Association of HLA genotypes, AB0 blood type and chemokine receptor 5 mutant CD195 with the clinical course of COVID-19
Background COVID-19, the pandemic disease caused by infection with SARS-CoV-2, may take highly variable clinical courses, ranging from symptom-free and pauci-symptomatic to fatal disease. The goal of the current study was to assess the association of COVID-19 clinical courses controlled by patients&...
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| Veröffentlicht in: | European journal of medical research 2021-09, Vol.26 (1), p.107-107, Article 107 |
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| creator | Fischer, Johannes C. Schmidt, Albrecht G. Boelke, Edwin Uhrberg, Markus Keitel, Verena Feldt, Torsten Jensen, Bjoern Haeussinger, Dieter Adams, Ortwin Schneider, E. Marion Balz, Vera Enczmann, Juergen Rox, Jutta Hermsen, Derik Schulze-Bosse, Karin Kindgen-Milles, Detlef Knoefel, Wolfram Trudo van Griensven, Martijn Haussmann, Jan Tamaskovics, Balint Plettenberg, Christian Scheckenbach, Kathrin Corradini, Stefanie Pedoto, Alessia Maas, Kitti Schmidt, Livia Grebe, Olaf Esposito, Irene Ehrhardt, Anja Peiper, Matthias Buhren, Bettina Alexandra Calles, Christian Stoehr, Andreas Lichtenberg, Artur Freise, Noemi F. Lutterbeck, Matthias Rezazadeh, Amir Budach, Wilfried Matuschek, Christiane |
| description | Background COVID-19, the pandemic disease caused by infection with SARS-CoV-2, may take highly variable clinical courses, ranging from symptom-free and pauci-symptomatic to fatal disease. The goal of the current study was to assess the association of COVID-19 clinical courses controlled by patients' adaptive immune responses without progression to severe disease with patients' Human Leukocyte Antigen (HLA) genetics, AB0 blood group antigens, and the presence or absence of near-loss-of-function delta 32 deletion mutant of the C-C chemokine receptor type 5 (CCR5). Patient and methods An exploratory observational study including 157 adult COVID-19 convalescent patients was performed with a median follow-up of 250 days. The impact of different HLA genotypes, AB0 blood group antigens, and the CCR5 mutant CD195 were investigated for their role in the clinical course of COVID-19. In addition, this study addressed levels of severity and morbidity of COVID-19. The association of the immunogenetic background parameters were further related to patients' humoral antiviral immune response patterns by longitudinal observation. Results Univariate HLA analyses identified putatively protective HLA alleles (HLA class II DRB1*01:01 and HLA class I B*35:01, with a trend for DRB1*03:01). They were associated with reduced durations of disease instead decreased (rather than increased) total anti-S IgG levels. They had a higher virus neutralizing capacity compared to non-carriers. Conversely, analyses also identified HLA alleles (HLA class II DQB1*03:02 und HLA class I B*15:01) not associated with such benefit in the patient cohort of this study. Hierarchical testing by Cox regression analyses confirmed the significance of the protective effect of the HLA alleles identified (when assessed in composite) in terms of disease duration, whereas AB0 blood group antigen heterozygosity was found to be significantly associated with disease severity (rather than duration) in our cohort. A suggestive association of a heterozygous CCR5 delta 32 mutation status with prolonged disease duration was implied by univariate analyses but could not be confirmed by hierarchical multivariate testing. Conclusion The current study shows that the presence of HLA class II DRB1*01:01 and HLA class I B*35:01 is of even stronger association with reduced disease duration in mild and moderate COVID-19 than age or any other potential risk factor assessed. Prospective studies in larger patient populations also in |
| doi_str_mv | 10.1186/s40001-021-00560-4 |
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Marion ; Balz, Vera ; Enczmann, Juergen ; Rox, Jutta ; Hermsen, Derik ; Schulze-Bosse, Karin ; Kindgen-Milles, Detlef ; Knoefel, Wolfram Trudo ; van Griensven, Martijn ; Haussmann, Jan ; Tamaskovics, Balint ; Plettenberg, Christian ; Scheckenbach, Kathrin ; Corradini, Stefanie ; Pedoto, Alessia ; Maas, Kitti ; Schmidt, Livia ; Grebe, Olaf ; Esposito, Irene ; Ehrhardt, Anja ; Peiper, Matthias ; Buhren, Bettina Alexandra ; Calles, Christian ; Stoehr, Andreas ; Lichtenberg, Artur ; Freise, Noemi F. ; Lutterbeck, Matthias ; Rezazadeh, Amir ; Budach, Wilfried ; Matuschek, Christiane</creator><creatorcontrib>Fischer, Johannes C. ; Schmidt, Albrecht G. ; Boelke, Edwin ; Uhrberg, Markus ; Keitel, Verena ; Feldt, Torsten ; Jensen, Bjoern ; Haeussinger, Dieter ; Adams, Ortwin ; Schneider, E. Marion ; Balz, Vera ; Enczmann, Juergen ; Rox, Jutta ; Hermsen, Derik ; Schulze-Bosse, Karin ; Kindgen-Milles, Detlef ; Knoefel, Wolfram Trudo ; van Griensven, Martijn ; Haussmann, Jan ; Tamaskovics, Balint ; Plettenberg, Christian ; Scheckenbach, Kathrin ; Corradini, Stefanie ; Pedoto, Alessia ; Maas, Kitti ; Schmidt, Livia ; Grebe, Olaf ; Esposito, Irene ; Ehrhardt, Anja ; Peiper, Matthias ; Buhren, Bettina Alexandra ; Calles, Christian ; Stoehr, Andreas ; Lichtenberg, Artur ; Freise, Noemi F. ; Lutterbeck, Matthias ; Rezazadeh, Amir ; Budach, Wilfried ; Matuschek, Christiane</creatorcontrib><description>Background COVID-19, the pandemic disease caused by infection with SARS-CoV-2, may take highly variable clinical courses, ranging from symptom-free and pauci-symptomatic to fatal disease. The goal of the current study was to assess the association of COVID-19 clinical courses controlled by patients' adaptive immune responses without progression to severe disease with patients' Human Leukocyte Antigen (HLA) genetics, AB0 blood group antigens, and the presence or absence of near-loss-of-function delta 32 deletion mutant of the C-C chemokine receptor type 5 (CCR5). Patient and methods An exploratory observational study including 157 adult COVID-19 convalescent patients was performed with a median follow-up of 250 days. The impact of different HLA genotypes, AB0 blood group antigens, and the CCR5 mutant CD195 were investigated for their role in the clinical course of COVID-19. In addition, this study addressed levels of severity and morbidity of COVID-19. The association of the immunogenetic background parameters were further related to patients' humoral antiviral immune response patterns by longitudinal observation. Results Univariate HLA analyses identified putatively protective HLA alleles (HLA class II DRB1*01:01 and HLA class I B*35:01, with a trend for DRB1*03:01). They were associated with reduced durations of disease instead decreased (rather than increased) total anti-S IgG levels. They had a higher virus neutralizing capacity compared to non-carriers. Conversely, analyses also identified HLA alleles (HLA class II DQB1*03:02 und HLA class I B*15:01) not associated with such benefit in the patient cohort of this study. Hierarchical testing by Cox regression analyses confirmed the significance of the protective effect of the HLA alleles identified (when assessed in composite) in terms of disease duration, whereas AB0 blood group antigen heterozygosity was found to be significantly associated with disease severity (rather than duration) in our cohort. A suggestive association of a heterozygous CCR5 delta 32 mutation status with prolonged disease duration was implied by univariate analyses but could not be confirmed by hierarchical multivariate testing. Conclusion The current study shows that the presence of HLA class II DRB1*01:01 and HLA class I B*35:01 is of even stronger association with reduced disease duration in mild and moderate COVID-19 than age or any other potential risk factor assessed. Prospective studies in larger patient populations also including novel SARS-CoV-2 variants will be required to assess the impact of HLA genetics on the capacity of mounting protective vaccination responses in the future.</description><identifier>ISSN: 0949-2321</identifier><identifier>ISSN: 2047-783X</identifier><identifier>EISSN: 2047-783X</identifier><identifier>DOI: 10.1186/s40001-021-00560-4</identifier><identifier>PMID: 34530915</identifier><language>eng</language><publisher>LONDON: Springer Nature</publisher><subject>ABO blood group ; ABO Blood-Group System - genetics ; Adult ; Aged ; Antibodies ; Antigens ; Antiviral agents ; Bar codes ; Biotechnology industry ; Blood groups ; CCR5 ; Chemokine receptor ; Chemokines ; Coronaviruses ; COVID-19 ; COVID-19 - epidemiology ; COVID-19 - etiology ; COVID-19 - genetics ; Development and progression ; Disease ; Epidemics ; Female ; Genes ; Genetic aspects ; Genetic Predisposition to Disease ; Genotype ; Health aspects ; Histocompatibility antigens ; Histocompatibility Antigens Class I - genetics ; HLA Antigens - genetics ; HLA class I genotypes ; HLA histocompatibility antigens ; HLA-DRB1 Chains - genetics ; Humans ; Immune response ; Immunogenetics ; Immunoglobulin G - blood ; Infections ; Life Sciences & Biomedicine ; Male ; Medical research ; Medicine, Experimental ; Medicine, Research & Experimental ; Middle Aged ; Morbidity ; Mutation ; Neutralizing antibodies ; Plasma ; Receptors, CCR5 - genetics ; Research & Experimental Medicine ; Risk factors ; SARS-CoV-2 ; Science & Technology ; Severe acute respiratory syndrome coronavirus 2 ; Severity of Illness Index ; Software ; United States</subject><ispartof>European journal of medical research, 2021-09, Vol.26 (1), p.107-107, Article 107</ispartof><rights>2021. The Author(s).</rights><rights>COPYRIGHT 2021 BioMed Central Ltd.</rights><rights>2021. This work is licensed under http://creativecommons.org/licenses/by/4.0/ (the “License”). Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>The Author(s) 2021</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>13</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000696520000001</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c594t-aa296451c5a161576eefd820d24a0229b383cb4f040f9563ee532df80bd4de723</citedby><cites>FETCH-LOGICAL-c594t-aa296451c5a161576eefd820d24a0229b383cb4f040f9563ee532df80bd4de723</cites><orcidid>0000-0001-9112-1024 ; 0000-0002-2533-0167 ; 0000-0003-1383-7662 ; 0000-0003-1626-4855 ; 0000-0001-5104-9881 ; 0000-0002-0554-2402 ; 0000-0002-2079-1845</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8444184/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC8444184/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,729,782,786,866,887,2104,2116,27931,27932,39265,53798,53800</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/34530915$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Fischer, Johannes C.</creatorcontrib><creatorcontrib>Schmidt, Albrecht G.</creatorcontrib><creatorcontrib>Boelke, Edwin</creatorcontrib><creatorcontrib>Uhrberg, Markus</creatorcontrib><creatorcontrib>Keitel, Verena</creatorcontrib><creatorcontrib>Feldt, Torsten</creatorcontrib><creatorcontrib>Jensen, Bjoern</creatorcontrib><creatorcontrib>Haeussinger, Dieter</creatorcontrib><creatorcontrib>Adams, Ortwin</creatorcontrib><creatorcontrib>Schneider, E. Marion</creatorcontrib><creatorcontrib>Balz, Vera</creatorcontrib><creatorcontrib>Enczmann, Juergen</creatorcontrib><creatorcontrib>Rox, Jutta</creatorcontrib><creatorcontrib>Hermsen, Derik</creatorcontrib><creatorcontrib>Schulze-Bosse, Karin</creatorcontrib><creatorcontrib>Kindgen-Milles, Detlef</creatorcontrib><creatorcontrib>Knoefel, Wolfram Trudo</creatorcontrib><creatorcontrib>van Griensven, Martijn</creatorcontrib><creatorcontrib>Haussmann, Jan</creatorcontrib><creatorcontrib>Tamaskovics, Balint</creatorcontrib><creatorcontrib>Plettenberg, Christian</creatorcontrib><creatorcontrib>Scheckenbach, Kathrin</creatorcontrib><creatorcontrib>Corradini, Stefanie</creatorcontrib><creatorcontrib>Pedoto, Alessia</creatorcontrib><creatorcontrib>Maas, Kitti</creatorcontrib><creatorcontrib>Schmidt, Livia</creatorcontrib><creatorcontrib>Grebe, Olaf</creatorcontrib><creatorcontrib>Esposito, Irene</creatorcontrib><creatorcontrib>Ehrhardt, Anja</creatorcontrib><creatorcontrib>Peiper, Matthias</creatorcontrib><creatorcontrib>Buhren, Bettina Alexandra</creatorcontrib><creatorcontrib>Calles, Christian</creatorcontrib><creatorcontrib>Stoehr, Andreas</creatorcontrib><creatorcontrib>Lichtenberg, Artur</creatorcontrib><creatorcontrib>Freise, Noemi F.</creatorcontrib><creatorcontrib>Lutterbeck, Matthias</creatorcontrib><creatorcontrib>Rezazadeh, Amir</creatorcontrib><creatorcontrib>Budach, Wilfried</creatorcontrib><creatorcontrib>Matuschek, Christiane</creatorcontrib><title>Association of HLA genotypes, AB0 blood type and chemokine receptor 5 mutant CD195 with the clinical course of COVID-19</title><title>European journal of medical research</title><addtitle>EUR J MED RES</addtitle><addtitle>Eur J Med Res</addtitle><description>Background COVID-19, the pandemic disease caused by infection with SARS-CoV-2, may take highly variable clinical courses, ranging from symptom-free and pauci-symptomatic to fatal disease. The goal of the current study was to assess the association of COVID-19 clinical courses controlled by patients' adaptive immune responses without progression to severe disease with patients' Human Leukocyte Antigen (HLA) genetics, AB0 blood group antigens, and the presence or absence of near-loss-of-function delta 32 deletion mutant of the C-C chemokine receptor type 5 (CCR5). Patient and methods An exploratory observational study including 157 adult COVID-19 convalescent patients was performed with a median follow-up of 250 days. The impact of different HLA genotypes, AB0 blood group antigens, and the CCR5 mutant CD195 were investigated for their role in the clinical course of COVID-19. In addition, this study addressed levels of severity and morbidity of COVID-19. The association of the immunogenetic background parameters were further related to patients' humoral antiviral immune response patterns by longitudinal observation. Results Univariate HLA analyses identified putatively protective HLA alleles (HLA class II DRB1*01:01 and HLA class I B*35:01, with a trend for DRB1*03:01). They were associated with reduced durations of disease instead decreased (rather than increased) total anti-S IgG levels. They had a higher virus neutralizing capacity compared to non-carriers. Conversely, analyses also identified HLA alleles (HLA class II DQB1*03:02 und HLA class I B*15:01) not associated with such benefit in the patient cohort of this study. Hierarchical testing by Cox regression analyses confirmed the significance of the protective effect of the HLA alleles identified (when assessed in composite) in terms of disease duration, whereas AB0 blood group antigen heterozygosity was found to be significantly associated with disease severity (rather than duration) in our cohort. A suggestive association of a heterozygous CCR5 delta 32 mutation status with prolonged disease duration was implied by univariate analyses but could not be confirmed by hierarchical multivariate testing. Conclusion The current study shows that the presence of HLA class II DRB1*01:01 and HLA class I B*35:01 is of even stronger association with reduced disease duration in mild and moderate COVID-19 than age or any other potential risk factor assessed. Prospective studies in larger patient populations also including novel SARS-CoV-2 variants will be required to assess the impact of HLA genetics on the capacity of mounting protective vaccination responses in the future.</description><subject>ABO blood group</subject><subject>ABO Blood-Group System - genetics</subject><subject>Adult</subject><subject>Aged</subject><subject>Antibodies</subject><subject>Antigens</subject><subject>Antiviral agents</subject><subject>Bar codes</subject><subject>Biotechnology industry</subject><subject>Blood groups</subject><subject>CCR5</subject><subject>Chemokine receptor</subject><subject>Chemokines</subject><subject>Coronaviruses</subject><subject>COVID-19</subject><subject>COVID-19 - epidemiology</subject><subject>COVID-19 - etiology</subject><subject>COVID-19 - genetics</subject><subject>Development and progression</subject><subject>Disease</subject><subject>Epidemics</subject><subject>Female</subject><subject>Genes</subject><subject>Genetic aspects</subject><subject>Genetic Predisposition to Disease</subject><subject>Genotype</subject><subject>Health aspects</subject><subject>Histocompatibility antigens</subject><subject>Histocompatibility Antigens Class I - genetics</subject><subject>HLA Antigens - genetics</subject><subject>HLA class I genotypes</subject><subject>HLA histocompatibility antigens</subject><subject>HLA-DRB1 Chains - genetics</subject><subject>Humans</subject><subject>Immune response</subject><subject>Immunogenetics</subject><subject>Immunoglobulin G - blood</subject><subject>Infections</subject><subject>Life Sciences & Biomedicine</subject><subject>Male</subject><subject>Medical research</subject><subject>Medicine, Experimental</subject><subject>Medicine, Research & Experimental</subject><subject>Middle Aged</subject><subject>Morbidity</subject><subject>Mutation</subject><subject>Neutralizing antibodies</subject><subject>Plasma</subject><subject>Receptors, CCR5 - genetics</subject><subject>Research & Experimental Medicine</subject><subject>Risk factors</subject><subject>SARS-CoV-2</subject><subject>Science & Technology</subject><subject>Severe acute respiratory syndrome coronavirus 2</subject><subject>Severity of Illness Index</subject><subject>Software</subject><subject>United States</subject><issn>0949-2321</issn><issn>2047-783X</issn><issn>2047-783X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2021</creationdate><recordtype>article</recordtype><sourceid>HGBXW</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>DOA</sourceid><recordid>eNqNkl-L1DAUxYso7rLuF_BBAoII2jX_27wI46y6Awv7ouJbSNPbmYydZGxSh_32pjPrsiM-mBAKt79zbnN7iuI5wReE1PJd5BhjUmKaDxYSl_xRcUoxr8qqZt8fF6dYcVVSRslJcR7jOtNYUlkp9bQ4YVwwrIg4LXazGIN1JrngUejQ1fUMLcGHdLuF-BbNPmDU9CG0aCog41tkV7AJP5wHNICFbQoDEmgzJuMTml8SJdDOpRVKK0C2d95Z0yMbxiHC5D-_-ba4LIl6VjzpTB_h_O55Vnz99PHL_Kq8vvm8mM-uSysUT6UxVEkuiBWGSCIqCdC1NcUt5QZTqhpWM9vwDnPcKSEZgGC07WrctLyFirKzYnHwbYNZ6-3gNma41cE4vS-EYanNkJztQbMGi6aVpmINcFbLplK8E0zR3JVajLPX-4PXdmw20FrwaTD9kenxG-9Wehl-6ZpzTmqeDV7fGQzh5wgx6Y2LFvreeAhj1FRUnOdfKKdeL_9C13mGPo9qT0mu6r3hHbU0-QLOdyH3tZOpnsmqzuFgnGXq4h9U3i1snA0eOpfrR4JXDwQrMH1axdCPU0jiMUgPoB1CjAN098MgWE8x1YeY6szrfUz19NEvHo7xXvInlBmoD8AOmtBF68BbuMemHCspKN4vMndpH955GH3K0jf_L2W_AdCG_go</recordid><startdate>20210916</startdate><enddate>20210916</enddate><creator>Fischer, Johannes C.</creator><creator>Schmidt, Albrecht G.</creator><creator>Boelke, Edwin</creator><creator>Uhrberg, Markus</creator><creator>Keitel, Verena</creator><creator>Feldt, Torsten</creator><creator>Jensen, Bjoern</creator><creator>Haeussinger, Dieter</creator><creator>Adams, Ortwin</creator><creator>Schneider, E. 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Marion ; Balz, Vera ; Enczmann, Juergen ; Rox, Jutta ; Hermsen, Derik ; Schulze-Bosse, Karin ; Kindgen-Milles, Detlef ; Knoefel, Wolfram Trudo ; van Griensven, Martijn ; Haussmann, Jan ; Tamaskovics, Balint ; Plettenberg, Christian ; Scheckenbach, Kathrin ; Corradini, Stefanie ; Pedoto, Alessia ; Maas, Kitti ; Schmidt, Livia ; Grebe, Olaf ; Esposito, Irene ; Ehrhardt, Anja ; Peiper, Matthias ; Buhren, Bettina Alexandra ; Calles, Christian ; Stoehr, Andreas ; Lichtenberg, Artur ; Freise, Noemi F. ; Lutterbeck, Matthias ; Rezazadeh, Amir ; Budach, Wilfried ; Matuschek, Christiane</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c594t-aa296451c5a161576eefd820d24a0229b383cb4f040f9563ee532df80bd4de723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2021</creationdate><topic>ABO blood group</topic><topic>ABO Blood-Group System - genetics</topic><topic>Adult</topic><topic>Aged</topic><topic>Antibodies</topic><topic>Antigens</topic><topic>Antiviral agents</topic><topic>Bar codes</topic><topic>Biotechnology industry</topic><topic>Blood groups</topic><topic>CCR5</topic><topic>Chemokine receptor</topic><topic>Chemokines</topic><topic>Coronaviruses</topic><topic>COVID-19</topic><topic>COVID-19 - epidemiology</topic><topic>COVID-19 - etiology</topic><topic>COVID-19 - genetics</topic><topic>Development and progression</topic><topic>Disease</topic><topic>Epidemics</topic><topic>Female</topic><topic>Genes</topic><topic>Genetic aspects</topic><topic>Genetic Predisposition to Disease</topic><topic>Genotype</topic><topic>Health aspects</topic><topic>Histocompatibility antigens</topic><topic>Histocompatibility Antigens Class I - genetics</topic><topic>HLA Antigens - genetics</topic><topic>HLA class I genotypes</topic><topic>HLA histocompatibility antigens</topic><topic>HLA-DRB1 Chains - genetics</topic><topic>Humans</topic><topic>Immune response</topic><topic>Immunogenetics</topic><topic>Immunoglobulin G - blood</topic><topic>Infections</topic><topic>Life Sciences & Biomedicine</topic><topic>Male</topic><topic>Medical research</topic><topic>Medicine, Experimental</topic><topic>Medicine, Research & Experimental</topic><topic>Middle Aged</topic><topic>Morbidity</topic><topic>Mutation</topic><topic>Neutralizing antibodies</topic><topic>Plasma</topic><topic>Receptors, CCR5 - genetics</topic><topic>Research & Experimental Medicine</topic><topic>Risk factors</topic><topic>SARS-CoV-2</topic><topic>Science & Technology</topic><topic>Severe acute respiratory syndrome coronavirus 2</topic><topic>Severity of Illness Index</topic><topic>Software</topic><topic>United States</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fischer, Johannes C.</creatorcontrib><creatorcontrib>Schmidt, Albrecht G.</creatorcontrib><creatorcontrib>Boelke, Edwin</creatorcontrib><creatorcontrib>Uhrberg, Markus</creatorcontrib><creatorcontrib>Keitel, Verena</creatorcontrib><creatorcontrib>Feldt, Torsten</creatorcontrib><creatorcontrib>Jensen, Bjoern</creatorcontrib><creatorcontrib>Haeussinger, Dieter</creatorcontrib><creatorcontrib>Adams, Ortwin</creatorcontrib><creatorcontrib>Schneider, E. Marion</creatorcontrib><creatorcontrib>Balz, Vera</creatorcontrib><creatorcontrib>Enczmann, Juergen</creatorcontrib><creatorcontrib>Rox, Jutta</creatorcontrib><creatorcontrib>Hermsen, Derik</creatorcontrib><creatorcontrib>Schulze-Bosse, Karin</creatorcontrib><creatorcontrib>Kindgen-Milles, Detlef</creatorcontrib><creatorcontrib>Knoefel, Wolfram Trudo</creatorcontrib><creatorcontrib>van Griensven, Martijn</creatorcontrib><creatorcontrib>Haussmann, Jan</creatorcontrib><creatorcontrib>Tamaskovics, Balint</creatorcontrib><creatorcontrib>Plettenberg, Christian</creatorcontrib><creatorcontrib>Scheckenbach, Kathrin</creatorcontrib><creatorcontrib>Corradini, Stefanie</creatorcontrib><creatorcontrib>Pedoto, Alessia</creatorcontrib><creatorcontrib>Maas, Kitti</creatorcontrib><creatorcontrib>Schmidt, Livia</creatorcontrib><creatorcontrib>Grebe, Olaf</creatorcontrib><creatorcontrib>Esposito, Irene</creatorcontrib><creatorcontrib>Ehrhardt, Anja</creatorcontrib><creatorcontrib>Peiper, Matthias</creatorcontrib><creatorcontrib>Buhren, Bettina Alexandra</creatorcontrib><creatorcontrib>Calles, Christian</creatorcontrib><creatorcontrib>Stoehr, Andreas</creatorcontrib><creatorcontrib>Lichtenberg, Artur</creatorcontrib><creatorcontrib>Freise, Noemi F.</creatorcontrib><creatorcontrib>Lutterbeck, Matthias</creatorcontrib><creatorcontrib>Rezazadeh, Amir</creatorcontrib><creatorcontrib>Budach, Wilfried</creatorcontrib><creatorcontrib>Matuschek, Christiane</creatorcontrib><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Web of Science - Science Citation Index Expanded - 2021</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Coronavirus Research Database</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Access via ProQuest (Open Access)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>European journal of medical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fischer, Johannes C.</au><au>Schmidt, Albrecht G.</au><au>Boelke, Edwin</au><au>Uhrberg, Markus</au><au>Keitel, Verena</au><au>Feldt, Torsten</au><au>Jensen, Bjoern</au><au>Haeussinger, Dieter</au><au>Adams, Ortwin</au><au>Schneider, E. Marion</au><au>Balz, Vera</au><au>Enczmann, Juergen</au><au>Rox, Jutta</au><au>Hermsen, Derik</au><au>Schulze-Bosse, Karin</au><au>Kindgen-Milles, Detlef</au><au>Knoefel, Wolfram Trudo</au><au>van Griensven, Martijn</au><au>Haussmann, Jan</au><au>Tamaskovics, Balint</au><au>Plettenberg, Christian</au><au>Scheckenbach, Kathrin</au><au>Corradini, Stefanie</au><au>Pedoto, Alessia</au><au>Maas, Kitti</au><au>Schmidt, Livia</au><au>Grebe, Olaf</au><au>Esposito, Irene</au><au>Ehrhardt, Anja</au><au>Peiper, Matthias</au><au>Buhren, Bettina Alexandra</au><au>Calles, Christian</au><au>Stoehr, Andreas</au><au>Lichtenberg, Artur</au><au>Freise, Noemi F.</au><au>Lutterbeck, Matthias</au><au>Rezazadeh, Amir</au><au>Budach, Wilfried</au><au>Matuschek, Christiane</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Association of HLA genotypes, AB0 blood type and chemokine receptor 5 mutant CD195 with the clinical course of COVID-19</atitle><jtitle>European journal of medical research</jtitle><stitle>EUR J MED RES</stitle><addtitle>Eur J Med Res</addtitle><date>2021-09-16</date><risdate>2021</risdate><volume>26</volume><issue>1</issue><spage>107</spage><epage>107</epage><pages>107-107</pages><artnum>107</artnum><issn>0949-2321</issn><issn>2047-783X</issn><eissn>2047-783X</eissn><abstract>Background COVID-19, the pandemic disease caused by infection with SARS-CoV-2, may take highly variable clinical courses, ranging from symptom-free and pauci-symptomatic to fatal disease. The goal of the current study was to assess the association of COVID-19 clinical courses controlled by patients' adaptive immune responses without progression to severe disease with patients' Human Leukocyte Antigen (HLA) genetics, AB0 blood group antigens, and the presence or absence of near-loss-of-function delta 32 deletion mutant of the C-C chemokine receptor type 5 (CCR5). Patient and methods An exploratory observational study including 157 adult COVID-19 convalescent patients was performed with a median follow-up of 250 days. The impact of different HLA genotypes, AB0 blood group antigens, and the CCR5 mutant CD195 were investigated for their role in the clinical course of COVID-19. In addition, this study addressed levels of severity and morbidity of COVID-19. The association of the immunogenetic background parameters were further related to patients' humoral antiviral immune response patterns by longitudinal observation. Results Univariate HLA analyses identified putatively protective HLA alleles (HLA class II DRB1*01:01 and HLA class I B*35:01, with a trend for DRB1*03:01). They were associated with reduced durations of disease instead decreased (rather than increased) total anti-S IgG levels. They had a higher virus neutralizing capacity compared to non-carriers. Conversely, analyses also identified HLA alleles (HLA class II DQB1*03:02 und HLA class I B*15:01) not associated with such benefit in the patient cohort of this study. Hierarchical testing by Cox regression analyses confirmed the significance of the protective effect of the HLA alleles identified (when assessed in composite) in terms of disease duration, whereas AB0 blood group antigen heterozygosity was found to be significantly associated with disease severity (rather than duration) in our cohort. A suggestive association of a heterozygous CCR5 delta 32 mutation status with prolonged disease duration was implied by univariate analyses but could not be confirmed by hierarchical multivariate testing. Conclusion The current study shows that the presence of HLA class II DRB1*01:01 and HLA class I B*35:01 is of even stronger association with reduced disease duration in mild and moderate COVID-19 than age or any other potential risk factor assessed. Prospective studies in larger patient populations also including novel SARS-CoV-2 variants will be required to assess the impact of HLA genetics on the capacity of mounting protective vaccination responses in the future.</abstract><cop>LONDON</cop><pub>Springer Nature</pub><pmid>34530915</pmid><doi>10.1186/s40001-021-00560-4</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-9112-1024</orcidid><orcidid>https://orcid.org/0000-0002-2533-0167</orcidid><orcidid>https://orcid.org/0000-0003-1383-7662</orcidid><orcidid>https://orcid.org/0000-0003-1626-4855</orcidid><orcidid>https://orcid.org/0000-0001-5104-9881</orcidid><orcidid>https://orcid.org/0000-0002-0554-2402</orcidid><orcidid>https://orcid.org/0000-0002-2079-1845</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | ABO blood group ABO Blood-Group System - genetics Adult Aged Antibodies Antigens Antiviral agents Bar codes Biotechnology industry Blood groups CCR5 Chemokine receptor Chemokines Coronaviruses COVID-19 COVID-19 - epidemiology COVID-19 - etiology COVID-19 - genetics Development and progression Disease Epidemics Female Genes Genetic aspects Genetic Predisposition to Disease Genotype Health aspects Histocompatibility antigens Histocompatibility Antigens Class I - genetics HLA Antigens - genetics HLA class I genotypes HLA histocompatibility antigens HLA-DRB1 Chains - genetics Humans Immune response Immunogenetics Immunoglobulin G - blood Infections Life Sciences & Biomedicine Male Medical research Medicine, Experimental Medicine, Research & Experimental Middle Aged Morbidity Mutation Neutralizing antibodies Plasma Receptors, CCR5 - genetics Research & Experimental Medicine Risk factors SARS-CoV-2 Science & Technology Severe acute respiratory syndrome coronavirus 2 Severity of Illness Index Software United States |
| title | Association of HLA genotypes, AB0 blood type and chemokine receptor 5 mutant CD195 with the clinical course of COVID-19 |
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