Author
Listed:
- Yong-Hong Zhang
(Beijing You'an Hospital, Capital Medical University)
- Yan Zhao
(Beijing You'an Hospital, Capital Medical University)
- Ning Li
(Beijing You'an Hospital, Capital Medical University)
- Yan-Chun Peng
(MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, Oxford University)
- Eleni Giannoulatou
(The Computational Biology Research Group, Weatherall Institute for Molecular Medicine, Oxford University)
- Rong-Hua Jin
(Beijing You'an Hospital, Capital Medical University)
- Hui-Ping Yan
(Beijing You'an Hospital, Capital Medical University)
- Hao Wu
(Beijing You'an Hospital, Capital Medical University)
- Jin-Hua Liu
(Beijing You'an Hospital, Capital Medical University)
- Ning Liu
(Beijing You'an Hospital, Capital Medical University)
- Da-Yan Wang
(Chinese National Influenza Center, National Institute for Viral Disease Control and Prevention, China CDC)
- Yue-Long Shu
(Chinese National Influenza Center, National Institute for Viral Disease Control and Prevention, China CDC)
- Ling-Pei Ho
(MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, Oxford University
Oxford Centre for Respiratory Medicine, Oxford University Hospital NHS Trust)
- Paul Kellam
(Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus
UCL/MRC Centre for Medical Molecular Virology, University College London, Gower Street, London WC1E 6BT, UK)
- Andrew McMichael
(MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, Oxford University)
- Tao Dong
(Beijing You'an Hospital, Capital Medical University
MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, Oxford University)
Abstract
The SNP rs12252-C allele alters the function of interferon-induced transmembrane protein-3 increasing the disease severity of influenza virus infection in Caucasians, but the allele is rare. However, rs12252-C is much more common in Han Chinese. Here we report that the CC genotype is found in 69% of Chinese patients with severe pandemic influenza A H1N1/09 virus infection compared with 25% in those with mild infection. Specifically, the CC genotype was estimated to confer a sixfold greater risk for severe infection than the CT and TT genotypes. More importantly, because the risk genotype occurs with such a high frequency, its effect translates to a large population-attributable risk of 54.3% for severe infection in the Chinese population studied compared with 5.4% in Northern Europeans. Interferon-induced transmembrane protein-3 genetic variants could, therefore, have a strong effect of the epidemiology of influenza in China and in people of Chinese descent.
Suggested Citation
Yong-Hong Zhang & Yan Zhao & Ning Li & Yan-Chun Peng & Eleni Giannoulatou & Rong-Hua Jin & Hui-Ping Yan & Hao Wu & Jin-Hua Liu & Ning Liu & Da-Yan Wang & Yue-Long Shu & Ling-Pei Ho & Paul Kellam & And, 2013.
"Interferon-induced transmembrane protein-3 genetic variant rs12252-C is associated with severe influenza in Chinese individuals,"
Nature Communications, Nature, vol. 4(1), pages 1-6, June.
Handle:
RePEc:nat:natcom:v:4:y:2013:i:1:d:10.1038_ncomms2433
DOI: 10.1038/ncomms2433
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Citations
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Cited by:
- Xianxian Yang & Bin Tan & Xipeng Zhou & Jian Xue & Xian Zhang & Peng Wang & Chuang Shao & Yingli Li & Chaorui Li & Huiming Xia & Jingfu Qiu, 2015.
"Interferon-Inducible Transmembrane Protein 3 Genetic Variant rs12252 and Influenza Susceptibility and Severity: A Meta-Analysis,"
PLOS ONE, Public Library of Science, vol. 10(5), pages 1-14, May.
- Parker J. Denz & Samuel Speaks & Adam D. Kenney & Adrian C. Eddy & Jonathan L. Papa & Jack Roettger & Sydney C. Scace & Adam Rubrum & Emily A. Hemann & Adriana Forero & Richard J. Webby & Andrew S. Bo, 2024.
"Innate immune control of influenza virus interspecies adaptation via IFITM3,"
Nature Communications, Nature, vol. 15(1), pages 1-11, December.
- M. Clement & J. L. Forbester & M. Marsden & P. Sabberwal & M. S. Sommerville & D. Wellington & S. Dimonte & S. Clare & K. Harcourt & Z. Yin & L. Nobre & R. Antrobus & B. Jin & M. Chen & S. Makvandi-Ne, 2022.
"IFITM3 restricts virus-induced inflammatory cytokine production by limiting Nogo-B mediated TLR responses,"
Nature Communications, Nature, vol. 13(1), pages 1-16, December.
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