Identification of genetic loci jointly influencing COVID-19 and coronary heart diseases
Abstract Background Comorbidities of coronavirus disease 2019 (COVID-19)/coronary heart disease (CHD) pose great threats to disease outcomes, yet little is known about their shared pathology. The study aimed to examine whether comorbidities of COVID-19/CHD involved shared genetic pathology, as well...
| Main Authors: | , , , , , , , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
| Published: |
BMC
2023-11-01
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| Series: | Human Genomics |
| Online Access: | https://doi.org/10.1186/s40246-023-00547-8 |
| _version_ | 1797557803001315328 |
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| author | Siyue Wang Hexiang Peng Feng Chen Chunfang Liu Qiwen Zheng Mengying Wang Jiating Wang Huan Yu Enci Xue Xi Chen Xueheng Wang Meng Fan Xueying Qin Yiqun Wu Jin Li Ying Ye Dafang Chen Yonghua Hu Tao Wu |
| author_facet | Siyue Wang Hexiang Peng Feng Chen Chunfang Liu Qiwen Zheng Mengying Wang Jiating Wang Huan Yu Enci Xue Xi Chen Xueheng Wang Meng Fan Xueying Qin Yiqun Wu Jin Li Ying Ye Dafang Chen Yonghua Hu Tao Wu |
| author_sort | Siyue Wang |
| collection | DOAJ |
| description | Abstract Background Comorbidities of coronavirus disease 2019 (COVID-19)/coronary heart disease (CHD) pose great threats to disease outcomes, yet little is known about their shared pathology. The study aimed to examine whether comorbidities of COVID-19/CHD involved shared genetic pathology, as well as to clarify the shared genetic variants predisposing risks common to COVID-19 severity and CHD risks. Methods By leveraging publicly available summary statistics, we assessed the genetically determined causality between COVID-19 and CHD with bidirectional Mendelian randomization. To further quantify the causality contributed by shared genetic variants, we interrogated their genetic correlation with the linkage disequilibrium score regression method. Bayesian colocalization analysis coupled with conditional/conjunctional false discovery rate analysis was applied to decipher the shared causal single nucleotide polymorphisms (SNPs). Findings Briefly, we observed that the incident CHD risks post COVID-19 infection were partially determined by shared genetic variants. The shared genetic variants contributed to the causality at a proportion of 0.18 (95% CI 0.18–0.19) to 0.23 (95% CI 0.23–0.24). The SNP (rs10490770) located near LZTFL1 suggested direct causality (SNPs → COVID-19 → CHD), and SNPs in ABO (rs579459, rs495828), ILRUN(rs2744961), and CACFD1(rs4962153, rs3094379) may simultaneously influence COVID-19 severity and CHD risks. Interpretation Five SNPs located near LZTFL1 (rs10490770), ABO (rs579459, rs495828), ILRUN (rs2744961), and CACFD1 (rs4962153, rs3094379) may simultaneously influence their risks. The current study suggested that there may be shared mechanisms predisposing to both COVID-19 severity and CHD risks. Genetic predisposition to COVID-19 is a causal risk factor for CHD, supporting that reducing the COVID-19 infection risk or alleviating COVID-19 severity among those with specific genotypes might reduce their subsequent CHD adverse outcomes. Meanwhile, the shared genetic variants identified may be of clinical implications for identifying the target population who are more vulnerable to adverse CHD outcomes post COVID-19 and may also advance treatments of ‘Long COVID-19.’ |
| first_indexed | 2024-03-10T17:21:21Z |
| format | Article |
| id | doaj.art-59aae5f8e40d4e0db37ea93a9929604e |
| institution | Directory Open Access Journal |
| issn | 1479-7364 |
| language | English |
| last_indexed | 2024-03-10T17:21:21Z |
| publishDate | 2023-11-01 |
| publisher | BMC |
| record_format | Article |
| series | Human Genomics |
| spelling | doaj.art-59aae5f8e40d4e0db37ea93a9929604e2023-11-20T10:18:47ZengBMCHuman Genomics1479-73642023-11-0117111110.1186/s40246-023-00547-8Identification of genetic loci jointly influencing COVID-19 and coronary heart diseasesSiyue Wang0Hexiang Peng1Feng Chen2Chunfang Liu3Qiwen Zheng4Mengying Wang5Jiating Wang6Huan Yu7Enci Xue8Xi Chen9Xueheng Wang10Meng Fan11Xueying Qin12Yiqun Wu13Jin Li14Ying Ye15Dafang Chen16Yonghua Hu17Tao Wu18Department of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Intensive Care Unit, PLA Rocket Force Characteristic Medical CenterSchool of Public Health, Baotou Medical CollegeCAS Key Laboratory of Genomic and Precision Medicine, Beijing Institute of Genomics, Chinese Academy of SciencesDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Local Diseases Control and Prevention, Fujian Provincial Center for Disease Control and PreventionDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityDepartment of Epidemiology and Biostatistics, School of Public Health, Peking UniversityAbstract Background Comorbidities of coronavirus disease 2019 (COVID-19)/coronary heart disease (CHD) pose great threats to disease outcomes, yet little is known about their shared pathology. The study aimed to examine whether comorbidities of COVID-19/CHD involved shared genetic pathology, as well as to clarify the shared genetic variants predisposing risks common to COVID-19 severity and CHD risks. Methods By leveraging publicly available summary statistics, we assessed the genetically determined causality between COVID-19 and CHD with bidirectional Mendelian randomization. To further quantify the causality contributed by shared genetic variants, we interrogated their genetic correlation with the linkage disequilibrium score regression method. Bayesian colocalization analysis coupled with conditional/conjunctional false discovery rate analysis was applied to decipher the shared causal single nucleotide polymorphisms (SNPs). Findings Briefly, we observed that the incident CHD risks post COVID-19 infection were partially determined by shared genetic variants. The shared genetic variants contributed to the causality at a proportion of 0.18 (95% CI 0.18–0.19) to 0.23 (95% CI 0.23–0.24). The SNP (rs10490770) located near LZTFL1 suggested direct causality (SNPs → COVID-19 → CHD), and SNPs in ABO (rs579459, rs495828), ILRUN(rs2744961), and CACFD1(rs4962153, rs3094379) may simultaneously influence COVID-19 severity and CHD risks. Interpretation Five SNPs located near LZTFL1 (rs10490770), ABO (rs579459, rs495828), ILRUN (rs2744961), and CACFD1 (rs4962153, rs3094379) may simultaneously influence their risks. The current study suggested that there may be shared mechanisms predisposing to both COVID-19 severity and CHD risks. Genetic predisposition to COVID-19 is a causal risk factor for CHD, supporting that reducing the COVID-19 infection risk or alleviating COVID-19 severity among those with specific genotypes might reduce their subsequent CHD adverse outcomes. Meanwhile, the shared genetic variants identified may be of clinical implications for identifying the target population who are more vulnerable to adverse CHD outcomes post COVID-19 and may also advance treatments of ‘Long COVID-19.’https://doi.org/10.1186/s40246-023-00547-8 |
| spellingShingle | Siyue Wang Hexiang Peng Feng Chen Chunfang Liu Qiwen Zheng Mengying Wang Jiating Wang Huan Yu Enci Xue Xi Chen Xueheng Wang Meng Fan Xueying Qin Yiqun Wu Jin Li Ying Ye Dafang Chen Yonghua Hu Tao Wu Identification of genetic loci jointly influencing COVID-19 and coronary heart diseases Human Genomics |
| title | Identification of genetic loci jointly influencing COVID-19 and coronary heart diseases |
| title_full | Identification of genetic loci jointly influencing COVID-19 and coronary heart diseases |
| title_fullStr | Identification of genetic loci jointly influencing COVID-19 and coronary heart diseases |
| title_full_unstemmed | Identification of genetic loci jointly influencing COVID-19 and coronary heart diseases |
| title_short | Identification of genetic loci jointly influencing COVID-19 and coronary heart diseases |
| title_sort | identification of genetic loci jointly influencing covid 19 and coronary heart diseases |
| url | https://doi.org/10.1186/s40246-023-00547-8 |
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