Recent studies highlight the crucial role of the gut microbiome in post-infectious complications, especially in patients recovering from severe COVID-19. Our research aimed to explore the connection between gut microbiome changes and the cytokine profile of patients with post-COVID syndrome. Using 16S rRNA amplicon sequencing, we analyzed the composition of the gut microbiome in 60 COVID-19 patients over the course of one year. We also measured the levels of serum cytokines and chemokines using the Milliplex system. Our results showed that severe SARS-CoV-2 infection cases, especially those complicated by pneumonia, induce a pro-inflammatory microbial milieu with heightened presence of Bacteroides, Faecalibacterium, and Prevotella_9. Furthermore, we found that post-COVID syndrome is characterized by a cross-correlation of various cytokines and chemokines MDC, IL-1b, Fractalkine, TNFa, FGF-2, EGF, IL-1RA, IFN-a2, IL-10, sCD40L, IL-8, Eotaxin, IL-12p40, and MIP-1b as well as a shift in the gut microbiome towards a pro-inflammatory profile. At the functional level, our analysis revealed associations with post-COVID-19 in homolactic fermentation, pentose phosphate, NAD salvage, and flavin biosynthesis. These findings highlight the intricate interplay between the gut microbiota, their metabolites, and systemic cytokines in shaping post-COVID symptoms. Unraveling the gut microbiome’s role in post-infectious complications opens avenues for new treatments for those patients with prolonged symptoms.

Background. Long COVID-19 symptoms appeared in many COVID-19 survivors. However, the prevalence and symptoms associated with long COVID-19 and its comorbidities have not been established. Methods. In total, 312 patients with long COVID-19 from 21 primary care centers were included in the study. At the six-month follow-up, their lung function was assessed by computerized tomography (CT) and spirometry, whereas cardiac function was assessed by electrocardiogram, Holter ECG, echocardiography, 24 h blood pressure monitoring, and a six-minute walk test (6MWT). Results. Of the 312 persons investigated, significantly higher systolic and diastolic blood pressure, left ventricular hypertrophy, and elevated NT-proBNP were revealed in participants with hypertension or type 2 diabetes. Left ventricular diastolic dysfunction was more frequently present in patients with hypertension. The most common registered CT abnormalities were fibrotic changes (83, 36.6%) and mediastinal lymphadenopathy (23, 10.1%). Among the tested biochemical parameters, three associations were found in long COVID-19 patients with hypertension but not diabetes: increased hemoglobin, fibrinogen, and ferritin. Nine patients had persisting IgM antibodies to SARS-CoV-2. Conclusions. We demonstrated a strong association between signs of cardiac dysfunction and lung fibrotic changes with comorbidities in a cohort of long COVID-19 subjects.

This study aimed to evaluate platform-specific immune memory trajectories in patients with breakthrough COVID-19 over a 12-month period. This prospective longitudinal study enrolled adults hospitalized with PCR-confirmed COVID-19. Participants were stratified according to prior COVID-19 vaccination status into three groups: unvaccinated, adenoviral-vector-vaccinated, and inactivated-virus-vaccinated. Comprehensive immune profiling included quantification of humoral responses and flow cytometric analysis of T- and B-cell memory subsets. Group differences were assessed using Kruskal–Wallis tests; longitudinal naïve CD8⁺ T-cell dynamics were modeled using linear mixed-effects models; multivariate immune signatures were identified using random forest classification with SHAP analysis. The most distinct cellular finding was a sustained reduction in naïve CD8⁺ T cells in the adenoviral-vector-vaccine group, which persisted for 12 months in patients without pneumonia. Machine learning models demonstrated high discriminative performance for patients without pneumonia (AUC = 0.89–0.92), identifying a specific triad of markers in the adenoviral-vector-vaccine group: decreased naïve CD8⁺ T cells, decreased double-negative effector memory T cells, and increased naïve CD19⁺ B cells. Linear mixed-effects modeling confirmed that contraction of the naïve CD8⁺ T-cell compartment over time was significant exclusively in AdV recipients, whereas pneumonia was the dominant predictor in unvaccinated individuals. No significant temporal or disease-related dynamics were observed in the inactivated vaccine group, whose immune profiles largely overlapped with those of unvaccinated individuals. COVID-19 vaccine platforms induce distinct, durable immune imprints that modulate responses to subsequent breakthrough infections. The adenoviral-vector platform was associated with unique phenotypic remodeling of the T-cell compartment, specifically persistent contraction of the naïve CD8⁺ pool. These findings suggest that the vaccine platform itself, beyond the target antigen, shapes the trajectory of immune competence and long-term memory.