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.

Tick-borne encephalitis (TBE) is the most prevalent viral infection of the central nervous system (CNS) in Poland. The disease is characterized by the presence of two stages. The first phase, called the viremic stage, presents with flu-like symptoms, while the second stage of TBE is characterized by damage to the nervous system and may follow a severe and dramatic course. The aim of this paper is to increase the awareness of the potential sequelae after TBE. In this study, we report cases of severe TBE in 36-year-old and 57-year-old female patients. The outcome of TBE varies from patient to patient, but there are some factors that can help to predict the severity of TBE infection. The risk factors presented in these patients were as follows: the monophasic course of TBE, high pleocytosis in cerebrospinal fluid (CSF) and older age. Both of our patients were not vaccinated despite the World Health Organization’s (WHO’s) recommendations. Both patients had no history of travel outside their region of residence prior to the onset of illness. The few risk factors shown in our patients and the serious sequelae of the disease may indicate the need to test patients for possible gene mutations.

The results of our study confirm the knowledge on immune response in the Polish population and add new information regarding correlations with the severity of the disease. The data in the literature concerning the correlation between antibodies response and sex are ambiguous, and we did not observe differences between antibodies production and gender, which also adds new information.

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: In the post-pandemic era, SARS-CoV-2 immunity is increasingly shaped by vaccination and previous infection. Understanding the relationship between cellular and humoral immune responses is important for characterizing immunity in vaccinated populations. Methods: This study included 629 participants from the Bialystok PLUS cohort, stratified according to anti-N serostatus into anti-N-seronegative (n = 159) and anti-N-seropositive (n = 470) groups. Cellular immune response measurements were available for a subset of 246 participants. Humoral response was assessed using anti-S and anti-N antibodies, while cellular response (OC) was evaluated by interferon-gamma (IFN-γ) release following SARS-CoV-2 antigen stimulation. Group differences were assessed using the Mann–Whitney U test, and associations were evaluated using Spearman’s rank correlations with Benjamini–Hochberg correction. Multivariable linear regression was used to assess the association between anti-N serostatus and cellular response after adjustment for age and sex. Results: Anti-N-seropositive participants had significantly higher cellular responses than anti-N-seronegative participants (median 1752.3 vs. 771.1; p < 0.001). After adjustment for age and sex, anti-N seropositivity remained significantly associated with higher cellular response, corresponding to a 3.57-fold higher geometric mean of OC + 1 (95% CI: 1.90–6.73; p < 0.001). Anti-S antibody levels showed moderate positive correlations with cellular response in both anti-N-seronegative and anti-N-seropositive participants (ρ = 0.45 and ρ = 0.37, respectively), and the association remained significant after adjustment for age, sex, and anti-N serostatus. No significant associations were observed between cellular response and anti-N antibody levels or routine laboratory parameters after correction for multiple comparisons. Conclusions: Anti-N seropositivity was associated with higher SARS-CoV-2-specific cellular immune response among vaccinated participants, and this association remained significant after adjustment for age and sex. The moderate association between anti-S antibody levels and cellular response suggests that humoral and cellular measures provide related but complementary information on SARS-CoV-2-specific immunity. Routine laboratory parameters were not significantly associated with cellular immune response in this cohort.