Introduction. The pandemic of the novel viral respiratory infection declared in 2020 demonstrated that coronaviruses are extremely dangerous human pathogens. They are characterised by high lethality and present a considerable medico-social threat owing to life-threatening complications.
Aim. To assess the impact of the COVID-19 pandemic on morbidity and mortality levels in the population of the Far Eastern Federal District (FEFD).
Materials and methods. A set of analytical, epidemiological and statistical studies was performed, together with a content analysis of relevant publications. Morbidity and mortality were evaluated according to ICD-10, using data from the state statistical monitoring system for 2000–2023 and the databases of the Federal State Statistics Service and the Ministry of Health of the Russian Federation.
Results. In the first pandemic year overall morbidity among adults fell sharply across all ICD-10 classes except “Diseases of the respiratory system”, which in the FEFD rose by 48.7% over the entire pandemic period. In 2020 the prevalence of COVID-19 among adults in the FEFD and in the Russian Federation was 2.4- and 3.2-fold higher, respectively, than among children. The pandemic was marked by high virulence and, accordingly, high adult case-fatality from COVID-19, which differed five-fold between FEFD regions. Among persons aged ≥ 60 years, COVID-19 accounted for 83.3% of deaths, whereas in the working-age group it accounted for 15.2% and in the 0- to 15-year group for 0.04%. The greatest share of deaths from respiratory diseases occurred in the 1- to 4-year age group (7.04%), while deaths from COVID-19 predominated in the 70- to 74-year group (9.28%). On average, respiratory diseases accounted for 4.51% of all deaths and COVID-19 for 6.76%. The pandemic markedly affected both the level and the structure of mortality across the full spectrum of causes. Particularly unprecedented was the rise in deaths from respiratory diseases: after years of steady decline (2000–2019), the rate increased by 48.7% in both Russia overall and the FEFD. During the pandemic years, total mortality among men in the region grew by 16.6% in 2021 versus 2019, and among women by 22.4%, reversing previous downward trends. The contribution of COVID-19 to overall mortality more than doubled the respective age-standardised death rates for respiratory and digestive diseases. In 2021 COVID-19 accounted for 14.6 % of all deaths in the FEFD, with regional shares ranging from 7.0% to 20.9%.
Conclusion. The COVID-19 pandemic substantially altered the level and structure of morbidity and mortality across all major nosological categories in the region. Socio-economic and natural-climatic conditions of the Far East produce wide inter-regional variation in these indicators. Forecasts that the recorded decline in morbidity during the pandemic would have negative consequences were confirmed: delayed detection and late diagnosis of chronic pathologies have led to progression, life-threatening complications and, consequently, increased mortality among people who did not receive timely and adequate medical care.

Aim. To assess the dynamics and age-specific patterns of bronchial asthma (BA) morbidity in the Republic of Crimea from 2017 to 2024.
Materials and methods. Data from the official statistical reporting form No. 12 ("Information on the Number of Diseases Registered Among Patients Residing in the Service Area of a Medical Organization") for the years 2017–2024 were analyzed. Regression analysis was used to quantitatively evaluate trends in BA morbidity.
Results. Overall BA morbidity increased from 796,570/0000 in 2017 to 936,16 0/0000 in 2024. Primary incidence rose from 37,430/0000 to 53,780/0000 over the same period. Age-specific trends varied: in the post-pandemic period, both overall and primary incidence declined among children and adolescents (0–14 and 15–17 years), whereas a clear increase was observed in adults aged 18–59 and those aged 60+. Regression analysis confirmed a statistically significant annual increase in BA incidence during the study period (β = 355.3 cases per year; p < 0.001).
Conclusion. Crimea has demonstrated a consistent upward trend in both overall and primary BA morbidity. Pre-pandemic years showed rising rates across all age groups. During the pandemic, primary incidence continued to increase while overall morbidity remained stable. In the post-pandemic period, incidence rose among adults (>18 years) but declined in those under 18 years of age.

Introduction. Acute respiratory viral infections (ARVIs) account for 90% of all infectious diseases in children. The COVID-19 pandemic has significantly impacted the epidemiological landscape of respiratory infections.
Aim. To determine the structure and circulation patterns of ARVI pathogens among children with bronchopulmonary diseases during 2023–2024.
Materials and methods. From February 2023 to January 2024, 128 pediatric patients presenting with clinical signs of ARVI were examined, including 87 children with recurrent respiratory infections, 28 diagnosed with community-acquired pneumonia, and 13 with bronchopulmonary dysplasia. Viral agents were detected by polymerase chain reaction (PCR) using the “ОRVI-COMPLEX” reagent kit (Russia).
Results. Etiological agents were identified in 70.3% of the tested children. Rhinoviruses were most frequently detected (24.22%), followed by seasonal coronaviruses (14.83%, predominantly HCoV-229E), and influenza viruses (10.15%). SARS-CoV-2 was detected in 5.47% of cases. Analysis of the circulating ARVI pathogen profile during the post-pandemic and post-COVID period (2023–2024) revealed a 16.7% increase in pathogen detection frequency compared to the pre-pandemic years (2018–2019).
Conclusion. The findings on the structure and circulation dynamics of influenza and ARVI pathogens in the post-COVID period are of significant importance for forecasting disease trends and implementing appropriate therapeutic, preventive, and anti-epidemic measures.

Introduction. In recent years, the proportion of viral pathogens in the etiology of community-acquired pneumonia has increased. Identification of the causative agent in postmortem (autopsy) material may provide a more accurate etiological cause of fatal pneumonias.
Aim. To analyze the species diversity of viral pathogens isolated from patients with fatal outcomes of community-acquired pneumonia, compared with the results of virological examination of respiratory samples from individuals with favorable disease outcomes.
Materials and Methods. The analysis included protocols of virological examination of autopsy material (lung tissue) from 140 individuals who died from pneumonia in Khabarovsk in 2023. The comparison group consisted of data from virological examinations of patients with clinical manifestations of community-acquired pneumonia and favorable outcomes, in which 1136 DNA and RNA viral agents were identified. The search targeted detecting DNA/RNA of 11 respiratory viral pathogens and four viruses causing opportunistic diseases. The study was performed using polymerase chain reaction with reagents produced by domestic manufacturers.
Results. DNA and RNA of respiratory viruses (10 types) were detected in autopsy material with a frequency of 46.43%. DNA of viruses causing opportunistic diseases (four types) was detected with a frequency of 27.14%. Clinical samples from patients with a favorable outcome more frequently contained rhinoviruses (25.6%), adenoviruses (13.03%), respiratory syncytial viruses (12.4%), and parainfluenza type 3 viruses (11.09%). In the spectrum of viruses isolated from clinical samples, rhinoviruses predominated (25.6%), followed by adenoviruses (13.03%), respiratory syncytial viruses (12.4%), and parainfluenza type 3 viruses (11.09%). SARS-CoV-2 viruses accounted for 6.6% of cases, and influenza A(H1N1) viruses for 1.1% of cases. Seasonal patterns in virus detection in fatal pneumonias were identified.
Conclusion. In cases of pneumonia with virologically confirmed etiology, fatal outcomes were determined in nearly half of cases by SARS-CoV-2 and influenza A(H1N1) viruses.

Aim. To delineate clinical profiles among the patients recovering from community-acquired pneumonia (CAP) based on their clinical and functional characteristics, in order to justify the need for and personalize subsequent rehabilitation programs.
Materials and methods. The study enrolled 104 patients. Collected data included demographics, medical history (including smoking status and pack-year index, prior CAP episodes, and previous COVID-19), complaints, laboratory parameters, lung function and chest computed tomography (CT) findings at the moment of CAP diagnosis and at admission to rehabilitation.
Results. The mean age of the patients was 47.3 ± 17.9 years; 57% were women. Severe CAP was present in 25% and correlated with age (ρ = 0.22; p = 0.029). The median hospital stay was 10 [8–13] days and increased with age (ρ = 0.30; p = 0.001) and comorbidity (p = 0.039). On initial chest CT bilateral lung involvement was observed in 48.5%; the median number of involved segments was 3 [2–6], decreasing to 1 [0–3] by the onset of rehabilitation. Predominant complaints were dyspnea (90.3%) and fatigue (87.4%); productive cough was more frequent in smokers, whereas dry cough predominated in non-smokers. Erythrocyte sedimentation rate correlated with length of hospitalization (ρ = 0.28; p = 0.0075). Dyspnea was associated with lower FEV1, FEV1/FVC, and FEF50 (ρ = 0.36–0.42; p < 0.05). Cluster analysis identified two clinical profiles differing in symptom severity, residual CT abnormalities, and degree of pulmonary function impairment.
Conclusions. These findings support a personalized approach to rehabilitation and highlight the need for further prospective studies and profile-oriented programs.

Aim. To assess lung function during the long-term follow-up period in convalescents of community-acquired viral pneumonia caused by SARS-CoV-2.
Materials and methods. Fifty patients who had recovered from SARSCoV- 2-associated community-acquired viral pneumonia were examined. Two observation groups were formed: Group 1 included 24 patients without a history of chronic obstructive airway diseases, and Group 2 comprised 26 patients with asthma (BA). The control group consisted of 20 apparently healthy volunteers with normal lung function and no history of community-acquired pneumonia. Lung function tests were performed at 1, 3, 6, and 12 months after hospital discharge. Evaluated parameters included vital capacity (VC), forced vital capacity (FVC), forced expiratory volume in one second (FEV1), FEV1/VC and FEV1/FVC ratios, forced expiratory flow at 25%, 50%, and 75% of FVC (FEF25, FEF50, FEF75, respectively), and maximal mid-expiratory flow (MMEF).
Results. In Group 1 patients, symptoms such as dyspnea, sensation of incomplete inspiration and expiration, and reduced mid-to-distal forced expiratory flow rates (FEF50, FEF75, and MMEF) persisted for up to 3 months and returned to normal values by 6 months after the viral pneumonia episode. In Group 2, at the 3-month follow-up, 78% of patients reported increased fatigue and 73% complained of dyspnea and incomplete expiration. Mild generalized bronchial obstruction, associated with persistent respiratory symptoms and poor asthma control, was observed in 75% of BA patients for up to 6 months and persisted at the mid-to-distal airway level for up to 12 months.
Conclusion. These findings suggest further research is needed to understand the mechanisms underlying prolonged respiratory dysfunction, particularly focusing on the immunometabolic consequences of SARS-CoV-2–induced communityacquired viral pneumonia.

Aim. To study the possibility of predicting frequent exacerbations of chronic obstructive pulmonary disease (COPD) by assessing parameters of lung function and echocardiographic indices.
Materials and methods. A oneyear prospective single-center study included 85 patients with COPD exacerbations, of whom two groups were formed based on the results of observation during the year. Group 1 included patients (n = 28) with one or no exacerbations per year, group 2 included patients (n = 57) with two or more exacerbations during the year (frequent exacerbations). It was found that patients in group 2 had more pronounced impairments of lung and cardiac function. A comprehensive clinical and functional examination included the CAT, mMRC, KOP-25 questionnaires, a study of lung function and an echocardiographic examination.
Results. Based on discriminant analysis data, two highly effective prediction models were developed to identify patients at increased risk of frequent exacerbations over the course of a year. Questionnaire results, respiratory parameters (FEV₁, FEF₅₀), and echocardiographic parameters (interventricular septal thickness and tricuspid annular systolic displacement (TAPSE)) were used as predictors.
Conclusion. These models can be used to develop a technology for predicting an unfavorable COPD course to ensure a personalized approach when choosing treatment for patients at high risk of exacerbations.

Aim. To evaluate the characteristics of inflammation in severe bronchial asthma in real-world clinical practice, using the city of Krasnoyarsk as an example.
Materials and methods. Eighty patients diagnosed with severe bronchial asthma were examined. Prior to enrollment, all patients had been receiving standard maintenance therapy corresponding to steps 4–5 according to the Russian federal clinical guidelines and exhibited uncontrolled asthma. The general clinical assessment included patient interviews, physical examination, and review of outpatient medical records and hospital discharge summaries. Pulmonary function tests were performed using a whole-body plethysmograph (Erich Eger, Germany). Serum levels of total IgE, interleukins (IL)-5, IL-4, IL-10, IL-9, IL-13, transforming growth factor beta (TGF-β), periostin, cathepsin S, and dipeptidyl peptidase-4 (DPP-4) were measured by solid-phase enzyme-linked immunosorbent assay (ELISA). Fractional exhaled nitric oxide (FeNO) was assessed using the portable analyzer «NObreath» (Bedfont Scientific Limited, UK).
Results. Fixed airflow obstruction (FAO) was present in 58% of patients with severe bronchial asthma. Evaluation of T2 inflammation biomarkers revealed that one marker was elevated in 15 (18.7%) patients, two markers in 34 (42.5%), and three markers in 31 (38.7%) patients. In one-third of patients with severe asthma, three T2 biomarkers were simultaneously elevated, which was associated with significantly higher peripheral blood eosinophil counts, total IgE levels, and FeNO values—although no corresponding increase in cytokine levels was observed. Compared to healthy controls, patients with severe asthma demonstrated significantly elevated concentrations of T2-associated cytokines (IL-4, IL-5, IL-13), as well as cathepsin S, periostin, and TGF-β. Notably, plasma periostin levels were significantly higher in patients with severe asthma and FAO compared to both those without FAO and healthy controls (p = 0.034). Correlation analysis revealed moderate-strength associations between cathepsin S, TGF-β, and DPP-4 levels and T2 cytokines. Furthermore, cathepsin S, TGF-β, DPP-4, and periostin were interrelated and correlated with lung function parameters.
Conclusion. Activation of three T2 inflammatory signaling pathways is associated with markedly elevated FeNO, blood eosinophils, and total IgE. A significant increase in plasma periostin levels in patients with severe asthma and fixed airflow obstruction suggests its potential role in T2 inflammation and airway remodeling.

Aim. To assess the efficacy of a fixed-dose combination of an angiotensin II receptor blocker and a calcium-channel blocker within combination therapy in patients with arterial hypertension (AH) combined with chronic obstructive pulmonary disease (COPD).
Materials and methods. Thirty patients aged 61–75 years with AH and COPD were examined and allocated to two equal groups. Group 1 received a fixed combination of candesartan 16 mg and amlodipine 5 mg once daily (Hyposart A, Akrikhin) as antihypertensive therapy; Group 2 received amlodipine 5 mg/day and lisinopril 20 mg/day. A full clinical, instrumental and laboratory evaluation was performed before treatment and after six weeks; office blood pressure (BP) was measured after two weeks, and 24-hour ambulatory BP monitoring (ABPM) was used to analyse BP variability and circadian profile.
Results. By week 6, the target BP was achieved in 100 % of Group 1 and in 86.7 % of Group 2. ABPM showed more pronounced favourable changes in Group 1. In Group 2 the variability of systolic (SBP) and diastolic BP (DBP) fell significantly only in daytime (p < 0.05); at night the decrease was not significant (p > 0.05). The nocturnal dip percentage of SBP in Group 1 increased by 24.6 % and that of DBP by 21.4 % (p < 0.01); no significant change was recorded in Group 2. In Group 1 the proportion of dippers rose from 20.0 % to 73.3 % owing to a decline in non-dippers (from 53.0 % to 20.0 %) and night-peakers (from 26.7 % to 6.1 %). In Group 2 the numbers of non-dippers (from 46.7 % to 40.0 %) and night-peakers (from 26.7 % to 20.0 %) fell, resulting in an increase in dippers to 40.0 %. Spirometry revealed significant improvement in airway patency in both groups.
Conclusion. In patients with concomitant AH and COPD, the fixed-dose combination of candesartan and amlodipine provides potent antihypertensive action, markedly normalises nocturnal BP variability in non-dippers and night-peakers, and improves bronchial patency.

Introduction. TRPV1 cation channels are known to be activated by cigarette smoke components, particulate matter, and reactive oxygen species, and their expression is increased in alveolar macrophages of patients with chronic obstructive pulmonary disease (COPD).
Aim. To analyze the features of the transcriptome profile of macrophages differentiating from peripheral blood monocytes in vitro under prolonged exposure to the TRPV1 agonist capsaicin.
Materials and methods. Monocytes were isolated from the peripheral blood of five apparently healthy male volunteers (52.2±3.89 years). The cells were differentiated for 10 days in RPMI-1640 medium (10% FCS, 1% penicillin/streptomycin) containing 50 ng/ml GM-CSF or GM-CSF at the same concentration and 50 μM capsaicin. Upon completion of differentiation, total RNA was extracted from the resulting macrophages, mRNA was enriched, and sequencing was performed on the MGISEQ-200 platform in SE50 mode. Data processing included read mapping (Salmon), differential expression analysis (DESeq2), and functional gene enrichment (Cytoscape). In addition, macrophage phenotype was assessed using the MacSpectrum platform.
Results. Macrophage differentiation in the presence of capsaicin was primarily accompanied by signs of activation of protein translation and transport processes, lipid metabolism, and maintenance of replicative potential. At the same time, suppression of biological processes associated with cytokine signaling, response to pathogens, ability to stimulate leukocyte activation and proliferation, as well as cytoskeletal organization and cell motility was observed. Analysis using MacSpectrum revealed a decrease in the polarization index (MPI) and differentiation index (AMDI) in macrophages differentiated in the presence of capsaicin, indicating inhibition of the development of a mature pro-inflammatory phenotype and the emegrence of a hyporesponsive, M0-like state.
Conclusion. Capsaicin, likely mediating its effect primarily through TRPV1, significantly influences macrophage differentiation, leading to the formation of hyporesponsive, incompletely differentiated cells that share several characteristics with alveolar macrophages found in the airways of COPD patients. These data suggest TRPV1-dependent modulation of macrophages as a possible pathogenetic mechanism contributing to this disease.

Introduction. Identifying single-nucleotide polymorphisms (SNPs) in immune-related genes and examining their associations with specific symptoms, syndromes, and diseases is one of the important directions in medical genetics.
Aim. To develop PCR-based assays for genotyping of selected SNPs in innate immunity and inflammatory response genes (TLR1, TLR4, MBL2, PELI1, IL1B, IL6, IL10, TNF, IFNG).
Materials and methods. SNP selection was based on public databases (PubMed, HapMap, RegulomeDB) and custom-developed software. Primers and probes for high-resolution melting (HRM) analysis of amplicons and for asymmetric Linear-After-The-Exponential (LATE) PCR coupled with molecular beacon probe melting analysis were designed in Vector NTI 11.0. Genomic DNA for genotyping was isolated from peripheral blood of 48 mothers with chronic herpesvirus infections and from umbilical cord blood of their newborns.
Results. Twenty SNPs across the target genes were selected. Oligonucleotide sequences and PCR conditions for genotyping were established.
Conclusions. The developed test systems enable genotyping of selected SNPs in TLR1, TLR4, MBL2, PELI1, IL1B, IL6, IL10, TNF, and IFNG genes, thereby facilitating further association studies with the course and outcomes of pregnancy in women with chronic herpesvirus infections and with developmental abnormalities in their newborns.

Introduction. Exacerbation of cytomegalovirus (CMV) infection during pregnancy is a significant risk factor for obstetric complications; however, the complex immunological and endocrine alterations preceding placental dysfunction remain poorly understood.
Aim. To develop a prognostic model for the development of chronic subcompensated placental insufficiency (PI) in pregnant women with CMV infection based on a comprehensive assessment of immune response markers (immunoglobulin (Ig) M, circulating immune complexes (CIC), tumor necrosis factor (TNF)-α, interleukins (IL)-1β and -4), endothelial function indicators (endothelin-1, nitrite anion (NO₂⁻)), and hormonal profile (progesterone, cortisol).
Materials and methods. The study included 27 pregnant women with exacerbation of chronic CMV infection in the second trimester and subsequent remission in the third trimester, complicated by subcompensated PI. The comparison group consisted of 35 CMV-seronegative pregnant women at comparable gestational ages. Study materials included peripheral blood, urine, and buccal epithelium. CMV-specific IgM and IgG, IgG avidity index, levels of IL-1β, IL-4, TNF-α, endothelin-1, NO2⁻, progesterone, cortisol, and total IgM were measured by enzyme-linked immunosorbent assay (ELISA). CIC levels were determined by turbidimetric analysis.
Results. CMV exacerbation in the second trimester was associated with significantly elevated concentrations of IL-1β (p < 0.0001), TNF-α (p < 0.0001), IgM (p < 0.001), CIC (p < 0.001), endothelin-1 (p < 0.0001), and cortisol (p < 0.0001), along with reduced levels of IL-4 (p < 0.0001), NO2⁻ (p < 0.01), and progesterone (p < 0.0001) in peripheral blood. A prognostic model for the development of subcompensated PI in the third trimester was developed based on these parameters in women with second-trimester CMV exacerbation.
Conclusion. Assessment of IgM, CIC, TNF-α, IL-1β, IL-4, endothelin-1, NO2⁻, progesterone, and cortisol can be integrated into a comprehensive diagnostic monitoring strategy for pregnant women with CMV infection to identify those at high risk of developing subcompensated placental insufficiency.

Introduction. Despite the well-established association between virus-induced structural liver remodeling and serum endotoxin accumulation, to date no studies have examined the morphofunctional characteristics of the liver in offspring of women with chronic respiratory disease during the acute phase of viral infection.
Aim. To evaluate echogenic and functional changes in the liver in newborns with cerebral ischemia born to mothers who experienced exacerbation of mild bronchial asthma associated with reactivation of chronic cytomegalovirus (CMV) infection during the second trimester of pregnancy.
Materials and methods. Hepatic echogenic structure, as well as levels of medium-molecular-weight peptides and seromucoid in umbilical cord serum, were assessed in 42 full-term newborns of mothers with uncomplicated pregnancies (control group) and in 68 newborns with cerebral ischemia that developed against a background of mild bronchial asthma exacerbation associated with reactivation of chronic CMV infection in their mothers during the second trimester of gestation (main group). The main group was subdivided into two subgroups: 36 newborns with grade I cerebral ischemia (subgroup 1) and 32 newborns with grade II cerebral ischemia (subgroup 2).
Results. Compared with the control group, newborns in subgroup 1 showed significantly lower Apgar scores at 1 minute (p < 0.001) and 5 minutes (p < 0.001), as well as lower birth weight (p < 0.01). However, no differences were found in ultrasound liver parameters or in serum levels of medium-molecular-weight peptides and seromucoid. In subgroup 2, compared with both the control group and subgroup 1, further reductions in Apgar scores at 1 minute (p < 0.001) and 5 minutes (p < 0.001), as well as birth weight (p < 0.01 and p < 0.001, respectively), were observed. Moreover, compared with subgroup 1, subgroup 2 exhibited significantly higher hepatic parenchymal echogenicity (p < 0.01), structural alterations in portal tracts (p < 0.05), small inclusions (p < 0.01), and gallbladder deformation (p < 0.05). Concentrations of medium-molecular-weight peptides increased to 0.280 ± 0.003 optical density units (p < 0.05), and seromucoid levels rose to 0.094 ± 0.002 optical density units (p < 0.05).
Conclusion. In newborns with grade II cerebral ischemia born to mothers with exacerbation of mild bronchial asthma associated with reactivation of chronic CMV infection during the second trimester of pregnancy, more pronounced alterations in liver ultrasound morphology and elevated levels of medium-molecular-weight peptides and seromucoid were observed compared to newborns with grade I cerebral ischemia under similar maternal somatic conditions. These findings reflect intensified cytotoxic effects of hypoxia and endotoxemia on the central nervous system in newborns with an adverse antenatal infectious history.

Introduction. Research into immunity in pregnant women with viral infections remains highly relevant.
Aim. To evaluate the characteristics of the humoral immune response in pregnant women with chronic placental insufficiency associated with exacerbation of cytomegalovirus (CMV) infection during the second trimester of pregnancy.
Materials and methods. A dynamic observational study was conducted in 165 pregnant women (main group) with chronic CMV infection—exacerbation in the second trimester and remission in the third trimester—including 138 patients with compensated chronic placental insufficiency (CCPI) (subgroup 1) and 27 with subcompensated chronic placental insufficiency (SCPI) (subgroup 2). The comparison group consisted of 35 CMV-seronegative pregnant women. Study materials included peripheral blood, urine, and buccal epithelium. CMV-specific immunoglobulins (Ig) M and G, CMV IgG avidity index, total IgA, IgM, and IgG, secretory sIgA, and circulating immune complexes (CIC) were measured using enzymelinked immunosorbent assay (ELISA) and turbidimetric analysis.
Results. In pregnant women with CMV exacerbation during the second trimester, a correlation was observed between the magnitude of the humoral immune response and the severity of placental insufficiency. High CMV IgG titers (1:1600 and 1:3200) were associated with more frequent viral DNA detection and significant humoral immune disturbances—namely, elevated levels of IgG (p < 0.01), IgM (p < 0.001), and CIC (p < 0.001), alongside reduced IgA (p < 0.001). An IgG titer of 1:3200 showed strong association with the development of CCPI, whereas a titer of 1:800 was linked to SCPI.
Conclusion. The findings indicate that the nature of the immune response in CMV infection—which determines disease severity and pregnancy outcomes—largely depends on the status of antiviral defense and humoral reactions, particularly the levels of CMV-specific IgG and sIgA, as confirmed by the established correlations.

Aim. To assess the content of phospholipids in leukocytes of peripheral blood in parturient women who had COVID-19 during the third trimester of pregnancy.
Materials and methods. The amount of the cytochemical reaction product for phospholipids in leukocytes of peripheral blood was determined using the reagent kit "DIAHIM-CYTOSTEINSCh" (Russia) in 102 parturient women. The first group included patients with mild course of COVID-19 (n = 34), the second group — patients with moderate course of COVID-19 (n = 32). The control group consisted of 36 women not infected with SARS-CoV-2.
Results. The phospholipid content in leukocytes of pregnant women who had COVID-19 differed significantly compared to the control group. In the control group, the mean cytochemical coefficient (MCC) was 2.67 ± 0.05 arbitrary units. In patients with COVID-19, a significant decrease in MCC was observed: in persons with a mild course of the disease to 2.42 ± 0.05 (p < 0.001), and in persons with a moderate course to 1.98 ± 0.04 arbitrary units (p < 0.001).
Conclusion. The data obtained suggest that COVID-19 infection affects the phospholipid content in the leukocytes of parturient women, reducing their amount. Further investigation of this issue may provide a detailed explanation of the impact of COVID-19 infection on pregnancy course and perinatal outcomes.

Introduction. The exacerbation of chronic cytomegalovirus (CMV) infection in women during gestation often leads to altered liver function in their offspring. This may initiate activation of enzymes – markers of cytolysis, cholestasis and glycolysis – which affect the reflex sphere, excitation and inhibition processes in the brain. Considering the important role of liver enzymes in the regulatory mechanisms of the central nervous system, the relationship between biochemical parameters of the liver in cerebral ischemia of varying severity in offspring of mothers who suffered an exacerbation of chronic CMV infection during gestation has not been studied to date.
Aim. To assess the functional state of the liver in cerebral ischemia of varying severity in newborns from mothers with exacerbation of chronic CMV infection in the second trimester of pregnancy.
Materials and methods. The study involved assessing the activity of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, gamma-glutamyl transferase, and lactate dehydrogenase in umbilical cord serum from 42 newborns with an uncomplicated antenatal history (control group) and 68 newborns with cerebral ischemia that developed against the background of exacerbation of chronic CMV infection in their mothers in the second trimester of gestation (main group). Depending on the severity of perinatal brain injury, two subgroups were identified: the first – 36 newborns with grade I cerebral ischemia; the second – 32 newborns with grade II cerebral ischemia. Depending on the severity of perinatal brain damage, two subgroups were identified: the first – 36 newborns with cerebral ischemia of the first degree; the second – 32 newborns with cerebral ischemia of the second degree.
Results. In the first subgroup of the main group, compared with the control group, lower Apgar scores at 1 minute (p <0.001) and 5 minutes (p <0.001), as well as lower birth weight (p <0.01), were recorded. At the same time, no differences in the activity of alanine aminotransferase, aspartate aminotransferase, alkaline phosphatase, and gamma-glutamyl transferase were detected in the blood serum from the umbilical vein against the background of an increase in lactate dehydrogenase levels. Newborns in the second subgroup, compared with both the control group and the first subgroup, showed a decrease in Apgar scores at 1 minute (p <0.001) and 5 minutes (p <0.001), as well as birth weight (p <0.01 and p <0.001, respectively). Biochemically, newborns in the second subgroup, compared with the first subgroup, showed higher levels of aspartate aminotransferase (p <0.05), alkaline phosphatase (p <0.05), gamma-glutamyl transferase (p <0.01), and lactate dehydrogenase (p <0.05).
Conclusion. Grade II cerebral ischemia in newborns of mothers with exacerbation of chronic CMV infection during the second trimester of pregnancy, compared with grade I cerebral ischemia in newborns under similar antenatal ontogenetic conditions, is characterized by more pronounced cytolysis, cholestasis, and glycolysis activation. This reflects the negative impact of intrauterine hypoxia associated with more severe cerebral pathology in newborns from mothers with exacerbation of chronic CMV infection during the second trimester of gestation.

The review systematizes the data of the scientific literature of recent years devoted to the problem of chronic cough. It provides modern information on the nomenclature, epidemiology, pathophysiology of chronic cough. A number of phenotypes of this syndrome, the features of its manifestations in various types of somatic pathology are discussed. Attention is focused on the refractory variant of chronic cough, which has a neurogenic origin associated with hypersensitivity to the cough reflex. The features of chronic cough in children and gender differences are described. Changes in the quality of life and social aspects of chronic cough are highlighted. A toolkit for assessing the quality of life associated with cough is provided.

Introduction. Psoriasis is one of the most common dermatoses among both adults and children. Its course associated with pulmonary diseases in adult patients has been described.
Aim. To analyze the accumulated data on the prevalence and possible pathophysiological mechanisms of inflammation in psoriasis and chronic bronchopulmonary diseases driven by shared processes and genetic predisposition, in order to assess the potential for future prognostic approaches and early prevention strategies.
Materials and methods. A literature search spanning more than 50 years was conducted in the PubMed, PlamX, ResearchGate, The BMJ, and Elsevier databases, selecting articles categorized as "Clinical Trial", "Meta-Analysis", "Review", and "Systematic Review".
Results. Analysis of published studies revealed a relatively low percentage of comorbidity between psoriasis and bronchopulmonary pathology. Several common pathogenetic mechanisms of inflammation and the effects of specialized therapies are presented. Shared risk factors contributing to the development of psoriasis and other diseases—particularly those affecting the bronchopulmonary system—have been identified. These similarities include immune processes, cytokine profiles, and types of immune cells involved. Several genetic variants linking psoriasis with impaired lung function have been analyzed, laying the groundwork for future research.
Conclusion. The insufficient study of the co-occurrence of these two nosological entities – especially in childhood necessitates further investigation and identification of – biomarkers at earlier stages of ontogenesis to enable timely diagnosis, prognosis, and evidence-based therapeutic interventions.