-replete patients remain uncertain. Oral nutritional supplementation is distinguished from intravenous pharmacologic ascorbate, with attention to route, formulation, dose division, gastrointestinal tolerance-limited adjustment, and safety monitoring. Because evidence for high-dose oral supplementation remains limited and condition-specific, such use should be individualized, time-limited, and clinician-monitored rather than presented as a population-level recommendation or evidence-defined therapeutic target. Taken together, the clinical value of vitamin C depends on baseline status, patient vulnerability, route, formulation, dosing interval, clinical endpoint, and safety review. Full article

This study aimed to investigate the therapeutic effects of camel milk (CM) on chronic fatigue syndrome (CFS) and elucidate the mechanisms underlying the microbiota–gut–brain axis. Using a murine model of CFS induced by chronic restraint and forced swimming stress, we administered lyophilized CM (1500 mg/kg/day, equivalent to approximately 121.5 mg/kg/day in humans based on body surface area conversion using the standard allometric scaling formula) orally. CM supplementation was significantly associated with ameliorated fatigue-like behaviors, as evidenced by prolonged swimming endurance and reduced immobility time. Metagenomic analysis revealed that CM was associated with reshaping of the small intestinal microbiota, including enrichment of beneficial Lactococcus lactis and suppression of pathobionts (H. hepaticus and H. typhlonius). These microbial shifts correlated with increased luminal lactic acid, improved intestinal barrier integrity (increased villus height, reduced crypt depth), and attenuated local inflammation (reduced TNF-α and IL-6, elevated IL-10). Consequently, CM was associated with reduced bacterial translocation and systemic inflammation, and normalization of hypothalamic–pituitary–adrenal (HPA) axis hyperactivity. We conclude that CM is associated with prevention of CFS-like symptoms through modulation of the gut ecosystem and strengthening of the intestinal barrier, potentially breaking the vicious cycle of gut inflammation and HPA axis dysfunction, although causality remains to be established through fecal microbiota transplantation or similar mechanistic studies. Full article

Background and Objectives: Fibromyalgia (FM) is a chronic primary pain syndrome. Its hallmark symptom is widespread pain, often accompanied by fatigue, sleep disturbances, and cognitive symptoms. Online surveys efficiently collect patient-reported data, but individuals recruited through this approach remain poorly characterized. This study aimed to describe a large online cohort of individuals with FM, providing data for comparison with the Italian Fibromyalgia Registry (IFR). Materials and Methods: Participants who self-reported a physician diagnosis of FM completed an online survey assessing socio-demographic and clinical characteristics, treatments and their perceived effectiveness, lifestyle, and impact variables. Disease severity and symptom burden were assessed using the Fibromyalgia Impact Questionnaire—Revised (FIQR), Widespread Pain Index (WPI), and Symptom Severity Scale (SSS). Participants were classified according to the 2016 American College of Rheumatology (ACR) criteria. Descriptive statistics were computed, and exploratory analyses assessed sex differences and differences according to ACR status using independent-samples t-tests with Bonferroni correction. Results: A total of 6022 participants were included (mean age 52.3 ± 10.3 years, 96.7% female). Nearly half (49.6%) reported pain duration > 10 years, and 50.4% had received conflicting diagnoses. Disease burden was high, with >70% classified as moderate-to-severe according to the FIQR. Overall, 79.4% fulfilled the 2016 ACR criteria. Participants not fulfilling the criteria showed lower symptom severity, although considerable clinical overlap was observed between groups. Pharmacological treatments were used by 81.1% of participants and non-pharmacological approaches by 55.1%, both with moderate perceived effectiveness. FM substantially affected daily life, particularly work and social functioning. After correction for multiple comparisons, sex differences were limited to FIQR functioning and symptom domains, with small effect sizes. Conclusions: Compared with published registry-based data, participants recruited through this online survey reported a higher symptom burden and longer pain duration, while showing a broadly similar symptom profile. Although the descriptive nature of the comparison precludes causal inferences, the findings suggest that online surveys and clinical registries may provide complementary perspectives on the FM population. Full article

Background/Objectives: Primary Sjögren’s syndrome (pSS) is a chronic autoimmune rheumatic disease that clinically presents with symptoms of xerostomia and xerophthalmia, as well as a wide range of other symptoms that may affect patients’ daily functioning and life satisfaction. The main purpose of this study was to assess their health-related quality of life (HRQoL) using both general and disease-specific questionnaires. Methods: This cross-sectional observational research with prospective data collection was conducted at the Rheumatology Clinic of the University Clinical Centre of Kragujevac. Participants were divided into two groups: patients with oral manifestations (oral manifestations group) and those presenting with xerostomia only, without other oral lesions or symptoms (xerostomia-only group). A complete clinical examination of the patient’s oral cavity was performed by one doctor of dental medicine. HRQoL was evaluated using various generic and disease-specific instruments. Results: A total of 80 participants were included in the study, of whom 40 were in the oral manifestations group and 40 in the xerostomia-only group. Patients with oral manifestations had significantly higher scores across all PSS-QoL domains compared with the xerostomia-only group (p < 0.001). A statistically significant difference in the total EQ-5D result was detected between groups (0.7 (0.3) vs. 0.8 (0.1), p < 0.001). In multivariable regression analysis (R² = 0.921), the ESSPRI score (β = 0.418, p < 0.001) and the presence of oral manifestations (β = −1.155, p < 0.001) were significant independent predictors of impaired HRQoL, while disease activity showed no significant association (p = 0.895). Conclusions: Patients with primary Sjögren’s syndrome presenting with oral manifestations have poorer HRQoL compared with participants with xerostomia only. Symptom burden, including dryness, pain, fatigue, and oral manifestations, may be associated with decreased HRQoL, in contrast to disease activity. Full article

Myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS) is a debilitating multisystem illness characterised by post-exertional malaise, non-restorative sleep, and cognitive impairment, yet no objective diagnostic biomarkers have been established. Untargeted plasma metabolomics provides a broad view of the biochemical disturbances underlying ME/CFS; however, the high dimensionality of omics datasets and the limited interpretability of conventional classifiers nevertheless hinder translation into clinical practice. This study evaluates three ensemble classifiers—Explainable Boosting Machine (EBM), XGBoost, and LightGBM—for binary ME/CFS classification using plasma metabolomic and lipidomic profiles from 197 participants (106 ME/CFS; 91 healthy controls; 888 features). Feature dimensionality was reduced using a Pareto-Guided Recursive Neural Network (PRNN) pipeline. Model performance was assessed via 50-repeat stratified hold-out validation. EBM achieved the highest accuracy (0.909; 95% CI: 0.868–0.949) and area under the receiver operating characteristic curve (AUC: 0.940; 95% CI: 0.909–0.983), with XGBoost and LightGBM performing comparably. Interpretability analyses revealed that pairwise metabolite interaction terms—particularly proline & indole-3-lactate, tyrosine & N-acetylornithine, and maleic acid & arachidic acid—contributed the greatest discriminative signal. An ablation analysis comparing the full interaction-augmented EBM (AUC = 0.940) with a main-effects-only EBM (AUC = 0.882) confirmed that pairwise metabolite co-variation contributes additional discriminative value beyond individual metabolite levels, implicating amino acid catabolism, tryptophan–kynurenine pathway dysregulation, mitochondrial energy impairment, and lipid remodelling as central pathophysiological features. Global and instance-level explanations jointly demonstrated population-level metabolic signatures alongside individual heterogeneity, highlighting the added clinical value of explainable artificial intelligence (XAI) in metabolomics. These findings support EBM-based metabolomic profiling as an internally validated approach for ME/CFS classification, subject to external validation, calibration assessment, and prospective testing. Full article

Chronic overlapping pain conditions (COPCs) refer to a set of chronic pain disorders that frequently co-occur and may involve partially overlapping mechanisms. The U.S. National Institutes of Health currently recognizes ten COPCs: fibromyalgia, painful temporomandibular disorders, chronic low back pain, chronic migraine headache, chronic tension-type headache, irritable bowel syndrome, endometriosis, interstitial cystitis/bladder pain syndrome, vulvodynia, and myalgic encephalomyelitis/chronic fatigue syndrome. When multiple COPCs coexist, they are associated with a disproportionate multimorbidity burden, including greater pain, poorer psychological well-being, functional limitations, disability, fatigue, sleep disturbances, diminished quality of life, and increased healthcare utilization. Despite their impact, COPCs remain under-recognized, underdiagnosed, and undertreated. Combining structured literature searches and citation tracking with narrative syntheses, this review examines comorbid relationships, the burden of multimorbidity, and potentially overlapping nociplastic mechanisms. By adopting a multimorbidity-based perspective rather than a one-disease, one-treatment approach, it highlights barriers to care—including limited clinical awareness, under-recognition of additional COPCs, limited mechanistic understanding, and fragmented care—and proposes integrated strategies emphasizing prevention, systematic screening, mechanism-informed assessment, and coordinated, patient-centered multimodal management. Full article

Human herpesvirus-6 consists of a pair of viral species, HHV-6A and HHV-6B, which are neurotropic with the ability to invade, persist, and reactivate within the nervous system. Accumulating evidence links HHV-6 to epilepsy and other neuropathologies, including: multiple sclerosis, chronic fatigue syndrome, and neurodegeneration. Yet, mechanisms by which these viruses induce neurological disorders, including their role in epileptogenesis, remain unknown. It has been demonstrated that HHV-6 exhibits tropism for astrocytes, oligodendrocytes, and neurons. Thus, HHV-6 can perturb cellular homeostasis, neuronal signaling, and immune regulation, astrocytic glutamate clearance, GABAergic inhibition, and cholinergic or monoaminergic neurotransmission yielding network hyperexcitability. It is also reported that HHV-6 can activate neuroinflammation through Toll-Like Receptor (TLR), cytokine, and/or NF-$\kappa$B activation, which facilitates neuronal injury and network instability. Indeed, a suite of converging processes suggest a multifactorial nature for HHV-6 related neuropathology. Despite robust experimental and clinical data, definitive causal relationships between HHV-6 and epilepsy (or induction of neurodegeneration) remain elusive. This review discusses evidence for roseolovirus-induced neurological dysfunction and disorders commonly associated with HHV-6A and HHV-6B infections. A preponderance of clinical and experimental evidence suggests that differential tropism for distinct neuronal neurotransmitter chemotypes and glia as well as systemic effects are involved in roseolovirus-mediated neurological disease. Full article