Association between ACE (rs4343 and rs1799752), AGTR1 (rs5186), and PAI-1 (rs2227631) polymorphisms in the host and the severity of Covid-19 infection
Özet
Objective: It is necessary to identify appropriate clinical, biochemical, epidemiological and genetic biomarkers to elucidate the underlying mechanisms of the coronavirus disease-2019 (COVID-19) disease. The study focused on not only the link between disease severity (non-intense unit care (non-ICU) versus intensive unit care (ICU) and genetic susceptibility in COVID-19 patients but also the connection between comorbidity and genetic susceptibility affecting the severity of COVID-19. Subject and methods: One hundred and sixty-two COVID-19 patients treated in the non-ICU and ICU in Kayseri City Hospital were included. All volunteers underwent a physical examination and biochemical evaluation. Angiotensin-converting enzyme (ACE p.T776T G > A(rs4343) and g.16471_16472delinsALU (also referred to as I/D polymorphism; rs1799752), angiotensin II receptor type-1 (AGTR1) c.*86A > C (also referred to as A1166C; rs5186), and plasminogen activator inhibitor-1 (PAI-1-844 G > A (rs2227631) polymorphisms were analysed as well. Results: To have ACE “ID” genotype did not change the severity of the disease (OR: 0.92, 95% CI: 0.41–2.1, p = 0.84), but decreased the mortality risk 2.9-fold (OR: 2.9, 95% CI: 1.1–7.0, p = 0.03). In PAI-1-844 G > A, having the “AA” genotype in the “A” recessive model increased the risk of the diabetes mellitus (DM) 2.3-fold (OR: 2.3 95%, CI: 1.16–4.66, p = 0.018). In the “G” recessive model, to have the GG genotype increased the risk of chronic kidney disease (CKD) 4.8-fold (OR:4.8, 95% CI: 1.5–15.5, p = 0.008). “GG” genotype in the DM group had a higher fibrinogen level compared to those with the “AG” genotype (AG:4847.2 mg/L (1704.3) versus GG:6444.67 mg/L (1861.62) p = 0.019) and “AA” genotype in the CKD group had lower platelet levels and those with “GG” had higher platelet levels (AA:149 µL (18–159) versus GG: 228 µL (146–357) p = 0.022). Conclusion: This study was shown that genetic predispositions that causes comorbidities were also likely to affect the prognosis of COVID-19. © 2024 Taylor & Francis Group, LLC.
Anahtar Kelimeler
Tam Kayıt
| Alan | Değer | Dil |
|---|---|---|
| dc.contributor.author | Polat, Seher | |
| dc.contributor.author | Şimşek, Zühal Özer | |
| dc.date.accessioned | 2026-10-18T20:26:12.807020011Z | |
| dc.date.available | 2026-10-18T20:26:12.807020011Z | |
| dc.date.issued | 2025 | |
| dc.description.abstract | Objective: It is necessary to identify appropriate clinical, biochemical, epidemiological and genetic biomarkers to elucidate the underlying mechanisms of the coronavirus disease-2019 (COVID-19) disease. The study focused on not only the link between disease severity (non-intense unit care (non-ICU) versus intensive unit care (ICU) and genetic susceptibility in COVID-19 patients but also the connection between comorbidity and genetic susceptibility affecting the severity of COVID-19. Subject and methods: One hundred and sixty-two COVID-19 patients treated in the non-ICU and ICU in Kayseri City Hospital were included. All volunteers underwent a physical examination and biochemical evaluation. Angiotensin-converting enzyme (ACE p.T776T G > A(rs4343) and g.16471_16472delinsALU (also referred to as I/D polymorphism; rs1799752), angiotensin II receptor type-1 (AGTR1) c.*86A > C (also referred to as A1166C; rs5186), and plasminogen activator inhibitor-1 (PAI-1-844 G > A (rs2227631) polymorphisms were analysed as well. Results: To have ACE “ID” genotype did not change the severity of the disease (OR: 0.92, 95% CI: 0.41–2.1, p = 0.84), but decreased the mortality risk 2.9-fold (OR: 2.9, 95% CI: 1.1–7.0, p = 0.03). In PAI-1-844 G > A, having the “AA” genotype in the “A” recessive model increased the risk of the diabetes mellitus (DM) 2.3-fold (OR: 2.3 95%, CI: 1.16–4.66, p = 0.018). In the “G” recessive model, to have the GG genotype increased the risk of chronic kidney disease (CKD) 4.8-fold (OR:4.8, 95% CI: 1.5–15.5, p = 0.008). “GG” genotype in the DM group had a higher fibrinogen level compared to those with the “AG” genotype (AG:4847.2 mg/L (1704.3) versus GG:6444.67 mg/L (1861.62) p = 0.019) and “AA” genotype in the CKD group had lower platelet levels and those with “GG” had higher platelet levels (AA:149 µL (18–159) versus GG: 228 µL (146–357) p = 0.022). Conclusion: This study was shown that genetic predispositions that causes comorbidities were also likely to affect the prognosis of COVID-19. © 2024 Taylor & Francis Group, LLC. | |
| dc.identifier.doi | 10.1080/15257770.2024.2387033 | |
| dc.identifier.eissn | 1532-2335 | |
| dc.identifier.endpage | 78 | |
| dc.identifier.issn | 1525-7770 | |
| dc.identifier.issue | 1 | |
| dc.identifier.pmid | 39092900 | |
| dc.identifier.scopus | 2-s2.0-85200234608 | |
| dc.identifier.startpage | 57 | |
| dc.identifier.uri | https://rdlopen.rawdatalibrary.net/r/ebyu/11111 | |
| dc.identifier.volume | 44 | |
| dc.identifier.wos | WOS:001283391000001 | |
| dc.language.iso | en | |
| dc.publisher | Taylor and Francis Ltd. | |
| dc.relation.ispartof | Nucleosides, Nucleotides and Nucleic Acids | |
| dc.rights | info:eu-repo/semantics/openAccess | |
| dc.subject | biomarker | |
| dc.subject | comorbidities | |
| dc.subject | Covid-19 | |
| dc.subject | genetic susceptibility | |
| dc.subject | risk assessment | |
| dc.subject | Adult | |
| dc.subject | Aged | |
| dc.subject | Female | |
| dc.subject | Genetic Predisposition to Disease | |
| dc.subject | Humans | |
| dc.subject | Intensive Care Units | |
| dc.subject | Male | |
| dc.subject | Middle Aged | |
| dc.subject | Peptidyl-Dipeptidase A | |
| dc.subject | Plasminogen Activator Inhibitor 1 | |
| dc.subject | Polymorphism, Single Nucleotide | |
| dc.subject | Receptor, Angiotensin, Type 1 | |
| dc.subject | SARS-CoV-2 | |
| dc.subject | Severity of Illness Index | |
| dc.subject | angiotensin receptor | |
| dc.subject | angiotensin receptor type 1 | |
| dc.subject | biological marker | |
| dc.subject | C reactive protein | |
| dc.subject | creatinine | |
| dc.subject | D dimer | |
| dc.subject | dipeptidyl carboxypeptidase | |
| dc.subject | ferritin | |
| dc.subject | fibrinogen | |
| dc.subject | genomic DNA | |
| dc.subject | glucose | |
| dc.title | Association between ACE (rs4343 and rs1799752), AGTR1 (rs5186), and PAI-1 (rs2227631) polymorphisms in the host and the severity of Covid-19 infection | |
| dc.type | Article | |
| dspace.entity.type | Publication | |
| rdl.citation.scopus | 2 | |
| rdl.citation.wos | 0 | |
| rdl.department | Medical Faculty, Department of Medical Genetics, Erzincan Binali Yildirim University, Erzincan, Türkiye. | |
| rdl.source.index | SCOPUS | |
| rdl.source.index | WOS | |
| rdl.source.index | PUBMED | |
| rdl.wos.index | Science Citation Index Expanded (SCI-EXPANDED) |
