Association between ACE (rs4343 and rs1799752), AGTR1 (rs5186), and PAI-1 (rs2227631) polymorphisms in the host and the severity of Covid-19 infection

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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.

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AlanDeğerDil
dc.contributor.authorPolat, Seher
dc.contributor.authorŞimşek, Zühal Özer
dc.date.accessioned2026-10-18T20:26:12.807020011Z
dc.date.available2026-10-18T20:26:12.807020011Z
dc.date.issued2025
dc.description.abstractObjective: 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.doi10.1080/15257770.2024.2387033
dc.identifier.eissn1532-2335
dc.identifier.endpage78
dc.identifier.issn1525-7770
dc.identifier.issue1
dc.identifier.pmid39092900
dc.identifier.scopus2-s2.0-85200234608
dc.identifier.startpage57
dc.identifier.urihttps://rdlopen.rawdatalibrary.net/r/ebyu/11111
dc.identifier.volume44
dc.identifier.wosWOS:001283391000001
dc.language.isoen
dc.publisherTaylor and Francis Ltd.
dc.relation.ispartofNucleosides, Nucleotides and Nucleic Acids
dc.rightsinfo:eu-repo/semantics/openAccess
dc.subjectbiomarker
dc.subjectcomorbidities
dc.subjectCovid-19
dc.subjectgenetic susceptibility
dc.subjectrisk assessment
dc.subjectAdult
dc.subjectAged
dc.subjectFemale
dc.subjectGenetic Predisposition to Disease
dc.subjectHumans
dc.subjectIntensive Care Units
dc.subjectMale
dc.subjectMiddle Aged
dc.subjectPeptidyl-Dipeptidase A
dc.subjectPlasminogen Activator Inhibitor 1
dc.subjectPolymorphism, Single Nucleotide
dc.subjectReceptor, Angiotensin, Type 1
dc.subjectSARS-CoV-2
dc.subjectSeverity of Illness Index
dc.subjectangiotensin receptor
dc.subjectangiotensin receptor type 1
dc.subjectbiological marker
dc.subjectC reactive protein
dc.subjectcreatinine
dc.subjectD dimer
dc.subjectdipeptidyl carboxypeptidase
dc.subjectferritin
dc.subjectfibrinogen
dc.subjectgenomic DNA
dc.subjectglucose
dc.titleAssociation between ACE (rs4343 and rs1799752), AGTR1 (rs5186), and PAI-1 (rs2227631) polymorphisms in the host and the severity of Covid-19 infection
dc.typeArticle
dspace.entity.typePublication
rdl.citation.scopus2
rdl.citation.wos0
rdl.departmentMedical Faculty, Department of Medical Genetics, Erzincan Binali Yildirim University, Erzincan, Türkiye.
rdl.source.indexSCOPUS
rdl.source.indexWOS
rdl.source.indexPUBMED
rdl.wos.indexScience Citation Index Expanded (SCI-EXPANDED)