Coronavirus disease (COVID-19) and its outcomes remain one of the most challenging problems today. COVID-19 in children could be asymptomatic, but can result in a fatal outcome; therefore, predictions of the disease severity are important. The goal was to investigate the human genetic factors that could be associated with COVID-19 severity in children. Single-nucleotide polymorphisms of the following genes were studied: ACE2 (rs2074192), IFNAR2 (rs2236757), TYK2 (rs2304256), OAS1 (rs10774671), OAS3 (rs10735079), CD40 (rs4813003), FCGR2A (rs1801274) and CASP3 (rs113420705). In the case–control study were 30 children with mild or moderate course of the disease; 30 with severe COVID-19 symptoms and multisystem inflammatory syndrome in children (MIS-C) and 15 who were healthy, and who did not have SARS-CoV-2 (PCR negative, Ig G negative). The study revealed that ACE2 rs2074192 (allele T), IFNAR2 rs2236757 (allele A), OAS1 rs10774671 (allele A), CD40 rs4813003 (allele C), CASP3 rs113420705 (allele C) and male sex contribute to severe COVID-19 course and MIS-C in 85.6% of cases. The World Health Organization reported that new SARS-CoV-2 variants may cause previously unseen symptoms in children. Although the study has limitations due to cohort size, the findings can help provide a better understanding of SARS-CoV-2 infection and proactive pediatric patient management.

ACE2’s impact on the severity of COVID-19 is widely discussed but still controversial. To estimate its role in aspects of the main risk factors and comorbidities, we involved post-COVID-19 patients in Ternopil region (Ukraine). The recruitment period was from July 2020 to December 2021. Medical records, treatment modalities, and outcomes were recorded and analyzed. The serum human ACE2 protein was measured with Cusabio ELISA kits (Houston, TX, USA). Statistical analysis was performed with SPSS21.0 software (SPSS Inc., Chicago, IL, USA). The level of the ACE2 serum protein was significantly higher (p < 0.001) in patients with mild symptoms compared to a more severe course of the disease, and inversely had changed from 1 to 90 days after recovery. In patients with mild COVID-19, ACE2 levels significantly decreased over time, while among critical patients, it increased by 34.1 percent. Such results could be explained by ACE2 shedding from tissues into circulation. Loss of the membrane-bound form of the enzyme decreases the virus’ entry into cells. Our studies did not identify a sex-related ACE2 serum level correlation. The most common comorbidities were hypertension, cardiovascular diseases, respiratory diseases, and diabetes mellitus. All abovementioned comorbidities except respiratory diseases contribute to the severity of the disease and correlate with ACE2 blood serum levels.

Introduction: Recent studies have underscored the importance of genetic factors in predicting COVID-19 susceptibility and severity. While cytokine storms are crucial in disease severity, genetic predisposition significantly influences immune responses. Our study examined genes related to SARS-CoV-2 invasion (ACE2 rs2074192) and interferon-induced immunity (IFNAR2 rs2236757, TYK2 rs2304256, OAS1 rs10774671, OAS3 rs10735079). Additionally, we investigated genes linked to Kawasaki disease (CD40 rs4813003, FCGR2A rs1801274, CASP3 rs113420705) that play roles in immunogenesis.Methods: The pilot study, which involved 75 pediatric patients aged one month to 17 years [43 patients with active COVID-19, 17 children with multisystem inflammatory syndrome in children (MIS-C), and 15 healthy controls], was conducted in Ternopil, Ukraine. Gene polymorphism was studied for all patients. ELISA kits were used for interleukin studies, including Human IL-1β (Interleukin 1 Beta), Human IL-6 (Interleukin 6), Human IL-8 (Interleukin 8), Human IL-12 (Interleukin 12), Human IFN-α (Interferon Alpha), and Human TNF-α (Tumor Necrosis Factor Alpha). Statistical analysis was performed using IBM SPSS Statistics 21 and GraphPad Prism 8.4.3.Results: The analysis identified significant gene-cytokine associations in pediatric COVID-19 patients. The ACE2 rs2074192 T allele correlated with increased IL-1β, IL-6, IL-8, and TNF-α. The IFNAR2 rs2236757 A allele was linked to elevated IL-1β and IL-12 levels and low IFN-α levels, while OAS1 rs10774671 A allele carriers also exhibited lower IFN-α levels. OAS1 rs10774671 was prognostically crucial for determining IL-8 levels in children infected with SARS-CoV-2. OAS3 gene polymorphism rs10735079 was associated with changes in IL-6 levels, precisely a high level. The CD40 rs4813003 T allele increased IFN-α levels, while carriers of allele C had higher levels of IL-12. The results of our study revealed a correlation between IL-8 levels and the FCGR2A gene polymorphism rs1801274 (A/G). The CASP3 gene polymorphism rs113420705 led to an increase in IL-6.Conclusion: These findings enhance our understanding of pediatric COVID-19 and may hold promise for developing targeted interventions and providing a personalized medical approach for each patient.

ACE2 impact on the severity of COVID-19 is widely discussed but still controversial. To estimate its role in aspects of the main risk factors and comorbidities, we involved post-COVID-19 patients in Ternopil region (Ukraine). Recruitment period was July 2020 to December 2021. Medical records, treatment modalities and outcomes were recorded and analyzed. Serum human ACE2 protein was measured with Cusabio ELISA kits (Houston, TX, USA). Statistical analysis was performed with SPSS21.0 software (SPSS Inc., Chicago, IL, USA). The level of ACE2 serum protein was significantly higher (p < 0.001) in patients with mild symptoms compared to more severe course of disease, and inversely had changed from 1 to 90 days after recovery. In patients with mild COVID-19, ACE2 level significantly decreased over time, while among critical patients, it increased by 34.1percent. Such results could be explained by ACE2 shedding from tissues into circulation. Loss of the membrane-bound form of the enzyme decreases the virus entry into cells. Our studies did not identify any sex-related ACE2 serum levels correlation. The most common comorbidities were hypertension, cardiovascular diseases, respiratory diseases and diabetes mellitus. All comorbidities except respiratory diseases contribute to the severity of disease and correlate with ACE2 blood serum level.

The problem of thyroid dysfunction related to SARS-CoV-2 infection remains unclear in children. Therefore, the study aimed to reveal the interrelationship between thyroid dysfunction and COVID-19 severity­ as well as to determine optimal cut-off values for screening for thyroid disorders in children. A total number of 90 children aged from 1 month to 17 years were involved in the study. Patients with known thyroid disease were not recruited for the research. A thyroid panel was assessed for all participants that included: free triiodothyronine (FT3), free thyroxine (FT4), thyroid-stimulating hormone (TSH) and anti-thyroid peroxidase (ATPO) antibodies. Statistical analysis was done using the computer software Statistica 13.0. Research has revealed euthyroid sick syndrome (ESS) in 14.10% of SARS-CoV-2 infected children more often among patients with severe COVID-19 and multisystem inflammatory syndrome (33.33%) compared to mild COVID-19 course (6.67%) and moderate disease severity (8.89%) (P < 0.05). Significant correlation relationships were revealed for next values – FT3 and erythrocyte sedimentation rate (ESR) (rs = -0.22; P < 0.05); FT3 and C-reactive protein (CRP) (rs = -0.33; P < 0.05); FT3 and procalcitonin (rs = -0.43; P < 0.05). The next cut-off values for ESS determination were revealed: ESR 18.5 mm/h (AUC 0.803); CRP 11.5 mg/l (AUC 0.763); ferritin 84.8 ng/ml (AUC 0.733). Results suggest that pediatricians should pay attention to the endocrine disruptions by COVID-19 in children. Keywords: COVID-19, euthyroid sick syndrome in children, inflammatory markers

Background: Chronic obstructive pulmonary disease (COPD) continues to cause a heavy health and economic burden in the Europe and around the world. Arterial hypertension (AH) is considered as one of the principal COPD-associated comorbidi-ties. However, no data for association between gene polymorphism and AH in patients with COPD in Ukraine have ever been internationally published. We assessed the genotype and allele frequencies of angiotensinogen (AGT) M235T polymorphisms in patients with COPD and comorbid AH. Methods: The study group consisted of 96 patients: Group 1 (25 individuals with COPD), Group 2 (23 individuals with AH) and Group 3 (28 individuals with COPD and AH). The control group consisted of 20 healthy subjects. M/T genotypes of AGT were determined by polymerase chain reaction amplification. Results: The results of the study have not demonstrated any significant impact of alleles of AGT genes on the occurrence of diseases such as COPD, AH and combinations thereof. However, analysis of odds ratio has demonstrated the presence of a trend towards a protective role of the M allele of the AGT gene concerning occurrence of COPD, AH and their combinations. At the same time, the presence of the T allele of the AGT gene may increase the risk for occurrence of the above-mentioned diseases. Conclusions: The study that we have conducted suggests that the presence of T allele of the AGT gene at position 235 of the peptide chain both in homozygous and heterozygous states may increase the risk for AH in patients with COPD.