Department of Personalized and Molecular Medicine, Era University, Lucknow 226003, Uttar Pradesh, India.
Department of Personalized and Molecular Medicine, Era University, Lucknow 226003, Uttar Pradesh, India; Department of Microbiology, Era University, Lucknow 226003, Uttar Pradesh, India.
Infect Genet Evol. 2021 Jul;91:104801. doi: 10.1016/j.meegid.2021.104801. Epub 2021 Mar 4.
Severe acute respiratory syndrome corona virus-2 (SARS-CoV-2) has first emerged from China in December 2019 and causes coronavirus induced disease 19 (COVID-19). Since then researchers worldwide have been struggling to detect the possible pathogenesis of this disease. COVID-19 showed a wide range of clinical behavior from asymptomatic to severe acute respiratory disease syndrome. However, the etiology of susceptibility to severe lung injury is not yet fully understood. Angiotensin-converting enzyme1 (ACE1) convert angiotensin I into Angiotensin II that was further metabolized by ACE 2 (ACE2). The binding ACE2 receptor to SARS-CoV-2 facilitate its enter into the host cell. The interaction and imbalance between ACE1 and ACE2 play a crucial role in the pathogenesis of lung injury. Thus, the aim of this study was to investigate the association of ACE1 I/D polymorphism with severity of Covid-19. The study included RT-PCR confirmed 269 cases of Covid-19. All cases were genotyped for ACE1 I/D polymorphism using polymerase chain reaction and followed by statistical analysis (SPSS, version 15.0). We found that ACE1 DD genotype, frequency of D allele, older age (≥46 years), unmarried status, and presence of diabetes and hypertension were significantly higher in severe COVID-19 patient. ACE1 ID genotype was significantly independently associated with high socio-economic COVID-19 patients (OR: 2.48, 95% CI: 1.331-4.609). These data suggest that the ACE1 genotype may impact the incidence and clinical outcome of COVID-19 and serve as a predictive marker for COVID-19 risk and severity.
严重急性呼吸综合征冠状病毒 2(SARS-CoV-2)于 2019 年 12 月首次在中国出现,导致冠状病毒引起的疾病 19(COVID-19)。从那时起,世界各地的研究人员一直在努力探索这种疾病的可能发病机制。COVID-19 的临床表现从无症状到严重急性呼吸窘迫综合征不等。然而,对易发生严重肺损伤的病因尚不完全了解。血管紧张素转换酶 1(ACE1)将血管紧张素 I 转化为血管紧张素 II,血管紧张素 II 进一步被 ACE2(ACE2)代谢。SARS-CoV-2 与 ACE2 受体结合,有助于其进入宿主细胞。ACE1 和 ACE2 之间的相互作用和失衡在肺损伤的发病机制中起着至关重要的作用。因此,本研究旨在探讨 ACE1 I/D 多态性与 COVID-19 严重程度的关系。该研究纳入了 269 例经 RT-PCR 确诊的 COVID-19 病例。所有病例均采用聚合酶链反应(PCR)对 ACE1 I/D 多态性进行基因分型,并进行统计分析(SPSS,版本 15.0)。结果发现,DD 基因型、D 等位基因频率、年龄≥46 岁、未婚、合并糖尿病和高血压在重症 COVID-19 患者中显著升高。ACE1 ID 基因型与高社会经济 COVID-19 患者显著相关(OR:2.48,95%CI:1.331-4.609)。这些数据表明,ACE1 基因型可能影响 COVID-19 的发病和临床结局,并可作为 COVID-19 风险和严重程度的预测标志物。