{"title":"宿主中 ACE（rs4343 和 rs1799752）、AGTR1（rs5186）和 PAI-1（rs2227631）多态性与 Covid-19 感染严重程度之间的关系。","authors":"Seher Polat, Zühal Özer Şimşek","doi":"10.1080/15257770.2024.2387033","DOIUrl":null,"url":null,"abstract":"<p><strong>Objective: </strong>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.</p><p><strong>Subject and methods: </strong>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 (<i>ACE</i> p.T776T G > A(rs4343) and g.16471_16472delinsALU (also referred to as I/D polymorphism; rs1799752), angiotensin II receptor type-1 (<i>AGTR1)</i> c.*86A > C (also referred to as A1166C; rs5186), and plasminogen activator inhibitor-1 (<i>PAI-1</i>-844 G > A (rs2227631) polymorphisms were analysed as well.</p><p><strong>Results: </strong>To have ACE \"ID\" genotype did not change the severity of the disease (OR: 0.92, 95% CI: 0.41-2.1, <i>p</i> = 0.84), but decreased the mortality risk 2.9-fold (OR: 2.9, 95% CI: 1.1-7.0, <i>p</i> = 0.03). In <i>PAI-1</i>-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, <i>p</i> = 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, <i>p</i> = 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) <i>p</i> = 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) <i>p</i> = 0.022).</p><p><strong>Conclusion: </strong>This study was shown that genetic predispositions that causes comorbidities were also likely to affect the prognosis of COVID-19.</p>","PeriodicalId":19343,"journal":{"name":"Nucleosides, Nucleotides & Nucleic Acids","volume":null,"pages":null},"PeriodicalIF":1.1000,"publicationDate":"2024-08-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Association between <i>ACE</i> (rs4343 and rs1799752), <i>AGTR1</i> (rs5186), and <i>PAI-1</i> (rs2227631) polymorphisms in the host and the severity of Covid-19 infection.\",\"authors\":\"Seher Polat, Zühal Özer Şimşek\",\"doi\":\"10.1080/15257770.2024.2387033\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><strong>Objective: </strong>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.</p><p><strong>Subject and methods: </strong>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 (<i>ACE</i> p.T776T G > A(rs4343) and g.16471_16472delinsALU (also referred to as I/D polymorphism; rs1799752), angiotensin II receptor type-1 (<i>AGTR1)</i> c.*86A > C (also referred to as A1166C; rs5186), and plasminogen activator inhibitor-1 (<i>PAI-1</i>-844 G > A (rs2227631) polymorphisms were analysed as well.</p><p><strong>Results: </strong>To have ACE \\\"ID\\\" genotype did not change the severity of the disease (OR: 0.92, 95% CI: 0.41-2.1, <i>p</i> = 0.84), but decreased the mortality risk 2.9-fold (OR: 2.9, 95% CI: 1.1-7.0, <i>p</i> = 0.03). In <i>PAI-1</i>-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, <i>p</i> = 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, <i>p</i> = 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) <i>p</i> = 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) <i>p</i> = 0.022).</p><p><strong>Conclusion: </strong>This study was shown that genetic predispositions that causes comorbidities were also likely to affect the prognosis of COVID-19.</p>\",\"PeriodicalId\":19343,\"journal\":{\"name\":\"Nucleosides, Nucleotides & Nucleic Acids\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":1.1000,\"publicationDate\":\"2024-08-02\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Nucleosides, Nucleotides & Nucleic Acids\",\"FirstCategoryId\":\"99\",\"ListUrlMain\":\"https://doi.org/10.1080/15257770.2024.2387033\",\"RegionNum\":4,\"RegionCategory\":\"生物学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q4\",\"JCRName\":\"BIOCHEMISTRY & MOLECULAR BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nucleosides, Nucleotides & Nucleic Acids","FirstCategoryId":"99","ListUrlMain":"https://doi.org/10.1080/15257770.2024.2387033","RegionNum":4,"RegionCategory":"生物学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q4","JCRName":"BIOCHEMISTRY & MOLECULAR BIOLOGY","Score":null,"Total":0}
引用次数: 0
摘要
目的：有必要确定适当的临床、生化、流行病学和遗传生物标志物，以阐明冠状病毒病-2019（COVID-19）疾病的潜在机制。该研究不仅关注COVID-19患者的疾病严重程度（非重症监护室（non-intense unit care，ICU）与重症监护室（intensive unit care，ICU）和遗传易感性之间的联系，还关注影响COVID-19严重程度的合并症和遗传易感性之间的联系：纳入 162 名在开塞利市医院非重症监护室和重症监护室接受治疗的 COVID-19 患者。所有志愿者均接受了身体检查和生化评估。血管紧张素转换酶（ACE p.T776T G > A(rs4343)和 g.16471_16472delinsALU（也称为 I/D 多态性；rs1799752）、血管紧张素 II 受体 1 型（AGTR1）c.*86A > C（也称为 A1166C；rs5186）和纤溶酶原激活剂抑制剂 1 型（PAI-1-844 G > A（rs2227631）多态性也进行了分析：结果：ACE "ID "基因型不会改变疾病的严重程度（OR：0.92，95% CI：0.41-2.1，p = 0.84），但会将死亡风险降低 2.9 倍（OR：2.9，95% CI：1.1-7.0，p = 0.03）。在 PAI-1-844 G > A 中，"A "隐性模型中的 "AA "基因型会使糖尿病（DM）风险增加 2.3 倍（OR：2.3 95%，CI：1.16-4.66，p = 0.018）。在 "G "隐性模型中，GG 基因型会使慢性肾病（CKD）的风险增加 4.8 倍（OR：4.8，95% CI：1.5-15.5，p = 0.008）。与 "AG "基因型的人相比，DM 组中 "GG "基因型的人纤维蛋白原水平更高（AG:4847.2 mg/L (1704.3) 对 GG:6444.67 mg/L (1861.62) p = 0.019），CKD 组中 "AA "基因型的人血小板水平更低，而 "GG "基因型的人血小板水平更高（AA:149 µL (18-159) 对 GG:228 µL (146-357) p = 0.022）：本研究表明，导致合并症的遗传倾向也可能影响 COVID-19 的预后。
Association between ACE (rs4343 and rs1799752), AGTR1 (rs5186), and PAI-1 (rs2227631) polymorphisms in the host and the severity of Covid-19 infection.
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.
期刊介绍：
Nucleosides, Nucleotides & Nucleic Acids publishes research articles, short notices, and concise, critical reviews of related topics that focus on the chemistry and biology of nucleosides, nucleotides, and nucleic acids.
Complete with experimental details, this all-inclusive journal emphasizes the synthesis, biological activities, new and improved synthetic methods, and significant observations related to new compounds.
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