Justyna Adamczuk

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.

Introduction and objective: Data concerning the occurrence of intestinal parasites among the Polish population remain limited. The aim of the study is to assess the carriage of intestinal parasites among adults from north-eastern Poland and to identify demographic and clinical factors...

Background: Furuncular cutaneous myiasis caused by Cordylobia anthropophaga is a rare condition in non-endemic regions and may mimic furunculosis or skin abscesses, posing a diagnostic challenge. Case presentation: A previously healthy 24-year-old woman presented eight days after returning from Zanzibar with multiple tender erythematous nodules on the buttocks and left forearm. One larva was self-extracted, and others were removed under medical supervision. Ultrasound showed subcutaneous tracts consistent with larval infestation. Morphological analysis confirmed C. anthropophaga. The patient was treated with extraction and topical therapy. Lesions gradually resolved, leaving minimal residual marks after three months. Conclusions: Clinicians should consider furuncular myiasis in travelers returning from sub-Saharan Africa who present with boil-like nodules. Early recognition and extraction of larvae prevent complications. Traveler education on preventive measures remains essential.

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.

Tularemia, caused by the bacterium Francisella tularensis, is a zoonotic disease that has been reported in many countries across the globe. It may manifest in many forms, like pneumonic, oropharyngeal, glandular, ulceroglandular, or oculoglandular. In Poland, one of the most common types of tularemia is ulceroglandular. Typical symptoms of ulceroglandular tularemia include painful ulcers at the site of the insect or animal bite, along with systemic flu-like symptoms. Tularemia is generally effectively treated with appropriate antibiotics, however, frequent misdiagnosis and subsequent improper treatment remain significant clinical challenges. We present a case of a 54-year-old patient diagnosed with the ulceroglandular form of tularemia. Physicians in endemic areas are obliged to be aware of a high index of suspicion for tularemia. It should be included in the differential diagnosis when evaluating patients presenting with flu-like symptoms, lymphadenopathy, and non-healing ulcers.

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.

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.

Background In tick-borne encephalitis (TBE), central nervous system is infiltrated by a mixed leukocyte population detectable as cerebrospinal fluid (CSF) pleocytosis, contributing both to an infection control and immune-mediated pathology. The chemotactic pathways controlling this leukocyte influx are not well defined. Results We studied serum and CSF samples from 103 TBE patients, using normal serum (n=19) and CSF (n=12) as controls. We measured concentrations of the chemotactic cytokines IL-16, CXCL1, CXCL2, CXCL5, CXCL6, IL-8, CXCL9, CXCL10, CXCL11, CXCL13, CCL2, CCL3, CCL4, CCL5, CCL7, CCL8, CCL11, CCL13, CCL17, CCL19, CCL20, CCL21, CX3CL1 and XCL1 with a micro-bead assay and of CXCL12 with ELISA. The CSF lymphocyte subpopulations were counted cytometrically with a fluorescent-labeled monoclonal antibody kit. DNA was isolated from patients’ blood samples and 10 polymorphisms in CCR2, CCL5, CCR5, CXCR3, CXCL10, CXCL11 and CX3CR1 genes studied with real-time PCR. We analyzed results with non-parametric tests and created multivariate linear regression models of leukocyte population counts in CSF and of the clinical severity dependent on chemokine CSF levels. Except of CXCL2, CCL5 and XCL1, all the CSF chemokine concentrations were increased and the concentration index values favored their intrathecal synthesis. CXCL1, IL-8, CXCL10, CCL2, CCL3, CCL19 and CCL20 created chemotactic gradients towards CSF in 90-100% and CCL4, CCL7, CCL8 in about half of patients. The neutrophils associated predominantly with CXCL1 and IL-8 and the lymphocytes with IL-16, CCL19, CCL20, CCL4, CXCL12 and CXCL13, with consistent negative associations with CX₃CL1 and CCL2. CCL11, CCL19, CXCL10 and CXCL13 associated with milder and CXCL1 and CCL20 with a more severe presentation. There were associations between the genotypes of CCR2, CCL5, CXCR3 and CX3CR1 and concentrations of the relevant chemokines. Conclusions CXCL1/CXCR2, IL-8/CXCR1, CCL19/CCR7, CCL20/CCR6, CCL4/CCR5, CXCL12/CXCR4, CXCL13/CXCR5 and possibly other signaling axes contribute to pleocytosis in TBE. IL-16 associates with pleocytosis in an unclear mechanism and CX₃CL1 may be an antagonist of the leukocyte influx. The protective/immunopathogenic effects of chemokines are can be distinguished from their chemotactic effects, suggesting a complex relation between the inflammatory infiltrate and the clinical outcome. The genetic background influences chemokine expression in TBE.

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.