Susceptibilities of Human ACE2 Genetic Variants in Coronavirus Infection
There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. The coronaviru...
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| Published in | Journal of virology Vol. 96; no. 1; p. e0149221 |
|---|---|
| Main Authors | , , , , , , , , , , , , , , , , , |
| Format | Journal Article |
| Language | English |
| Published |
United States
American Society for Microbiology
12.01.2022
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| Subjects | |
| Online Access | Get full text |
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| Abstract | There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells.
The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in more than 235 million cases worldwide and 4.8 million deaths (October 2021), with various incidences and mortalities among regions/ethnicities. The coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize the angiotensin-converting enzyme 2 (ACE2) as the receptor to enter cells. We hypothesized that the genetic variability in ACE2 may contribute to the variable clinical outcomes of COVID-19. To test this hypothesis, we first conducted an
in silico
investigation of single-nucleotide polymorphisms (SNPs) in the coding region of ACE2. We then applied an integrated approach of genetics, biochemistry, and virology to explore the capacity of select ACE2 variants to bind coronavirus spike proteins and mediate viral entry. We identified the ACE2 D355N variant that restricts the spike protein-ACE2 interaction and consequently limits infection both
in vitro
and
in vivo
. In conclusion, ACE2 polymorphisms could modulate susceptibility to SARS-CoV-2, which may lead to variable disease severity.
IMPORTANCE
There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. We found that several missense ACE2 single-nucleotide variants (SNVs) that showed significantly altered binding with the spike proteins of SARS-CoV, SARS-CoV-2, and NL63-HCoV. We identified an ACE2 SNP, D355N, that restricts the spike protein-ACE2 interaction and consequently has the potential to protect individuals against SARS-CoV-2 infection. Our study highlights that ACE2 polymorphisms could impact human susceptibility to SARS-CoV-2, which may contribute to ethnic and geographical differences in SARS-CoV-2 spread and pathogenicity. |
|---|---|
| AbstractList | The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in more than 235 million cases worldwide and 4.8 million deaths (October 2021), with various incidences and mortalities among regions/ethnicities. The coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize the angiotensin-converting enzyme 2 (ACE2) as the receptor to enter cells. We hypothesized that the genetic variability in ACE2 may contribute to the variable clinical outcomes of COVID-19. To test this hypothesis, we first conducted an in silico investigation of single-nucleotide polymorphisms (SNPs) in the coding region of ACE2. We then applied an integrated approach of genetics, biochemistry, and virology to explore the capacity of select ACE2 variants to bind coronavirus spike proteins and mediate viral entry. We identified the ACE2 D355N variant that restricts the spike protein-ACE2 interaction and consequently limits infection both in vitro and in vivo. In conclusion, ACE2 polymorphisms could modulate susceptibility to SARS-CoV-2, which may lead to variable disease severity. IMPORTANCE There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. We found that several missense ACE2 single-nucleotide variants (SNVs) that showed significantly altered binding with the spike proteins of SARS-CoV, SARS-CoV-2, and NL63-HCoV. We identified an ACE2 SNP, D355N, that restricts the spike protein-ACE2 interaction and consequently has the potential to protect individuals against SARS-CoV-2 infection. Our study highlights that ACE2 polymorphisms could impact human susceptibility to SARS-CoV-2, which may contribute to ethnic and geographical differences in SARS-CoV-2 spread and pathogenicity. The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in more than 235 million cases worldwide and 4.8 million deaths (October 2021), with various incidences and mortalities among regions/ethnicities. The coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize the angiotensin-converting enzyme 2 (ACE2) as the receptor to enter cells. We hypothesized that the genetic variability in ACE2 may contribute to the variable clinical outcomes of COVID-19. To test this hypothesis, we first conducted an in silico investigation of single-nucleotide polymorphisms (SNPs) in the coding region of ACE2. We then applied an integrated approach of genetics, biochemistry, and virology to explore the capacity of select ACE2 variants to bind coronavirus spike proteins and mediate viral entry. We identified the ACE2 D355N variant that restricts the spike protein-ACE2 interaction and consequently limits infection both in vitro and in vivo . In conclusion, ACE2 polymorphisms could modulate susceptibility to SARS-CoV-2, which may lead to variable disease severity. IMPORTANCE There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. We found that several missense ACE2 single-nucleotide variants (SNVs) that showed significantly altered binding with the spike proteins of SARS-CoV, SARS-CoV-2, and NL63-HCoV. We identified an ACE2 SNP, D355N, that restricts the spike protein-ACE2 interaction and consequently has the potential to protect individuals against SARS-CoV-2 infection. Our study highlights that ACE2 polymorphisms could impact human susceptibility to SARS-CoV-2, which may contribute to ethnic and geographical differences in SARS-CoV-2 spread and pathogenicity. There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in more than 235 million cases worldwide and 4.8 million deaths (October 2021), with various incidences and mortalities among regions/ethnicities. The coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize the angiotensin-converting enzyme 2 (ACE2) as the receptor to enter cells. We hypothesized that the genetic variability in ACE2 may contribute to the variable clinical outcomes of COVID-19. To test this hypothesis, we first conducted an in silico investigation of single-nucleotide polymorphisms (SNPs) in the coding region of ACE2. We then applied an integrated approach of genetics, biochemistry, and virology to explore the capacity of select ACE2 variants to bind coronavirus spike proteins and mediate viral entry. We identified the ACE2 D355N variant that restricts the spike protein-ACE2 interaction and consequently limits infection both in vitro and in vivo . In conclusion, ACE2 polymorphisms could modulate susceptibility to SARS-CoV-2, which may lead to variable disease severity. IMPORTANCE There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. We found that several missense ACE2 single-nucleotide variants (SNVs) that showed significantly altered binding with the spike proteins of SARS-CoV, SARS-CoV-2, and NL63-HCoV. We identified an ACE2 SNP, D355N, that restricts the spike protein-ACE2 interaction and consequently has the potential to protect individuals against SARS-CoV-2 infection. Our study highlights that ACE2 polymorphisms could impact human susceptibility to SARS-CoV-2, which may contribute to ethnic and geographical differences in SARS-CoV-2 spread and pathogenicity. The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in more than 235 million cases worldwide and 4.8 million deaths (October 2021), with various incidences and mortalities among regions/ethnicities. The coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize the angiotensin-converting enzyme 2 (ACE2) as the receptor to enter cells. We hypothesized that the genetic variability in ACE2 may contribute to the variable clinical outcomes of COVID-19. To test this hypothesis, we first conducted an in silico investigation of single-nucleotide polymorphisms (SNPs) in the coding region of ACE2. We then applied an integrated approach of genetics, biochemistry, and virology to explore the capacity of select ACE2 variants to bind coronavirus spike proteins and mediate viral entry. We identified the ACE2 D355N variant that restricts the spike protein-ACE2 interaction and consequently limits infection both in vitro and in vivo. In conclusion, ACE2 polymorphisms could modulate susceptibility to SARS-CoV-2, which may lead to variable disease severity. IMPORTANCE There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. We found that several missense ACE2 single-nucleotide variants (SNVs) that showed significantly altered binding with the spike proteins of SARS-CoV, SARS-CoV-2, and NL63-HCoV. We identified an ACE2 SNP, D355N, that restricts the spike protein-ACE2 interaction and consequently has the potential to protect individuals against SARS-CoV-2 infection. Our study highlights that ACE2 polymorphisms could impact human susceptibility to SARS-CoV-2, which may contribute to ethnic and geographical differences in SARS-CoV-2 spread and pathogenicity.The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in more than 235 million cases worldwide and 4.8 million deaths (October 2021), with various incidences and mortalities among regions/ethnicities. The coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize the angiotensin-converting enzyme 2 (ACE2) as the receptor to enter cells. We hypothesized that the genetic variability in ACE2 may contribute to the variable clinical outcomes of COVID-19. To test this hypothesis, we first conducted an in silico investigation of single-nucleotide polymorphisms (SNPs) in the coding region of ACE2. We then applied an integrated approach of genetics, biochemistry, and virology to explore the capacity of select ACE2 variants to bind coronavirus spike proteins and mediate viral entry. We identified the ACE2 D355N variant that restricts the spike protein-ACE2 interaction and consequently limits infection both in vitro and in vivo. In conclusion, ACE2 polymorphisms could modulate susceptibility to SARS-CoV-2, which may lead to variable disease severity. IMPORTANCE There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. We found that several missense ACE2 single-nucleotide variants (SNVs) that showed significantly altered binding with the spike proteins of SARS-CoV, SARS-CoV-2, and NL63-HCoV. We identified an ACE2 SNP, D355N, that restricts the spike protein-ACE2 interaction and consequently has the potential to protect individuals against SARS-CoV-2 infection. Our study highlights that ACE2 polymorphisms could impact human susceptibility to SARS-CoV-2, which may contribute to ethnic and geographical differences in SARS-CoV-2 spread and pathogenicity. The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in more than 235 million cases worldwide and 4.8 million deaths (October 2021), with various incidences and mortalities among regions/ethnicities. The coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize the angiotensin-converting enzyme 2 (ACE2) as the receptor to enter cells. We hypothesized that the genetic variability in ACE2 may contribute to the variable clinical outcomes of COVID-19. To test this hypothesis, we first conducted an investigation of single-nucleotide polymorphisms (SNPs) in the coding region of ACE2. We then applied an integrated approach of genetics, biochemistry, and virology to explore the capacity of select ACE2 variants to bind coronavirus spike proteins and mediate viral entry. We identified the ACE2 D355N variant that restricts the spike protein-ACE2 interaction and consequently limits infection both and . In conclusion, ACE2 polymorphisms could modulate susceptibility to SARS-CoV-2, which may lead to variable disease severity. There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect disease outcome, and the coronaviruses SARS-CoV, SARS-CoV-2, and HCoV-NL63 utilize human ACE2 as the receptor to enter cells. We found that several missense ACE2 single-nucleotide variants (SNVs) that showed significantly altered binding with the spike proteins of SARS-CoV, SARS-CoV-2, and NL63-HCoV. We identified an ACE2 SNP, D355N, that restricts the spike protein-ACE2 interaction and consequently has the potential to protect individuals against SARS-CoV-2 infection. Our study highlights that ACE2 polymorphisms could impact human susceptibility to SARS-CoV-2, which may contribute to ethnic and geographical differences in SARS-CoV-2 spread and pathogenicity. |
| Author | Chen, Hedi Zhao, Xiaomin Saeed, Mohsan Ding, Qiang Wang, Yuyan Zhou, Dongming Feng, Fei Shi, Hongyang Chen, Da-Yuan Lan, Jun Wu, Jianping Wang, Xinquan Ren, Wenlin Tian, Boxue Zhang, Rong Close, Brianna Zhu, Yunkai Yuan, Zhenghong |
| Author_xml | – sequence: 1 givenname: Wenlin surname: Ren fullname: Ren, Wenlin organization: Center for Infectious Disease Research, School of Medicine, Tsinghua University, Beijing, China – sequence: 2 givenname: Yunkai surname: Zhu fullname: Zhu, Yunkai organization: Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China – sequence: 3 givenname: Jun surname: Lan fullname: Lan, Jun organization: School of Life Sciences, Tsinghua University, Beijing, China – sequence: 4 givenname: Hedi surname: Chen fullname: Chen, Hedi organization: School of Pharmaceutical Sciences, Tsinghua University, Beijing, China – sequence: 5 givenname: Yuyan surname: Wang fullname: Wang, Yuyan organization: Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China – sequence: 6 givenname: Hongyang surname: Shi fullname: Shi, Hongyang organization: CAS Key Laboratory of Molecular Virology and Immunology, Institut Pasteur of Shanghai, Chinese Academy of Sciences, Shanghai, China – sequence: 7 givenname: Fei surname: Feng fullname: Feng, Fei organization: Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China – sequence: 8 givenname: Da-Yuan surname: Chen fullname: Chen, Da-Yuan organization: Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts, USA, National Emerging Infectious Diseases Laboratories, Boston University, Boston, Massachusetts, USA – sequence: 9 givenname: Brianna surname: Close fullname: Close, Brianna organization: Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts, USA, National Emerging Infectious Diseases Laboratories, Boston University, Boston, Massachusetts, USA – sequence: 10 givenname: Xiaomin surname: Zhao fullname: Zhao, Xiaomin organization: Center for Infectious Disease Research, School of Medicine, Tsinghua University, Beijing, China – sequence: 11 givenname: Jianping surname: Wu fullname: Wu, Jianping organization: Key Laboratory of Structural Biology of Zhejiang Province, School of Life Sciences, Westlake University, Hangzhou, Zhejiang Province, China – sequence: 12 givenname: Boxue surname: Tian fullname: Tian, Boxue organization: School of Pharmaceutical Sciences, Tsinghua University, Beijing, China – sequence: 13 givenname: Zhenghong surname: Yuan fullname: Yuan, Zhenghong organization: Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China – sequence: 14 givenname: Dongming surname: Zhou fullname: Zhou, Dongming organization: Department of Pathogen Biology, School of Basic Medical Sciences, Tianjin Medical University, Tianjin, China – sequence: 15 givenname: Mohsan orcidid: 0000-0001-8505-7054 surname: Saeed fullname: Saeed, Mohsan organization: Department of Biochemistry, Boston University School of Medicine, Boston, Massachusetts, USA, National Emerging Infectious Diseases Laboratories, Boston University, Boston, Massachusetts, USA – sequence: 16 givenname: Xinquan surname: Wang fullname: Wang, Xinquan organization: School of Life Sciences, Tsinghua University, Beijing, China – sequence: 17 givenname: Rong surname: Zhang fullname: Zhang, Rong organization: Key Laboratory of Medical Molecular Virology (MOE/NHC/CAMS), School of Basic Medical Sciences, Shanghai Medical College, Biosafety Level 3 Laboratory, Fudan University, Shanghai, China – sequence: 18 givenname: Qiang orcidid: 0000-0002-6226-869X surname: Ding fullname: Ding, Qiang organization: Center for Infectious Disease Research, School of Medicine, Tsinghua University, Beijing, China |
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| Cites_doi | 10.1042/CS20060020 10.1038/nm0397-252 10.1007/s00109-005-0718-5 10.1056/NEJMoa1211721 10.1038/s41586-020-2008-3 10.1371/journal.ppat.1009392 10.1038/s41586-020-2179-y 10.1073/pnas.2025373118 10.1016/S0140-6736(05)62411-7 10.1038/s41586-020-2012-7 10.1038/nature02145 10.1016/j.cell.2020.03.045 10.1186/s12933-018-0771-3 10.1038/nm1196-1240 10.1038/s41579-018-0118-9 10.1056/NEJMoa2020283 10.1007/s00439-008-0524-6 10.1073/pnas.0908837106 10.1073/pnas.0409465102 10.1038/s41598-020-73820-8 10.1016/j.chom.2021.02.017 10.1073/pnas.2002589117 10.1146/annurev.mi.44.100190.001511 10.1063/1.2408420 10.1126/science.abd4570 10.1038/sj.jhh.1001107 10.1038/s41586-020-2818-3 10.1038/s41579-020-00459-7 10.1016/j.antiviral.2013.08.014 10.1016/j.cell.2020.06.011 10.1002/path.2162 10.1161/01.res.87.5.e1 10.1021/acs.jctc.9b00591 10.1038/s41440-018-0166-6 10.1186/s12944-018-0890-6 10.1093/nar/gkz383 10.1016/j.tim.2020.05.012 10.1038/s41431-020-0636-6 10.1128/JVI.02615-14 10.1016/S0140-6736(20)31748-7 10.1126/science.1116480 10.1126/science.abd4585 10.1146/annurev-micro-110520-023212 10.1007/s00439-020-02142-6 10.1016/j.cell.2020.05.016 10.1016/j.cell.2020.08.021 10.1099/jgv.0.001584 10.1146/annurev-micro-020518-115759 10.1002/(SICI)1096-987X(199709)18:12<1463::AID-JCC4>3.0.CO;2-H 10.1016/j.cell.2020.05.027 10.1063/1.448118 10.1056/NEJMoa030781 10.1002/jcc.20291 10.1038/s41586-020-2180-5 10.1016/j.cell.2020.02.052 10.1128/JVI.00442-08 |
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| License | All Rights Reserved. This article is made available via the PMC Open Access Subset for unrestricted noncommercial re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. https://doi.org/10.1128/ASMCopyrightv2 All Rights Reserved. This article is made available via the PMC Open Access Subset for unrestricted noncommercial re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic. |
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| Notes | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 Wenlin Ren, Yunkai Zhu, Jun Lan, and Hedi Chen contributed equally to this work. Author order was determined based on project leadership. |
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| References | e_1_3_2_26_2 e_1_3_2_49_2 e_1_3_2_28_2 e_1_3_2_41_2 e_1_3_2_20_2 e_1_3_2_43_2 e_1_3_2_22_2 e_1_3_2_45_2 e_1_3_2_24_2 e_1_3_2_47_2 e_1_3_2_9_2 e_1_3_2_16_2 e_1_3_2_37_2 e_1_3_2_7_2 e_1_3_2_18_2 e_1_3_2_39_2 e_1_3_2_54_2 e_1_3_2_10_2 e_1_3_2_31_2 e_1_3_2_52_2 e_1_3_2_5_2 e_1_3_2_12_2 e_1_3_2_33_2 e_1_3_2_3_2 e_1_3_2_14_2 e_1_3_2_35_2 e_1_3_2_56_2 e_1_3_2_50_2 e_1_3_2_27_2 e_1_3_2_48_2 e_1_3_2_29_2 e_1_3_2_40_2 e_1_3_2_21_2 e_1_3_2_42_2 e_1_3_2_23_2 e_1_3_2_44_2 e_1_3_2_25_2 e_1_3_2_46_2 e_1_3_2_15_2 e_1_3_2_38_2 e_1_3_2_8_2 e_1_3_2_17_2 e_1_3_2_6_2 e_1_3_2_19_2 e_1_3_2_30_2 e_1_3_2_53_2 e_1_3_2_32_2 e_1_3_2_51_2 e_1_3_2_11_2 e_1_3_2_34_2 e_1_3_2_57_2 e_1_3_2_4_2 e_1_3_2_13_2 e_1_3_2_36_2 e_1_3_2_55_2 e_1_3_2_2_2 Bastard, P, Rosen, LB, Zhang, Q, Michailidis, E, Hoffmann, HH, Zhang, Y, Dorgham, K, Philippot, Q, Rosain, J, Beziat, V, Manry, J, Shaw, E, Haljasmagi, L, Peterson, P, Lorenzo, L, Bizien, L, Trouillet-Assant, S, Dobbs, K, de Jesus, AA, Belot, A, Kallaste, A, Catherinot, E, Tandjaoui-Lambiotte, Y, Le Pen, J, Kerner, G, Bigio, B, Seeleuthner, Y, Yang, R, Bolze, A, Spaan, AN, Delmonte, OM, Abers, MS, Aiuti, A, Casari, G, Lampasona, V, Piemonti, L, Ciceri, F, Bilguvar, K, Lifton, RP, Vasse, M, Smadja, DM, Migaud, M, Hadjadj, J, Terrier, B, Duffy, D, Quintana-Murci, L, van de Beek, D, Roussel, L, Vinh, DC, Tangye, SG (B17) 2020; 370 Zaki, AM, van Boheemen, S, Bestebroer, TM, Osterhaus, AD, Fouchier, RA (B4) 2012; 367 Liu, C, Li, Y, Guan, T, Lai, Y, Shen, Y, Zeyaweiding, A, Zhao, H, Li, F, Maimaiti, T (B25) 2018; 17 Casanova, JL, Su, HC, Effort, CHG (B13) 2020; 181 Luo, Y, Liu, C, Guan, T, Li, Y, Lai, Y, Li, F, Zhao, H, Maimaiti, T, Zeyaweiding, A (B24) 2019; 42 Ellinghaus, D, Degenhardt, F, Bujanda, L, Buti, M, Albillos, A, Invernizzi, P, Fernandez, J, Prati, D, Baselli, G, Asselta, R, Grimsrud, MM, Milani, C, Aziz, F, Kassens, J, May, S, Wendorff, M, Wienbrandt, L, Uellendahl-Werth, F, Zheng, T, Yi, X, de Pablo, R, Chercoles, AG, Palom, A, Garcia-Fernandez, AE, Rodriguez-Frias, F, Zanella, A, Bandera, A, Protti, A, Aghemo, A, Lleo, A, Biondi, A, Caballero-Garralda, A, Gori, A, Tanck, A, Carreras Nolla, A, Latiano, A, Fracanzani, AL, Peschuck, A, Julia, A, Pesenti, A, Voza, A, Jimenez, D, Mateos, B, Jimenez, BN, Quereda, C, Paccapelo, C, Gassner, C, Angelini, C, Cea, C (B15) 2020; 383 Donoghue, M, Hsieh, F, Baronas, E, Godbout, K, Gosselin, M, Stagliano, N, Donovan, M, Woolf, B, Robison, K, Jeyaseelan, R, Breitbart, RE, Acton, S (B29) 2000; 87 Morens, DM, Fauci, AS (B5) 2020; 182 Hofmann, H, Pyrc, K, van der Hoek, L, Geier, M, Berkhout, B, Pohlmann, S (B22) 2005; 102 Ksiazek, TG, Erdman, D, Goldsmith, CS, Zaki, SR, Peret, T, Emery, S, Tong, S, Urbani, C, Comer, JA, Lim, W, Rollin, PE, Dowell, SF, Ling, AE, Humphrey, CD, Shieh, WJ, Guarner, J, Paddock, CD, Rota, P, Fields, B, DeRisi, J, Yang, JY, Cox, N, Hughes, JM, LeDuc, JW, Bellini, WJ, Anderson, LJ (B3) 2003; 348 Wang, YT, Landeras-Bueno, S, Hsieh, LE, Terada, Y, Kim, K, Ley, K, Shresta, S, Saphire, EO, Regla-Nava, JA (B8) 2020; 28 Kariuki, SN, Williams, TN (B12) 2020; 139 van der Merwe, L, Cloete, R, Revera, M, Heradien, M, Goosen, A, Corfield, VA, Brink, PA, Moolman-Smook, JC (B48) 2008; 124 Cui, J, Li, F, Shi, ZL (B6) 2019; 17 Li, F, Li, W, Farzan, M, Harrison, SC (B35) 2005; 309 Fung, TS, Liu, DX (B20) 2021; 75 Lieb, W, Graf, J, Gotz, A, Konig, IR, Mayer, B, Fischer, M, Stritzke, J, Hengstenberg, C, Holmer, SR, Doring, A, Lowel, H, Schunkert, H, Erdmann, J (B28) 2006; 84 Hu, B, Guo, H, Zhou, P, Shi, ZL (B23) 2021; 19 Wu, A, Wang, L, Zhou, HY, Ji, CY, Xia, SZ, Cao, Y, Meng, J, Ding, X, Gold, S, Jiang, T, Cheng, G (B51) 2021; 29 Berendsen, HJC, Postma, JPM, Gunsteren, WFv, DiNola, A, Haak, JR (B56) 1984; 81 Hess, B, Bekker, H, Berendsen, HJC, Fraaije, JGEM (B54) 1997; 18 Zhang, Q, Bastard, P, Liu, Z, Le Pen, J, Moncada-Velez, M, Chen, J, Ogishi, M, Sabli, IKD, Hodeib, S, Korol, C, Rosain, J, Bilguvar, K, Ye, J, Bolze, A, Bigio, B, Yang, R, Arias, AA, Zhou, Q, Zhang, Y, Onodi, F, Korniotis, S, Karpf, L, Philippot, Q, Chbihi, M, Bonnet-Madin, L, Dorgham, K, Smith, N, Schneider, WM, Razooky, BS, Hoffmann, HH, Michailidis, E, Moens, L, Han, JE, Lorenzo, L, Bizien, L, Meade, P, Neehus, AL, Ugurbil, AC, Corneau, A, Kerner, G, Zhang, P, Rapaport, F, Seeleuthner, Y, Manry, J, Masson, C, Schmitt, Y, Schluter, A, Le Voyer, T, Khan, T, Li, J (B18) 2020; 370 Yang, W, Huang, W, Su, S, Li, B, Zhao, W, Chen, S, Gu, D (B26) 2006; 111 Hassan, AO, Case, JB, Winkler, ES, Thackray, LB, Kafai, NM, Bailey, AL, McCune, BT, Fox, JM, Chen, RE, Alsoussi, WB, Turner, JS, Schmitz, AJ, Lei, T, Shrihari, S, Keeler, SP, Fremont, DH, Greco, S, McCray, PB, Perlman, S, Holtzman, MJ, Ellebedy, AH, Diamond, MS (B40) 2020; 182 Wu, F, Zhao, S, Yu, B, Chen, Y-M, Wang, W, Song, Z-G, Hu, Y, Tao, Z-W, Tian, J-H, Pei, Y-Y, Yuan, M-L, Zhang, Y-L, Dai, F-H, Liu, Y, Wang, Q-M, Zheng, J-J, Xu, L, Holmes, EC, Zhang, Y-Z (B7) 2020; 579 Lai, MM (B2) 1990; 44 Shang, J, Ye, G, Shi, K, Wan, Y, Luo, C, Aihara, H, Geng, Q, Auerbach, A, Li, F (B32) 2020; 581 Wu, K, Li, W, Peng, G, Li, F (B34) 2009; 106 Pan, Y, Wang, T, Li, Y, Guan, T, Lai, Y, Shen, Y, Zeyaweiding, A, Maimaiti, T, Li, F, Zhao, H, Liu, C (B47) 2018; 17 Liu, Y, Hu, G, Wang, Y, Ren, W, Zhao, X, Ji, F, Zhu, Y, Feng, F, Gong, M, Ju, X, Zhu, Y, Cai, X, Lan, J, Guo, J, Xie, M, Dong, L, Zhu, Z, Na, J, Wu, J, Lan, X, Xie, Y, Wang, X, Yuan, Z, Zhang, R, Ding, Q (B38) 2021; 118 Li, W, Moore, MJ, Vasilieva, N, Sui, J, Wong, SK, Berne, MA, Somasundaran, M, Sullivan, JL, Luzuriaga, K, Greenough, TC, Choe, H, Farzan, M (B21) 2003; 426 Hamming, I, Cooper, ME, Haagmans, BL, Hooper, NM, Korstanje, R, Osterhaus, AD, Timens, W, Turner, AJ, Navis, G, van Goor, H (B27) 2007; 212 Li, F (B45) 2013; 100 Fung, TS, Liu, DX (B1) 2019; 73 Huang, Y, Paxton, WA, Wolinsky, SM, Neumann, AU, Zhang, L, He, T, Kang, S, Ceradini, D, Jin, Z, Yazdanbakhsh, K, Kunstman, K, Erickson, D, Dragon, E, Landau, NR, Phair, J, Ho, DD, Koup, RA (B11) 1996; 2 Van Der Spoel, D, Lindahl, E, Hess, B, Groenhof, G, Mark, AE, Berendsen, HJ (B52) 2005; 26 Zhou, P, Yang, XL, Wang, XG, Hu, B, Zhang, L, Zhang, W, Si, HR, Zhu, Y, Li, B, Huang, CL, Chen, HD, Chen, J, Luo, Y, Guo, H, Jiang, RD, Liu, MQ, Chen, Y, Shen, XR, Wang, X, Zheng, XS, Zhao, K, Chen, QJ, Deng, F, Liu, LL, Yan, B, Zhan, FX, Wang, YY, Xiao, GF, Shi, ZL (B19) 2020; 579 Initiative, C-HG (B14) 2020; 28 Bhopal, SS, Bhopal, R (B42) 2020; 396 Frossard, PM, Malloy, MJ, Lestringant, GG, Kane, JP (B30) 2001; 15 Theodorou, I, Meyer, L, Magierowska, M, Katlama, C, Rouzioux, C (B10) 1997; 349 Peacock, TP, Penrice-Randal, R, Hiscox, JA, Barclay, WS (B50) 2021; 102 Ren, W, Zhu, Y, Wang, Y, Shi, H, Yu, Y, Hu, G, Feng, F, Zhao, X, Lan, J, Wu, J, Kenney, DJ, Douam, F, Tong, Y, Zhong, J, Xie, Y, Wang, X, Yuan, Z, Zhou, D, Zhang, R, Ding, Q (B39) 2021; 17 Tian, C, Kasavajhala, K, Belfon, KAA, Raguette, L, Huang, H, Migues, AN, Bickel, J, Wang, Y, Pincay, J, Wu, Q, Simmerling, C (B53) 2020; 16 Rodrigues, CHM, Myung, Y, Pires, DEV, Ascher, DB (B36) 2019; 47 Zeberg, H, Paabo, S (B16) 2020; 587 Jiang, RD, Liu, MQ, Chen, Y, Shan, C, Zhou, YW, Shen, XR, Li, Q, Zhang, L, Zhu, Y, Si, HR, Wang, Q, Min, J, Wang, X, Zhang, W, Li, B, Zhang, HJ, Baric, RS, Zhou, P, Yang, XL, Shi, ZL (B41) 2020; 182 Li, F (B46) 2015; 89 Bussi, G, Donadio, D, Parrinello, M (B55) 2007; 126 Wang, Q, Zhang, Y, Wu, L, Niu, S, Song, C, Zhang, Z, Lu, G, Qiao, C, Hu, Y, Yuen, K-Y, Wang, Q, Zhou, H, Yan, J, Qi, J (B33) 2020; 181 Matsuyama, S, Nao, N, Shirato, K, Kawase, M, Saito, S, Takayama, I, Nagata, N, Sekizuka, T, Katoh, H, Kato, F, Sakata, M, Tahara, M, Kutsuna, S, Ohmagari, N, Kuroda, M, Suzuki, T, Kageyama, T, Takeda, M (B49) 2020; 117 Lan, J, Ge, J, Yu, J, Shan, S, Zhou, H, Fan, S, Zhang, Q, Shi, X, Wang, Q, Zhang, L, Wang, X (B31) 2020; 581 Li, F (B44) 2008; 82 Hoffmann, M, Kleine-Weber, H, Schroeder, S, Kruger, N, Herrler, T, Erichsen, S, Schiergens, TS, Herrler, G, Wu, NH, Nitsche, A, Muller, MA, Drosten, C, Pohlmann, S (B43) 2020; 181 Lim, H, Baek, A, Kim, J, Kim, MS, Liu, J, Nam, KY, Yoon, J, No, KT (B37) 2020; 10 Biti, R, Ffrench, R, Young, J, Bennetts, B, Stewart, G, Liang, T (B9) 1997; 3 |
| References_xml | – ident: e_1_3_2_27_2 doi: 10.1042/CS20060020 – ident: e_1_3_2_10_2 doi: 10.1038/nm0397-252 – ident: e_1_3_2_29_2 doi: 10.1007/s00109-005-0718-5 – ident: e_1_3_2_5_2 doi: 10.1056/NEJMoa1211721 – ident: e_1_3_2_8_2 doi: 10.1038/s41586-020-2008-3 – ident: e_1_3_2_40_2 doi: 10.1371/journal.ppat.1009392 – ident: e_1_3_2_33_2 doi: 10.1038/s41586-020-2179-y – ident: e_1_3_2_39_2 doi: 10.1073/pnas.2025373118 – ident: e_1_3_2_11_2 doi: 10.1016/S0140-6736(05)62411-7 – ident: e_1_3_2_20_2 doi: 10.1038/s41586-020-2012-7 – ident: e_1_3_2_22_2 doi: 10.1038/nature02145 – ident: e_1_3_2_34_2 doi: 10.1016/j.cell.2020.03.045 – ident: e_1_3_2_26_2 doi: 10.1186/s12933-018-0771-3 – ident: e_1_3_2_12_2 doi: 10.1038/nm1196-1240 – ident: e_1_3_2_7_2 doi: 10.1038/s41579-018-0118-9 – ident: e_1_3_2_16_2 doi: 10.1056/NEJMoa2020283 – ident: e_1_3_2_49_2 doi: 10.1007/s00439-008-0524-6 – ident: e_1_3_2_35_2 doi: 10.1073/pnas.0908837106 – ident: e_1_3_2_23_2 doi: 10.1073/pnas.0409465102 – ident: e_1_3_2_38_2 doi: 10.1038/s41598-020-73820-8 – ident: e_1_3_2_52_2 doi: 10.1016/j.chom.2021.02.017 – ident: e_1_3_2_50_2 doi: 10.1073/pnas.2002589117 – ident: e_1_3_2_3_2 doi: 10.1146/annurev.mi.44.100190.001511 – ident: e_1_3_2_56_2 doi: 10.1063/1.2408420 – ident: e_1_3_2_19_2 doi: 10.1126/science.abd4570 – ident: e_1_3_2_31_2 doi: 10.1038/sj.jhh.1001107 – ident: e_1_3_2_17_2 doi: 10.1038/s41586-020-2818-3 – ident: e_1_3_2_24_2 doi: 10.1038/s41579-020-00459-7 – ident: e_1_3_2_46_2 doi: 10.1016/j.antiviral.2013.08.014 – ident: e_1_3_2_41_2 doi: 10.1016/j.cell.2020.06.011 – ident: e_1_3_2_28_2 doi: 10.1002/path.2162 – ident: e_1_3_2_30_2 doi: 10.1161/01.res.87.5.e1 – ident: e_1_3_2_54_2 doi: 10.1021/acs.jctc.9b00591 – ident: e_1_3_2_25_2 doi: 10.1038/s41440-018-0166-6 – ident: e_1_3_2_48_2 doi: 10.1186/s12944-018-0890-6 – ident: e_1_3_2_37_2 doi: 10.1093/nar/gkz383 – ident: e_1_3_2_9_2 doi: 10.1016/j.tim.2020.05.012 – ident: e_1_3_2_15_2 doi: 10.1038/s41431-020-0636-6 – ident: e_1_3_2_47_2 doi: 10.1128/JVI.02615-14 – ident: e_1_3_2_43_2 doi: 10.1016/S0140-6736(20)31748-7 – ident: e_1_3_2_36_2 doi: 10.1126/science.1116480 – ident: e_1_3_2_18_2 doi: 10.1126/science.abd4585 – ident: e_1_3_2_21_2 doi: 10.1146/annurev-micro-110520-023212 – ident: e_1_3_2_13_2 doi: 10.1007/s00439-020-02142-6 – ident: e_1_3_2_14_2 doi: 10.1016/j.cell.2020.05.016 – ident: e_1_3_2_6_2 doi: 10.1016/j.cell.2020.08.021 – ident: e_1_3_2_51_2 doi: 10.1099/jgv.0.001584 – ident: e_1_3_2_2_2 doi: 10.1146/annurev-micro-020518-115759 – ident: e_1_3_2_55_2 doi: 10.1002/(SICI)1096-987X(199709)18:12<1463::AID-JCC4>3.0.CO;2-H – ident: e_1_3_2_42_2 doi: 10.1016/j.cell.2020.05.027 – ident: e_1_3_2_57_2 doi: 10.1063/1.448118 – ident: e_1_3_2_4_2 doi: 10.1056/NEJMoa030781 – ident: e_1_3_2_53_2 doi: 10.1002/jcc.20291 – ident: e_1_3_2_32_2 doi: 10.1038/s41586-020-2180-5 – ident: e_1_3_2_44_2 doi: 10.1016/j.cell.2020.02.052 – ident: e_1_3_2_45_2 doi: 10.1128/JVI.00442-08 – volume: 29 start-page: 503 year: 2021 end-page: 507 ident: B51 article-title: One year of SARS-CoV-2 evolution publication-title: Cell Host Microbe doi: 10.1016/j.chom.2021.02.017 – volume: 44 start-page: 303 year: 1990 end-page: 333 ident: B2 article-title: Coronavirus: organization, replication and expression of genome publication-title: Annu Rev Microbiol doi: 10.1146/annurev.mi.44.100190.001511 – volume: 348 start-page: 1953 year: 2003 end-page: 1966 ident: B3 article-title: A novel coronavirus associated with severe acute respiratory syndrome publication-title: N Engl J Med doi: 10.1056/NEJMoa030781 – volume: 367 start-page: 1814 year: 2012 end-page: 1820 ident: B4 article-title: Isolation of a novel coronavirus from a man with pneumonia in Saudi Arabia publication-title: N Engl J Med doi: 10.1056/NEJMoa1211721 – volume: 212 start-page: 1 year: 2007 end-page: 11 ident: B27 article-title: The emerging role of ACE2 in physiology and disease publication-title: J Pathol doi: 10.1002/path.2162 – volume: 84 start-page: 88 year: 2006 end-page: 96 ident: B28 article-title: Association of angiotensin-converting enzyme 2 (ACE2) gene polymorphisms with parameters of left ventricular hypertrophy in men. Results of the MONICA Augsburg echocardiographic substudy publication-title: J Mol Med (Berl) doi: 10.1007/s00109-005-0718-5 – volume: 18 start-page: 1463 year: 1997 end-page: 1472 ident: B54 article-title: LINCS: a linear constraint solver for molecular simulations publication-title: J Comput Chem doi: 10.1002/(SICI)1096-987X(199709)18:12<1463::AID-JCC4>3.0.CO;2-H – volume: 182 start-page: 1077 year: 2020 end-page: 1092 ident: B5 article-title: Emerging pandemic diseases: how we got to COVID-19 publication-title: Cell doi: 10.1016/j.cell.2020.08.021 – volume: 181 start-page: 271 year: 2020 end-page: 280.e8 ident: B43 article-title: SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor publication-title: Cell doi: 10.1016/j.cell.2020.02.052 – volume: 117 start-page: 7001 year: 2020 end-page: 7003 ident: B49 article-title: Enhanced isolation of SARS-CoV-2 by TMPRSS2-expressing cells publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.2002589117 – volume: 182 start-page: 744 year: 2020 end-page: 753.e4 ident: B40 article-title: A SARS-CoV-2 infection model in mice demonstrates protection by neutralizing antibodies publication-title: Cell doi: 10.1016/j.cell.2020.06.011 – volume: 426 start-page: 450 year: 2003 end-page: 454 ident: B21 article-title: Angiotensin-converting enzyme 2 is a functional receptor for the SARS coronavirus publication-title: Nature doi: 10.1038/nature02145 – volume: 100 start-page: 246 year: 2013 end-page: 254 ident: B45 article-title: Receptor recognition and cross-species infections of SARS coronavirus publication-title: Antiviral Res doi: 10.1016/j.antiviral.2013.08.014 – volume: 118 year: 2021 ident: B38 article-title: Functional and genetic analysis of viral receptor ACE2 orthologs reveals a broad potential host range of SARS-CoV-2 publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.2025373118 – volume: 81 start-page: 3684 year: 1984 end-page: 3690 ident: B56 article-title: Molecular dynamics with coupling to an external bath publication-title: J Chem Phys doi: 10.1063/1.448118 – volume: 579 start-page: 265 year: 2020 end-page: 269 ident: B7 article-title: A new coronavirus associated with human respiratory disease in China publication-title: Nature doi: 10.1038/s41586-020-2008-3 – volume: 102 start-page: 001584 year: 2021 ident: B50 article-title: SARS-CoV-2 one year on: evidence for ongoing viral adaptation publication-title: J Gen Virol doi: 10.1099/jgv.0.001584 – volume: 16 start-page: 528 year: 2020 end-page: 552 ident: B53 article-title: ff19SB: amino-acid-specific protein backbone parameters trained against quantum mechanics energy surfaces in solution publication-title: J Chem Theory Comput doi: 10.1021/acs.jctc.9b00591 – volume: 370 year: 2020 ident: B18 article-title: Inborn errors of type I IFN immunity in patients with life-threatening COVID-19 publication-title: Science doi: 10.1126/science.abd4570 – volume: 3 start-page: 252 year: 1997 end-page: 253 ident: B9 article-title: HIV-1 infection in an individual homozygous for the CCR5 deletion allele publication-title: Nat Med doi: 10.1038/nm0397-252 – volume: 581 start-page: 215 year: 2020 end-page: 220 ident: B31 article-title: Structure of the SARS-CoV-2 spike receptor-binding domain bound to the ACE2 receptor publication-title: Nature doi: 10.1038/s41586-020-2180-5 – volume: 10 start-page: 16862 year: 2020 ident: B37 article-title: Hot spot profiles of SARS-CoV-2 and human ACE2 receptor protein interaction obtained by density functional tight binding fragment molecular orbital method publication-title: Sci Rep doi: 10.1038/s41598-020-73820-8 – volume: 111 start-page: 333 year: 2006 end-page: 340 ident: B26 article-title: Association study of ACE2 (angiotensin I-converting enzyme 2) gene polymorphisms with coronary heart disease and myocardial infarction in a Chinese Han population publication-title: Clin Sci (Lond) doi: 10.1042/CS20060020 – volume: 17 start-page: 181 year: 2019 end-page: 192 ident: B6 article-title: Origin and evolution of pathogenic coronaviruses publication-title: Nat Rev Microbiol doi: 10.1038/s41579-018-0118-9 – volume: 370 year: 2020 ident: B17 article-title: Autoantibodies against type I IFNs in patients with life-threatening COVID-19 publication-title: Science doi: 10.1126/science.abd4585 – volume: 87 start-page: e1 year: 2000 end-page: e9 ident: B29 article-title: A novel angiotensin-converting enzyme-related carboxypeptidase (ACE2) converts angiotensin I to angiotensin 1–9 publication-title: Circ Res doi: 10.1161/01.res.87.5.e1 – volume: 17 year: 2021 ident: B39 article-title: Comparative analysis reveals the species-specific genetic determinants of ACE2 required for SARS-CoV-2 entry publication-title: PLoS Pathog doi: 10.1371/journal.ppat.1009392 – volume: 124 start-page: 57 year: 2008 end-page: 61 ident: B48 article-title: Genetic variation in angiotensin-converting enzyme 2 gene is associated with extent of left ventricular hypertrophy in hypertrophic cardiomyopathy publication-title: Hum Genet doi: 10.1007/s00439-008-0524-6 – volume: 28 start-page: 605 year: 2020 end-page: 618 ident: B8 article-title: Spiking pandemic potential: structural and immunological aspects of SARS-CoV-2 publication-title: Trends Microbiol doi: 10.1016/j.tim.2020.05.012 – volume: 89 start-page: 1954 year: 2015 end-page: 1964 ident: B46 article-title: Receptor recognition mechanisms of coronaviruses: a decade of structural studies publication-title: J Virol doi: 10.1128/JVI.02615-14 – volume: 75 start-page: 19 year: 2021 end-page: 47 ident: B20 article-title: Similarities and dissimilarities of COVID-19 and other coronavirus diseases publication-title: Annu Rev Microbiol doi: 10.1146/annurev-micro-110520-023212 – volume: 309 start-page: 1864 year: 2005 end-page: 1868 ident: B35 article-title: Structure of SARS coronavirus spike receptor-binding domain complexed with receptor publication-title: Science doi: 10.1126/science.1116480 – volume: 102 start-page: 7988 year: 2005 end-page: 7993 ident: B22 article-title: Human coronavirus NL63 employs the severe acute respiratory syndrome coronavirus receptor for cellular entry publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0409465102 – volume: 383 start-page: 1522 year: 2020 end-page: 1534 ident: B15 article-title: Genomewide association study of severe covid-19 with respiratory failure publication-title: N Engl J Med doi: 10.1056/NEJMoa2020283 – volume: 82 start-page: 6984 year: 2008 end-page: 6991 ident: B44 article-title: Structural analysis of major species barriers between humans and palm civets for severe acute respiratory syndrome coronavirus infections publication-title: J Virol doi: 10.1128/JVI.00442-08 – volume: 349 start-page: 1219 year: 1997 end-page: 1220 ident: B10 article-title: HIV-1 infection in an individual homozygous for CCR5 delta 32 publication-title: Lancet doi: 10.1016/S0140-6736(05)62411-7 – volume: 17 start-page: 127 year: 2018 ident: B25 article-title: ACE2 polymorphisms associated with cardiovascular risk in Uygurs with type 2 diabetes mellitus publication-title: Cardiovasc Diabetol doi: 10.1186/s12933-018-0771-3 – volume: 28 start-page: 715 year: 2020 end-page: 718 ident: B14 article-title: The COVID-19 Host Genetics Initiative, a global initiative to elucidate the role of host genetic factors in susceptibility and severity of the SARS-CoV-2 virus pandemic publication-title: Eur J Hum Genet doi: 10.1038/s41431-020-0636-6 – volume: 73 start-page: 529 year: 2019 end-page: 557 ident: B1 article-title: Human coronavirus: host-pathogen interaction publication-title: Annu Rev Microbiol doi: 10.1146/annurev-micro-020518-115759 – volume: 581 start-page: 221 year: 2020 end-page: 224 ident: B32 article-title: Structural basis of receptor recognition by SARS-CoV-2 publication-title: Nature doi: 10.1038/s41586-020-2179-y – volume: 396 start-page: 532 year: 2020 end-page: 533 ident: B42 article-title: Sex differential in COVID-19 mortality varies markedly by age publication-title: Lancet doi: 10.1016/S0140-6736(20)31748-7 – volume: 579 start-page: 270 year: 2020 end-page: 273 ident: B19 article-title: A pneumonia outbreak associated with a new coronavirus of probable bat origin publication-title: Nature doi: 10.1038/s41586-020-2012-7 – volume: 19 start-page: 141 year: 2021 end-page: 154 ident: B23 article-title: Characteristics of SARS-CoV-2 and COVID-19 publication-title: Nat Rev Microbiol doi: 10.1038/s41579-020-00459-7 – volume: 42 start-page: 681 year: 2019 end-page: 689 ident: B24 article-title: Association of ACE2 genetic polymorphisms with hypertension-related target organ damages in south Xinjiang publication-title: Hypertens Res doi: 10.1038/s41440-018-0166-6 – volume: 126 start-page: 014101 year: 2007 ident: B55 article-title: Canonical sampling through velocity rescaling publication-title: J Chem Phys doi: 10.1063/1.2408420 – volume: 2 start-page: 1240 year: 1996 end-page: 1243 ident: B11 article-title: The role of a mutant CCR5 allele in HIV-1 transmission and disease progression publication-title: Nat Med doi: 10.1038/nm1196-1240 – volume: 181 start-page: 1194 year: 2020 end-page: 1199 ident: B13 article-title: A global effort to define the human genetics of protective immunity to SARS-CoV-2 infection publication-title: Cell doi: 10.1016/j.cell.2020.05.016 – volume: 106 start-page: 19970 year: 2009 end-page: 19974 ident: B34 article-title: Crystal structure of NL63 respiratory coronavirus receptor-binding domain complexed with its human receptor publication-title: Proc Natl Acad Sci USA doi: 10.1073/pnas.0908837106 – volume: 587 start-page: 610 year: 2020 end-page: 612 ident: B16 article-title: The major genetic risk factor for severe COVID-19 is inherited from Neanderthals publication-title: Nature doi: 10.1038/s41586-020-2818-3 – volume: 47 start-page: W338 year: 2019 end-page: W344 ident: B36 article-title: mCSM-PPI2: predicting the effects of mutations on protein-protein interactions publication-title: Nucleic Acids Res doi: 10.1093/nar/gkz383 – volume: 17 start-page: 241 year: 2018 ident: B47 article-title: Association of ACE2 polymorphisms with susceptibility to essential hypertension and dyslipidemia in Xinjiang, China publication-title: Lipids Health Dis doi: 10.1186/s12944-018-0890-6 – volume: 15 start-page: 49 year: 2001 end-page: 55 ident: B30 article-title: Haplotypes of the human renin gene associated with essential hypertension and stroke publication-title: J Hum Hypertens doi: 10.1038/sj.jhh.1001107 – volume: 181 start-page: 894 year: 2020 end-page: 904.e9 ident: B33 article-title: Structural and functional basis of SARS-CoV-2 entry by using human ACE2 publication-title: Cell doi: 10.1016/j.cell.2020.03.045 – volume: 139 start-page: 801 year: 2020 end-page: 811 ident: B12 article-title: Human genetics and malaria resistance publication-title: Hum Genet doi: 10.1007/s00439-020-02142-6 – volume: 26 start-page: 1701 year: 2005 end-page: 1718 ident: B52 article-title: GROMACS: fast, flexible, and free publication-title: J Comput Chem doi: 10.1002/jcc.20291 – volume: 182 start-page: 50 year: 2020 end-page: 58.e8 ident: B41 article-title: Pathogenesis of SARS-CoV-2 in transgenic mice expressing human angiotensin-converting enzyme 2 publication-title: Cell doi: 10.1016/j.cell.2020.05.027 |
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| Snippet | There is considerable variation in disease severity among patients infected with SARS-CoV-2, the virus that causes COVID-19. Human genetic variation can affect... The coronavirus disease 2019 (COVID-19) pandemic, caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2), has resulted in more than 235 million... |
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| SubjectTerms | Angiotensin-Converting Enzyme 2 - genetics Angiotensin-Converting Enzyme 2 - metabolism COVID-19 - genetics Genetic Predisposition to Disease - genetics Genetic Variation Humans Polymorphism, Single Nucleotide Protein Binding SARS-CoV-2 - metabolism SARS-CoV-2 - pathogenicity Spike Glycoprotein, Coronavirus - metabolism Virology Virus Internalization Virus-Cell Interactions |
| Title | Susceptibilities of Human ACE2 Genetic Variants in Coronavirus Infection |
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