A host-based whole genome sequencing study reveals novel risk loci associated with severity of influenza A(H1N1)pdm09 infection
Influenza A(H1N1)pdm09 virus has remained in a seasonal circulation since being recognized in 2009. Although it followed a mild course in most patients, in others it caused a series of severe clinical illnesses. Epidemiologic studies have implicated that host factors have a major influence on the di...
| Main Authors: | , , , , , , , , , , , , |
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| Format: | Article |
| Language: | English |
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Taylor & Francis Group
2021-01-01
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| Series: | Emerging Microbes and Infections |
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| Online Access: | https://www.tandfonline.com/doi/10.1080/22221751.2020.1870412 |
| _version_ | 1818987798012624896 |
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| author | Mo Li Yongkun Chen Tao Chen Shixiong Hu Luan Chen Lu Shen Fangcai Li Jing Yang Yan Sun Dayan Wang Lin He Shengying Qin Yuelong Shu |
| author_facet | Mo Li Yongkun Chen Tao Chen Shixiong Hu Luan Chen Lu Shen Fangcai Li Jing Yang Yan Sun Dayan Wang Lin He Shengying Qin Yuelong Shu |
| author_sort | Mo Li |
| collection | DOAJ |
| description | Influenza A(H1N1)pdm09 virus has remained in a seasonal circulation since being recognized in 2009. Although it followed a mild course in most patients, in others it caused a series of severe clinical illnesses. Epidemiologic studies have implicated that host factors have a major influence on the disease severity of influenza A(H1N1)pdm09 infection. However, an understanding of relevant genetic variations and the underlying mechanisms is still limited. In this present study, we used a host-based whole genome sequencing (WGS) method to comprehensively explore the genetic risk loci associated with severity of influenza A(H1N1)pdm09 infection. From the common single-nucleotide variants (SNVs) analysis, we identified the abnormal nominally significant (P < 1 × 10−4) common SNVs enriched in PTBP3 gene. The results of rare functional SNVs analysis supported that there were several novel candidate genes might confer risk of severe influenza A(H1N1)pdm09 diseases, such as FTSJ3, CPVL, BST2, NOD2 and MAVS. Moreover, our results of gene set based analysis indicated that the HIF-1 transcription factor and IFN-γ pathway might play an important role in the underlying mechanism of severe influenza A(H1N1)pdm09. These findings will increase our knowledge about biological mechanism underlying the severe influenza A(H1N1)pdm09 and facilitate to design novel personalized treatments. |
| first_indexed | 2024-12-20T19:12:24Z |
| format | Article |
| id | doaj.art-063f525d5ee94c8a8ee3236dfee87d03 |
| institution | Directory Open Access Journal |
| issn | 2222-1751 |
| language | English |
| last_indexed | 2024-12-20T19:12:24Z |
| publishDate | 2021-01-01 |
| publisher | Taylor & Francis Group |
| record_format | Article |
| series | Emerging Microbes and Infections |
| spelling | doaj.art-063f525d5ee94c8a8ee3236dfee87d032022-12-21T19:29:10ZengTaylor & Francis GroupEmerging Microbes and Infections2222-17512021-01-0110112313110.1080/22221751.2020.1870412A host-based whole genome sequencing study reveals novel risk loci associated with severity of influenza A(H1N1)pdm09 infectionMo Li0Yongkun Chen1Tao Chen2Shixiong Hu3Luan Chen4Lu Shen5Fangcai Li6Jing Yang7Yan Sun8Dayan Wang9Lin He10Shengying Qin11Yuelong Shu12Bio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, People’s Republic of ChinaSchool of Public Health (Shenzhen), Sun Yat-sen University, Shenzhen, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaHunan Provincial Center for Disease Control and Prevention, Changsha, People’s Republic of ChinaBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, People’s Republic of ChinaBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, People’s Republic of ChinaHunan Provincial Center for Disease Control and Prevention, Changsha, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaChangsha Central Hospital, Changsha 410004, People’s Republic of ChinaNational Institute for Viral Disease Control and Prevention, Chinese Center for Disease Control and Prevention, Beijing, People’s Republic of ChinaBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, People’s Republic of ChinaBio-X Institutes, Key Laboratory for the Genetics of Developmental and Neuropsychiatric Disorders, Ministry of Education, Shanghai Jiao Tong University, Shanghai, People’s Republic of ChinaSchool of Public Health (Shenzhen), Sun Yat-sen University, Shenzhen, People’s Republic of ChinaInfluenza A(H1N1)pdm09 virus has remained in a seasonal circulation since being recognized in 2009. Although it followed a mild course in most patients, in others it caused a series of severe clinical illnesses. Epidemiologic studies have implicated that host factors have a major influence on the disease severity of influenza A(H1N1)pdm09 infection. However, an understanding of relevant genetic variations and the underlying mechanisms is still limited. In this present study, we used a host-based whole genome sequencing (WGS) method to comprehensively explore the genetic risk loci associated with severity of influenza A(H1N1)pdm09 infection. From the common single-nucleotide variants (SNVs) analysis, we identified the abnormal nominally significant (P < 1 × 10−4) common SNVs enriched in PTBP3 gene. The results of rare functional SNVs analysis supported that there were several novel candidate genes might confer risk of severe influenza A(H1N1)pdm09 diseases, such as FTSJ3, CPVL, BST2, NOD2 and MAVS. Moreover, our results of gene set based analysis indicated that the HIF-1 transcription factor and IFN-γ pathway might play an important role in the underlying mechanism of severe influenza A(H1N1)pdm09. These findings will increase our knowledge about biological mechanism underlying the severe influenza A(H1N1)pdm09 and facilitate to design novel personalized treatments.https://www.tandfonline.com/doi/10.1080/22221751.2020.1870412Influenza A(H1N1)pdm09host disease severitywhole genome sequencinghypoxia inducible factor-1interferon gamma |
| spellingShingle | Mo Li Yongkun Chen Tao Chen Shixiong Hu Luan Chen Lu Shen Fangcai Li Jing Yang Yan Sun Dayan Wang Lin He Shengying Qin Yuelong Shu A host-based whole genome sequencing study reveals novel risk loci associated with severity of influenza A(H1N1)pdm09 infection Emerging Microbes and Infections Influenza A(H1N1)pdm09 host disease severity whole genome sequencing hypoxia inducible factor-1 interferon gamma |
| title | A host-based whole genome sequencing study reveals novel risk loci associated with severity of influenza A(H1N1)pdm09 infection |
| title_full | A host-based whole genome sequencing study reveals novel risk loci associated with severity of influenza A(H1N1)pdm09 infection |
| title_fullStr | A host-based whole genome sequencing study reveals novel risk loci associated with severity of influenza A(H1N1)pdm09 infection |
| title_full_unstemmed | A host-based whole genome sequencing study reveals novel risk loci associated with severity of influenza A(H1N1)pdm09 infection |
| title_short | A host-based whole genome sequencing study reveals novel risk loci associated with severity of influenza A(H1N1)pdm09 infection |
| title_sort | host based whole genome sequencing study reveals novel risk loci associated with severity of influenza a h1n1 pdm09 infection |
| topic | Influenza A(H1N1)pdm09 host disease severity whole genome sequencing hypoxia inducible factor-1 interferon gamma |
| url | https://www.tandfonline.com/doi/10.1080/22221751.2020.1870412 |
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