Tick-borne encephalitis (TBE) is an emerging vector-borne disease in Europe caused by tick-borne encephalitis virus (TBEV), which belongs to Flaviviridae. Although most of the patients quickly recover from TBE, some require further neurological and psychiatric treatment due to persistent symptoms. The aim of the study was to evaluate the usefulness of an antibodies index for predicting the course of the disease and potential persistent sequalae. Sixty-six patients (49 males and 17 females, mean age 45.97 ± 13.69 years) with TBE hospitalized in the Department of Infectious Diseases and Neuroinfections, Medical University of Bialystok, Poland, in years 2016–2019 were included to the study. TBE antibodies titer in serum and CSF samples were measured with an Anti-TBEV ELISA (IgM, IgG) EUROIMMUN test. Patients who developed persistent sequelae after TBE had significantly lower IgG intrathecal index at admission. Additionally, IgG2/IgG1was significantly higher in patients who developed sequelae. IgG intrathecal index might be a useful tool for the prediction of TBE sequelae development.

Approximately 25% of HIV-infected patients are co-infected with HCV. Notably, the burden of HCV infection (e.g., viral persistence, viral load, or HCV-related liver symptoms) is more pronounced in the presence of HIV co-infection. However, to date, the underlying immune mechanisms accounting for accelerated disease progression in HIV/HCV-coinfected individuals have not been described in sufficient detail. We hypothesized that regulatory T cells (Treg) bearing potent immunosuppressive capacities could not only play a substantial role in the pathogenesis of HCV/HIV coinfection but also modulate the response to the standard anti-viral therapy. Materials and Methods: To this end, we studied alterations in frequencies of Treg cells in correlation with other Treg-related and virus-related parameters in both HCV and HCV/HIV-infected patients subjected to standard pegIFN-α/RBV therapy. Results: Notably, we found that pegIFN-α/RBV therapy significantly increased levels of Treg cells in HCV-infected but not in HIV/HCV-coinfected individuals. Furthermore, HIV/HCV-coinfection was demonstrated to inhibit expansion of regulatory T cells during anti-viral treatment; thus, it might probably be responsible for viral persistence and HCV-related liver damage. Conclusions: Therapy with pegIFN-α/RBV demonstrated a significant effect on regulatory T cells in the course of HIV and/or HCV infection indicating a crucial role in the anti-viral immune response.

The aim of this study was to evaluate the usefulness of IgM anti-Tick-Borne Encephalitis (anti-TBE) intrathecal synthesis in the diagnosis and prediction of the clinical course of the disease. Thirty-six patients were included in the study (patients reported symptoms such as fever, headache, fatigue, and nausea/vomiting). CRP, White Blood Cells (WBC), pleocytosis, Cerebrospinal Fluid (CSF) protein concentration, CSF albumin concentration, serum IgM, serum IgG, CSF IgM, CSF IgG, IgM Index, IgG Index, and IgG Index/IgM Index ratio were the parameters which were examined in the individuals. An analysis of correlation presented statistical significance between IgM Index and pleocytosis and protein concentration in CSF in the whole group of individuals. IgM Index and IgG Index/IgM Index ratio may be used in the prediction of severity of TBE. The most probable link between the IgM intrathecal production and severity of TBE may be a result of delayed seroconversion to IgG, and therefore not an adequate response to the virus presence.

Viral infections have been implicated in psychiatric outcomes through immune-mediated pathways. This 12-month prospective cohort study, designed as a pilot and hypothesis-generating investigation, compared psychiatric symptoms and inflammatory cytokine profiles in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), hepatitis C virus (HCV), and tick-borne encephalitis virus (TBEV), and explored their potential predictive value. Thirty-seven patients hospitalized with viral infections and 32 healthy controls were evaluated, acknowledging the limited sample size. Psychiatric interviews and the Hospital Anxiety and Depression Scale (HADS) were used for assessment. The study was divided into two stages. In Stage 1, during the acute infection, a psychiatric assessment was conducted, and cytokine levels were measured in the patients’ blood. In Stage 2, one year later, the psychiatric assessment was repeated. No significant differences were found in psychiatric diagnosis rates or symptom severity between infection groups, regardless of viral type or neuroinvasive capacity. However, these findings should be interpreted as preliminary given the limited sample size. Some cytokines, eg., interleukin-1β (IL-1β), tumor necrosis factor-alpha (TNF-α), interleukin-10 (IL-10), and soluble interleukin-2 receptor subunit alpha (sIL-2Rα), showed associations with individual symptoms, but these were inconsistent and did not demonstrate robust predictive value. Cluster analysis identified two distinct inflammatory profiles—one characterized by higher cytokine levels (predominantly in Coronavirus disease 2019 (COVID-19) and TBEV cases) and the other by lower cytokine levels (mostly in HCV and controls). However, different cytokine profiles did not correspond to clinical outcomes. The results suggest that psychiatric sequelae after viral infections are not directly driven by specific cytokines or infection type but rather emerge from a complex interaction of immune, psychological, and environmental factors. Single cytokine measurement is insufficient and cannot be used as a tool for assessing the risk of developing psychiatric disorders. Given the exploratory nature of the study, all results require confirmation in larger, adequately powered cohorts. Future studies should focus on composite biomarkers and systems-based models such as neuroimmune-metabolic-oxidative pathways (NIMETOX), or Immune-Inflammatory Response System (IRS)/Compensatory Immune Response System (CIRS)/Oxidative & Nitrosative Stress (O&NS) for improved predictive accuracy.

Viral infections have been implicated in psychiatric outcomes through immune-mediated pathways. This 12-month prospective cohort study compared psychiatric symptoms and inflammatory cytokine profiles in patients with severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), hepatitis C virus (HCV), and tick-borne encephalitis virus (TBEV), and assessed their predictive value. 37 patients hospitalized with viral infections and 32 healthy controls were evaluated using psychiatric interviews and the Hospital Anxiety and Depression Scale (HADS). The study was divided into two stages. In Stage 1, during the acute infection, a psychiatric assessment was conducted and cytokine levels were measured in the patients’ blood. In Stage 2, one year later, the psychiatric as-sessment was repeated. No significant differences were found in psychiatric diagnosis rates or symptom severity between infection groups, regardless of viral type or neu-roinvasive capacity. Some cytokines (eg., IL-1β, TNF-α, IL-10, and sIL-2Rα) showed as-sociations with individual symptoms, but these were inconsistent and not predictive. Cluster analysis identified two distinct inflammatory profiles - one characterized by higher cytokine levels (predominantly in COVID-19 and TBEV cases) and the other by lower cytokine levels (mostly in HCV and controls). However, different cytokine profiles did not correspond to clinical outcomes. The results suggest that psychiatric sequelae after viral infections are not directly driven by specific cytokines or infection type but rather emerge from a complex interaction of immune, psychological, and environmental factors. Single cytokine measurement is insufficient and cannot be used as a tool for assessing the risk of developing psychiatric disorders. Future studies should focus on composite bi-omarkers and systems-based models such as neuroimmune-metabolic-oxidative path-ways (NIMETOX), Immune-Inflammatory Response System (IRS)/ Compensatory Im-mune Response System (CIRS)/ Oxidative & Nitrosative Stress (O&NS) for improved predictive accuracy.

Background: Cardiovascular diseases remain important causes of morbidity and potential premature mortality in children. Although clinical imaging and electrophysiologic testing have advanced, early, minimally invasive biomarkers that can both detect myocardial injury and help differentiate among overlapping pediatric phenotypes are still limited. Circulating microRNAs (miRNAs; miRs) are becoming attractive biomarker candidates because many are abundant in the heart, actively released into the circulation, and remarkably stable in plasma. The study aimed to assess the expression of miR-1-3p, miR-let-7b-5p, miR-21-5p, and miR-26b-5p in children with cardiovascular disease. Methods: Children aged 10–18 years with cardiac arrhythmias, myocarditis, or cardio-myopathies were recruited. The control group consisted of healthy age- and sex-matched children. For each participant, peripheral venous blood was collected for plasma isolation and miRNA profiling. The expression of miR-1-3p, miR-let-7b-5p, miR-21-5p, miR-26b-5p, and UniSp6 molecules was analyzed using the comparative cycle threshold delta Ct (ΔCt) method. A p-value ≤ 0.05 was considered statistically significant. Results: miR-26b-5p was significantly downregulated in patients with cardiac disease compared with healthy controls. miR-21-5p and miR-26b-5p were downregulated in patients with ventricular arrhythmia. Moreover, miR-26b-5p was downregulated in arrhythmia in general. We found no significant difference in the expression of miR-1-3p, miR-let-7b-5p, miR-21b-5p, and miR-26b-5p between patients with and without myocarditis, as well as with and without hypertrophic cardiomyopathy. Conclusions: miR-26b-5p may distinguish young patients with cardiovascular disease and those with arrhythmias from healthy individuals. miR-21-5p and miR-26b-5p may also be seen as potential biomarkers of ventricular arrhythmia. Further studies involving a larger sample size are required to obtain sufficient data and validate these findings.