Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19

Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 sp...
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Autor*in:	Hocini, Hakim [verfasserIn] Wiedemann, Aurélie Blengio, Fabiola Lefebvre, Cécile Cervantes-Gonzalez, Minerva Foucat, Emile Tisserand, Pascaline Surenaud, Mathieu Coléon, Séverin Prague, Mélanie Guillaumat, Lydia Krief, Corinne Fenwick, Craig Laouénan, Cédric Bouadma, Lila Ghosn, Jade Pantaleo, Giuseppe Thiébaut, Rodolphe Lévy, Yves

Format:	E-Artikel
Sprache:	Englisch

Erschienen:	2023

Schlagwörter:	COVID-19 disease post-acute COVID-19 syndrome thrombosis

Anmerkung:	© The Author(s) 2023. corrected publication 2023

Übergeordnetes Werk:	Enthalten in: Journal of clinical immunology - Dordrecht [u.a.] : Springer Science + Business Media B.V, 1981, 43(2023), 5 vom: 21. März, Seite 882-893
Übergeordnetes Werk:	volume:43 ; year:2023 ; number:5 ; day:21 ; month:03 ; pages:882-893

Links:	Volltext

DOI / URN:	10.1007/s10875-023-01459-x

Katalog-ID:	SPR051924471

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520			\|a Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 spike-specific and neutralizing antibodies, and whole blood gene expression profiles in convalescent severe COVID-19 patients 1, 3, and 6 months following hospital discharge. Results We observed persistent abnormalities until month 6 marked by (i) high serum levels of monocyte/macrophage and endothelial activation markers, chemotaxis, and hematopoietic cytokines; (ii) a high frequency of central memory $ CD4^{+} $ and effector $ CD8^{+} $ T cells; (iii) a decrease in anti-SARS-CoV-2 spike and neutralizing antibodies; and (iv) an upregulation of genes related to platelet, neutrophil activation, erythrocytes, myeloid cell differentiation, and RUNX1 signaling. We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. Conclusion The lack of restoration of gene expression to a normal profile after up to 6 months of follow-up, even in asymptomatic patients who experienced severe COVID-19, signals the need to carefully extend their clinical follow-up and propose preventive measures.
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700	1		\|a Blengio, Fabiola \|4 aut
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700	1		\|a Cervantes-Gonzalez, Minerva \|4 aut
700	1		\|a Foucat, Emile \|4 aut
700	1		\|a Tisserand, Pascaline \|4 aut
700	1		\|a Surenaud, Mathieu \|4 aut
700	1		\|a Coléon, Séverin \|4 aut
700	1		\|a Prague, Mélanie \|4 aut
700	1		\|a Guillaumat, Lydia \|4 aut
700	1		\|a Krief, Corinne \|4 aut
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700	1		\|a Laouénan, Cédric \|4 aut
700	1		\|a Bouadma, Lila \|4 aut
700	1		\|a Ghosn, Jade \|4 aut
700	1		\|a Pantaleo, Giuseppe \|4 aut
700	1		\|a Thiébaut, Rodolphe \|4 aut
700	1		\|a Lévy, Yves \|0 (orcid)0000-0002-5549-6256 \|4 aut
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allfields	10.1007/s10875-023-01459-x doi (DE-627)SPR051924471 (SPR)s10875-023-01459-x-e DE-627 ger DE-627 rakwb eng Hocini, Hakim verfasserin aut Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 spike-specific and neutralizing antibodies, and whole blood gene expression profiles in convalescent severe COVID-19 patients 1, 3, and 6 months following hospital discharge. Results We observed persistent abnormalities until month 6 marked by (i) high serum levels of monocyte/macrophage and endothelial activation markers, chemotaxis, and hematopoietic cytokines; (ii) a high frequency of central memory $ CD4^{+} $ and effector $ CD8^{+} $ T cells; (iii) a decrease in anti-SARS-CoV-2 spike and neutralizing antibodies; and (iv) an upregulation of genes related to platelet, neutrophil activation, erythrocytes, myeloid cell differentiation, and RUNX1 signaling. We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. Conclusion The lack of restoration of gene expression to a normal profile after up to 6 months of follow-up, even in asymptomatic patients who experienced severe COVID-19, signals the need to carefully extend their clinical follow-up and propose preventive measures. COVID-19 disease (dpeaa)DE-He213 post-acute COVID-19 syndrome (dpeaa)DE-He213 thrombosis (dpeaa)DE-He213 Wiedemann, Aurélie aut Blengio, Fabiola aut Lefebvre, Cécile aut Cervantes-Gonzalez, Minerva aut Foucat, Emile aut Tisserand, Pascaline aut Surenaud, Mathieu aut Coléon, Séverin aut Prague, Mélanie aut Guillaumat, Lydia aut Krief, Corinne aut Fenwick, Craig aut Laouénan, Cédric aut Bouadma, Lila aut Ghosn, Jade aut Pantaleo, Giuseppe aut Thiébaut, Rodolphe aut Lévy, Yves (orcid)0000-0002-5549-6256 aut Enthalten in Journal of clinical immunology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1981 43(2023), 5 vom: 21. März, Seite 882-893 (DE-627)320573362 (DE-600)2016755-6 1573-2592 nnns volume:43 year:2023 number:5 day:21 month:03 pages:882-893 https://dx.doi.org/10.1007/s10875-023-01459-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2023 5 21 03 882-893
spelling	10.1007/s10875-023-01459-x doi (DE-627)SPR051924471 (SPR)s10875-023-01459-x-e DE-627 ger DE-627 rakwb eng Hocini, Hakim verfasserin aut Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 spike-specific and neutralizing antibodies, and whole blood gene expression profiles in convalescent severe COVID-19 patients 1, 3, and 6 months following hospital discharge. Results We observed persistent abnormalities until month 6 marked by (i) high serum levels of monocyte/macrophage and endothelial activation markers, chemotaxis, and hematopoietic cytokines; (ii) a high frequency of central memory $ CD4^{+} $ and effector $ CD8^{+} $ T cells; (iii) a decrease in anti-SARS-CoV-2 spike and neutralizing antibodies; and (iv) an upregulation of genes related to platelet, neutrophil activation, erythrocytes, myeloid cell differentiation, and RUNX1 signaling. We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. Conclusion The lack of restoration of gene expression to a normal profile after up to 6 months of follow-up, even in asymptomatic patients who experienced severe COVID-19, signals the need to carefully extend their clinical follow-up and propose preventive measures. COVID-19 disease (dpeaa)DE-He213 post-acute COVID-19 syndrome (dpeaa)DE-He213 thrombosis (dpeaa)DE-He213 Wiedemann, Aurélie aut Blengio, Fabiola aut Lefebvre, Cécile aut Cervantes-Gonzalez, Minerva aut Foucat, Emile aut Tisserand, Pascaline aut Surenaud, Mathieu aut Coléon, Séverin aut Prague, Mélanie aut Guillaumat, Lydia aut Krief, Corinne aut Fenwick, Craig aut Laouénan, Cédric aut Bouadma, Lila aut Ghosn, Jade aut Pantaleo, Giuseppe aut Thiébaut, Rodolphe aut Lévy, Yves (orcid)0000-0002-5549-6256 aut Enthalten in Journal of clinical immunology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1981 43(2023), 5 vom: 21. März, Seite 882-893 (DE-627)320573362 (DE-600)2016755-6 1573-2592 nnns volume:43 year:2023 number:5 day:21 month:03 pages:882-893 https://dx.doi.org/10.1007/s10875-023-01459-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2023 5 21 03 882-893
allfields_unstemmed	10.1007/s10875-023-01459-x doi (DE-627)SPR051924471 (SPR)s10875-023-01459-x-e DE-627 ger DE-627 rakwb eng Hocini, Hakim verfasserin aut Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 spike-specific and neutralizing antibodies, and whole blood gene expression profiles in convalescent severe COVID-19 patients 1, 3, and 6 months following hospital discharge. Results We observed persistent abnormalities until month 6 marked by (i) high serum levels of monocyte/macrophage and endothelial activation markers, chemotaxis, and hematopoietic cytokines; (ii) a high frequency of central memory $ CD4^{+} $ and effector $ CD8^{+} $ T cells; (iii) a decrease in anti-SARS-CoV-2 spike and neutralizing antibodies; and (iv) an upregulation of genes related to platelet, neutrophil activation, erythrocytes, myeloid cell differentiation, and RUNX1 signaling. We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. Conclusion The lack of restoration of gene expression to a normal profile after up to 6 months of follow-up, even in asymptomatic patients who experienced severe COVID-19, signals the need to carefully extend their clinical follow-up and propose preventive measures. COVID-19 disease (dpeaa)DE-He213 post-acute COVID-19 syndrome (dpeaa)DE-He213 thrombosis (dpeaa)DE-He213 Wiedemann, Aurélie aut Blengio, Fabiola aut Lefebvre, Cécile aut Cervantes-Gonzalez, Minerva aut Foucat, Emile aut Tisserand, Pascaline aut Surenaud, Mathieu aut Coléon, Séverin aut Prague, Mélanie aut Guillaumat, Lydia aut Krief, Corinne aut Fenwick, Craig aut Laouénan, Cédric aut Bouadma, Lila aut Ghosn, Jade aut Pantaleo, Giuseppe aut Thiébaut, Rodolphe aut Lévy, Yves (orcid)0000-0002-5549-6256 aut Enthalten in Journal of clinical immunology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1981 43(2023), 5 vom: 21. März, Seite 882-893 (DE-627)320573362 (DE-600)2016755-6 1573-2592 nnns volume:43 year:2023 number:5 day:21 month:03 pages:882-893 https://dx.doi.org/10.1007/s10875-023-01459-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2023 5 21 03 882-893
allfieldsGer	10.1007/s10875-023-01459-x doi (DE-627)SPR051924471 (SPR)s10875-023-01459-x-e DE-627 ger DE-627 rakwb eng Hocini, Hakim verfasserin aut Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 spike-specific and neutralizing antibodies, and whole blood gene expression profiles in convalescent severe COVID-19 patients 1, 3, and 6 months following hospital discharge. Results We observed persistent abnormalities until month 6 marked by (i) high serum levels of monocyte/macrophage and endothelial activation markers, chemotaxis, and hematopoietic cytokines; (ii) a high frequency of central memory $ CD4^{+} $ and effector $ CD8^{+} $ T cells; (iii) a decrease in anti-SARS-CoV-2 spike and neutralizing antibodies; and (iv) an upregulation of genes related to platelet, neutrophil activation, erythrocytes, myeloid cell differentiation, and RUNX1 signaling. We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. Conclusion The lack of restoration of gene expression to a normal profile after up to 6 months of follow-up, even in asymptomatic patients who experienced severe COVID-19, signals the need to carefully extend their clinical follow-up and propose preventive measures. COVID-19 disease (dpeaa)DE-He213 post-acute COVID-19 syndrome (dpeaa)DE-He213 thrombosis (dpeaa)DE-He213 Wiedemann, Aurélie aut Blengio, Fabiola aut Lefebvre, Cécile aut Cervantes-Gonzalez, Minerva aut Foucat, Emile aut Tisserand, Pascaline aut Surenaud, Mathieu aut Coléon, Séverin aut Prague, Mélanie aut Guillaumat, Lydia aut Krief, Corinne aut Fenwick, Craig aut Laouénan, Cédric aut Bouadma, Lila aut Ghosn, Jade aut Pantaleo, Giuseppe aut Thiébaut, Rodolphe aut Lévy, Yves (orcid)0000-0002-5549-6256 aut Enthalten in Journal of clinical immunology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1981 43(2023), 5 vom: 21. März, Seite 882-893 (DE-627)320573362 (DE-600)2016755-6 1573-2592 nnns volume:43 year:2023 number:5 day:21 month:03 pages:882-893 https://dx.doi.org/10.1007/s10875-023-01459-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2023 5 21 03 882-893
allfieldsSound	10.1007/s10875-023-01459-x doi (DE-627)SPR051924471 (SPR)s10875-023-01459-x-e DE-627 ger DE-627 rakwb eng Hocini, Hakim verfasserin aut Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19 2023 Text txt rdacontent Computermedien c rdamedia Online-Ressource cr rdacarrier © The Author(s) 2023. corrected publication 2023 Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 spike-specific and neutralizing antibodies, and whole blood gene expression profiles in convalescent severe COVID-19 patients 1, 3, and 6 months following hospital discharge. Results We observed persistent abnormalities until month 6 marked by (i) high serum levels of monocyte/macrophage and endothelial activation markers, chemotaxis, and hematopoietic cytokines; (ii) a high frequency of central memory $ CD4^{+} $ and effector $ CD8^{+} $ T cells; (iii) a decrease in anti-SARS-CoV-2 spike and neutralizing antibodies; and (iv) an upregulation of genes related to platelet, neutrophil activation, erythrocytes, myeloid cell differentiation, and RUNX1 signaling. We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. Conclusion The lack of restoration of gene expression to a normal profile after up to 6 months of follow-up, even in asymptomatic patients who experienced severe COVID-19, signals the need to carefully extend their clinical follow-up and propose preventive measures. COVID-19 disease (dpeaa)DE-He213 post-acute COVID-19 syndrome (dpeaa)DE-He213 thrombosis (dpeaa)DE-He213 Wiedemann, Aurélie aut Blengio, Fabiola aut Lefebvre, Cécile aut Cervantes-Gonzalez, Minerva aut Foucat, Emile aut Tisserand, Pascaline aut Surenaud, Mathieu aut Coléon, Séverin aut Prague, Mélanie aut Guillaumat, Lydia aut Krief, Corinne aut Fenwick, Craig aut Laouénan, Cédric aut Bouadma, Lila aut Ghosn, Jade aut Pantaleo, Giuseppe aut Thiébaut, Rodolphe aut Lévy, Yves (orcid)0000-0002-5549-6256 aut Enthalten in Journal of clinical immunology Dordrecht [u.a.] : Springer Science + Business Media B.V, 1981 43(2023), 5 vom: 21. März, Seite 882-893 (DE-627)320573362 (DE-600)2016755-6 1573-2592 nnns volume:43 year:2023 number:5 day:21 month:03 pages:882-893 https://dx.doi.org/10.1007/s10875-023-01459-x kostenfrei Volltext GBV_USEFLAG_A SYSFLAG_A GBV_SPRINGER GBV_ILN_11 GBV_ILN_20 GBV_ILN_22 GBV_ILN_23 GBV_ILN_24 GBV_ILN_31 GBV_ILN_32 GBV_ILN_39 GBV_ILN_40 GBV_ILN_60 GBV_ILN_62 GBV_ILN_63 GBV_ILN_69 GBV_ILN_70 GBV_ILN_73 GBV_ILN_74 GBV_ILN_90 GBV_ILN_95 GBV_ILN_100 GBV_ILN_101 GBV_ILN_105 GBV_ILN_110 GBV_ILN_120 GBV_ILN_138 GBV_ILN_150 GBV_ILN_151 GBV_ILN_152 GBV_ILN_161 GBV_ILN_170 GBV_ILN_171 GBV_ILN_187 GBV_ILN_213 GBV_ILN_224 GBV_ILN_230 GBV_ILN_250 GBV_ILN_281 GBV_ILN_285 GBV_ILN_293 GBV_ILN_370 GBV_ILN_602 GBV_ILN_636 GBV_ILN_702 GBV_ILN_2001 GBV_ILN_2003 GBV_ILN_2004 GBV_ILN_2005 GBV_ILN_2006 GBV_ILN_2007 GBV_ILN_2008 GBV_ILN_2009 GBV_ILN_2010 GBV_ILN_2011 GBV_ILN_2014 GBV_ILN_2015 GBV_ILN_2020 GBV_ILN_2021 GBV_ILN_2025 GBV_ILN_2026 GBV_ILN_2027 GBV_ILN_2031 GBV_ILN_2034 GBV_ILN_2037 GBV_ILN_2038 GBV_ILN_2039 GBV_ILN_2044 GBV_ILN_2048 GBV_ILN_2049 GBV_ILN_2050 GBV_ILN_2055 GBV_ILN_2056 GBV_ILN_2057 GBV_ILN_2059 GBV_ILN_2061 GBV_ILN_2064 GBV_ILN_2065 GBV_ILN_2068 GBV_ILN_2088 GBV_ILN_2093 GBV_ILN_2106 GBV_ILN_2107 GBV_ILN_2108 GBV_ILN_2110 GBV_ILN_2111 GBV_ILN_2112 GBV_ILN_2113 GBV_ILN_2118 GBV_ILN_2122 GBV_ILN_2129 GBV_ILN_2143 GBV_ILN_2144 GBV_ILN_2147 GBV_ILN_2148 GBV_ILN_2152 GBV_ILN_2153 GBV_ILN_2188 GBV_ILN_2190 GBV_ILN_2232 GBV_ILN_2336 GBV_ILN_2446 GBV_ILN_2470 GBV_ILN_2472 GBV_ILN_2507 GBV_ILN_2522 GBV_ILN_2548 GBV_ILN_4035 GBV_ILN_4037 GBV_ILN_4046 GBV_ILN_4112 GBV_ILN_4125 GBV_ILN_4126 GBV_ILN_4242 GBV_ILN_4246 GBV_ILN_4249 GBV_ILN_4251 GBV_ILN_4305 GBV_ILN_4306 GBV_ILN_4307 GBV_ILN_4313 GBV_ILN_4322 GBV_ILN_4323 GBV_ILN_4324 GBV_ILN_4325 GBV_ILN_4326 GBV_ILN_4328 GBV_ILN_4333 GBV_ILN_4334 GBV_ILN_4335 GBV_ILN_4336 GBV_ILN_4338 GBV_ILN_4393 GBV_ILN_4700 AR 43 2023 5 21 03 882-893
language	English
source	Enthalten in Journal of clinical immunology 43(2023), 5 vom: 21. März, Seite 882-893 volume:43 year:2023 number:5 day:21 month:03 pages:882-893
sourceStr	Enthalten in Journal of clinical immunology 43(2023), 5 vom: 21. März, Seite 882-893 volume:43 year:2023 number:5 day:21 month:03 pages:882-893
format_phy_str_mv	Article
institution	findex.gbv.de
topic_facet	COVID-19 disease post-acute COVID-19 syndrome thrombosis
isfreeaccess_bool	true
container_title	Journal of clinical immunology
authorswithroles_txt_mv	Hocini, Hakim @@aut@@ Wiedemann, Aurélie @@aut@@ Blengio, Fabiola @@aut@@ Lefebvre, Cécile @@aut@@ Cervantes-Gonzalez, Minerva @@aut@@ Foucat, Emile @@aut@@ Tisserand, Pascaline @@aut@@ Surenaud, Mathieu @@aut@@ Coléon, Séverin @@aut@@ Prague, Mélanie @@aut@@ Guillaumat, Lydia @@aut@@ Krief, Corinne @@aut@@ Fenwick, Craig @@aut@@ Laouénan, Cédric @@aut@@ Bouadma, Lila @@aut@@ Ghosn, Jade @@aut@@ Pantaleo, Giuseppe @@aut@@ Thiébaut, Rodolphe @@aut@@ Lévy, Yves @@aut@@
publishDateDaySort_date	2023-03-21T00:00:00Z
hierarchy_top_id	320573362
id	SPR051924471
language_de	englisch
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We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. 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author	Hocini, Hakim
spellingShingle	Hocini, Hakim misc COVID-19 disease misc post-acute COVID-19 syndrome misc thrombosis Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19
authorStr	Hocini, Hakim
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topic_title	Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19 COVID-19 disease (dpeaa)DE-He213 post-acute COVID-19 syndrome (dpeaa)DE-He213 thrombosis (dpeaa)DE-He213
topic	misc COVID-19 disease misc post-acute COVID-19 syndrome misc thrombosis
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title	Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19
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title_full	Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19
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author_browse	Hocini, Hakim Wiedemann, Aurélie Blengio, Fabiola Lefebvre, Cécile Cervantes-Gonzalez, Minerva Foucat, Emile Tisserand, Pascaline Surenaud, Mathieu Coléon, Séverin Prague, Mélanie Guillaumat, Lydia Krief, Corinne Fenwick, Craig Laouénan, Cédric Bouadma, Lila Ghosn, Jade Pantaleo, Giuseppe Thiébaut, Rodolphe Lévy, Yves
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author-letter	Hocini, Hakim
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title_sort	neutrophil activation and immune thrombosis profiles persist in convalescent covid-19
title_auth	Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19
abstract	Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 spike-specific and neutralizing antibodies, and whole blood gene expression profiles in convalescent severe COVID-19 patients 1, 3, and 6 months following hospital discharge. Results We observed persistent abnormalities until month 6 marked by (i) high serum levels of monocyte/macrophage and endothelial activation markers, chemotaxis, and hematopoietic cytokines; (ii) a high frequency of central memory $ CD4^{+} $ and effector $ CD8^{+} $ T cells; (iii) a decrease in anti-SARS-CoV-2 spike and neutralizing antibodies; and (iv) an upregulation of genes related to platelet, neutrophil activation, erythrocytes, myeloid cell differentiation, and RUNX1 signaling. We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. Conclusion The lack of restoration of gene expression to a normal profile after up to 6 months of follow-up, even in asymptomatic patients who experienced severe COVID-19, signals the need to carefully extend their clinical follow-up and propose preventive measures. © The Author(s) 2023. corrected publication 2023
abstractGer	Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 spike-specific and neutralizing antibodies, and whole blood gene expression profiles in convalescent severe COVID-19 patients 1, 3, and 6 months following hospital discharge. Results We observed persistent abnormalities until month 6 marked by (i) high serum levels of monocyte/macrophage and endothelial activation markers, chemotaxis, and hematopoietic cytokines; (ii) a high frequency of central memory $ CD4^{+} $ and effector $ CD8^{+} $ T cells; (iii) a decrease in anti-SARS-CoV-2 spike and neutralizing antibodies; and (iv) an upregulation of genes related to platelet, neutrophil activation, erythrocytes, myeloid cell differentiation, and RUNX1 signaling. We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. Conclusion The lack of restoration of gene expression to a normal profile after up to 6 months of follow-up, even in asymptomatic patients who experienced severe COVID-19, signals the need to carefully extend their clinical follow-up and propose preventive measures. © The Author(s) 2023. corrected publication 2023
abstract_unstemmed	Purpose Following a severe COVID-19 infection, a proportion of individuals develop prolonged symptoms. We investigated the immunological dysfunction that underlies the persistence of symptoms months after the resolution of acute COVID-19. Methods We analyzed cytokines, cell phenotypes, SARS-CoV-2 spike-specific and neutralizing antibodies, and whole blood gene expression profiles in convalescent severe COVID-19 patients 1, 3, and 6 months following hospital discharge. Results We observed persistent abnormalities until month 6 marked by (i) high serum levels of monocyte/macrophage and endothelial activation markers, chemotaxis, and hematopoietic cytokines; (ii) a high frequency of central memory $ CD4^{+} $ and effector $ CD8^{+} $ T cells; (iii) a decrease in anti-SARS-CoV-2 spike and neutralizing antibodies; and (iv) an upregulation of genes related to platelet, neutrophil activation, erythrocytes, myeloid cell differentiation, and RUNX1 signaling. We identified a “core gene signature” associated with a history of thrombotic events, with upregulation of a set of genes involved in neutrophil activation, platelet, hematopoiesis, and blood coagulation. Conclusion The lack of restoration of gene expression to a normal profile after up to 6 months of follow-up, even in asymptomatic patients who experienced severe COVID-19, signals the need to carefully extend their clinical follow-up and propose preventive measures. © The Author(s) 2023. corrected publication 2023
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container_issue	5
title_short	Neutrophil Activation and Immune Thrombosis Profiles Persist in Convalescent COVID-19
url	https://dx.doi.org/10.1007/s10875-023-01459-x
remote_bool	true
author2	Wiedemann, Aurélie Blengio, Fabiola Lefebvre, Cécile Cervantes-Gonzalez, Minerva Foucat, Emile Tisserand, Pascaline Surenaud, Mathieu Coléon, Séverin Prague, Mélanie Guillaumat, Lydia Krief, Corinne Fenwick, Craig Laouénan, Cédric Bouadma, Lila Ghosn, Jade Pantaleo, Giuseppe Thiébaut, Rodolphe Lévy, Yves
author2Str	Wiedemann, Aurélie Blengio, Fabiola Lefebvre, Cécile Cervantes-Gonzalez, Minerva Foucat, Emile Tisserand, Pascaline Surenaud, Mathieu Coléon, Séverin Prague, Mélanie Guillaumat, Lydia Krief, Corinne Fenwick, Craig Laouénan, Cédric Bouadma, Lila Ghosn, Jade Pantaleo, Giuseppe Thiébaut, Rodolphe Lévy, Yves
ppnlink	320573362
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doi_str	10.1007/s10875-023-01459-x
up_date	2024-07-04T00:27:40.486Z
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