SrasV1, PascalFrancis, Corpus, bibRecord, 000073

Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway

Identifieur interne : 000073 ( PascalFrancis/Corpus ); précédent : 000072; suivant : 000074

Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway

Auteurs : Martial Jaume ; Ming S. Yip ; Chung Y. Cheung ; Hiu L. Leung ; Ping H. Li ; Francois Kien ; Isabelle Dutry ; Benoit Callendret ; Nicolas Escriou ; Ralf Altmeyer ; Beatrice Nal ; Marc Daëron ; Roberto Bruzzone ; J. S. Malik Peiris

Source :

Journal of virology [ 0022-538X ] ; 2011.

RBID : Pascal:12-0111133

Descripteurs français

Pascal (Inist)
- Coronavirus, Homme, Anticorps, Cysteine endopeptidases, Récepteur FcγR, Syndrome respiratoire aigu sévère.

English descriptors

KwdEn :
- Antibody, Coronavirus, Cysteine endopeptidases, FcγR receptor, Human, Severe acute respiratory syndrome.

Abstract

Public health measures successfully contained outbreaks of the severe acute respiratory syndrome coronavirus (SARS-CoV) infection. However, the precursor of the SARS-CoV remains in its natural bat reservoir, and reemergence of a human-adapted SARS-like coronavirus remains a plausible public health concern. Vaccination is a major strategy for containing resurgence of SARS in humans, and a number of vaccine candidates have been tested in experimental animal models. We previously reported that antibody elicited by a SARS-CoV vaccine candidate based on recombinant full-length Spike-protein trimers potentiated infection of human B cell lines despite eliciting in vivo a neutralizing and protective immune response in rodents. These observations prompted us to investigate the mechanisms underlying antibody-dependent enhancement (ADE) of SARS-CoV infection in vitro. We demonstrate here that anti-Spike immune serum, while inhibiting viral entry in a permissive cell line, potentiated infection of immune cells by SARS-CoV Spike-pseudotyped lentiviral particles, as well as replication-competent SARS coronavirus. Antibody-mediated infection was dependent on Fcγ receptor II but did not use the endosomal/lysosomal pathway utilized by angiotensin I converting enzyme 2 (ACE2), the accepted receptor for SARS-CoV. This suggests that ADE of SARS-CoV utilizes a novel cell entry mechanism into immune cells. Different SARS vaccine candidates elicit sera that differ in their capacity to induce ADE in immune cells despite their comparable potency to neutralize infection in ACE2-bearing cells. Our results suggest a novel mechanism by which SARS-CoV can enter target cells and illustrate the potential pitfalls associated with immunization against it. These findings should prompt further investigations into SARS pathogenesis.

Notice en format standard (ISO 2709)

Pour connaître la documentation sur le format Inist Standard.

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A14	`02`			`@1 Department of Microbiology, The University of Hong Kong, 21 Sassoon Road @3 HKG @Z 3 aut. @Z 7 aut.`
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Format Inist (serveur)

NO :	PASCAL 12-0111133 INIST
ET :	Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway
AU :	JAUME (Martial); YIP (Ming S.); CHEUNG (Chung Y.); LEUNG (Hiu L.); LI (Ping H.); KIEN (Francois); DUTRY (Isabelle); CALLENDRET (Benoit); ESCRIOU (Nicolas); ALTMEYER (Ralf); NAL (Beatrice); DAËRON (Marc); BRUZZONE (Roberto); MALIK PEIRIS (J. S.)
AF :	HKU-Pasteur Research Centre, 8 Sassoon Road/Hong-Kong (1 aut., 2 aut., 4 aut., 5 aut., 6 aut., 7 aut., 10 aut., 11 aut., 13 aut., 14 aut.); Department of Microbiology, The University of Hong Kong, 21 Sassoon Road/Hong-Kong (3 aut., 7 aut.); Institut Pasteur, Unité de Génétique Moléculaire des Virus à ARN, Département de Virologie, 25 Rue du Docteur Roux/75015 Paris/France (8 aut., 9 aut.); CNRS, UPA3015/75015 Paris/France (8 aut., 9 aut.); Department of Anatomy, The University of Hong Kong, 21 Sassoon Road/Hong-Kong (11 aut.); Institut Pasteur, Département d'lmmunologie, Unité d'Allergologie Moléculaire et Cellulaire, 25 Rue du Docteur Roux/75015 Paris/France (12 aut.); INSERM, Unité 760, 25 Rue du Docteur Roux/75015 Paris/France (12 aut.); Institut Pasteur, Department of Cell Biology and Infection, 25 Rue du Docteur Roux/75015 Paris/France (13 aut.)
DT :	Publication en série; Niveau analytique
SO :	Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2011; Vol. 85; No. 20; Pp. 10582-10597; Bibl. 76 ref.
LA :	Anglais
EA :	Public health measures successfully contained outbreaks of the severe acute respiratory syndrome coronavirus (SARS-CoV) infection. However, the precursor of the SARS-CoV remains in its natural bat reservoir, and reemergence of a human-adapted SARS-like coronavirus remains a plausible public health concern. Vaccination is a major strategy for containing resurgence of SARS in humans, and a number of vaccine candidates have been tested in experimental animal models. We previously reported that antibody elicited by a SARS-CoV vaccine candidate based on recombinant full-length Spike-protein trimers potentiated infection of human B cell lines despite eliciting in vivo a neutralizing and protective immune response in rodents. These observations prompted us to investigate the mechanisms underlying antibody-dependent enhancement (ADE) of SARS-CoV infection in vitro. We demonstrate here that anti-Spike immune serum, while inhibiting viral entry in a permissive cell line, potentiated infection of immune cells by SARS-CoV Spike-pseudotyped lentiviral particles, as well as replication-competent SARS coronavirus. Antibody-mediated infection was dependent on Fcγ receptor II but did not use the endosomal/lysosomal pathway utilized by angiotensin I converting enzyme 2 (ACE2), the accepted receptor for SARS-CoV. This suggests that ADE of SARS-CoV utilizes a novel cell entry mechanism into immune cells. Different SARS vaccine candidates elicit sera that differ in their capacity to induce ADE in immune cells despite their comparable potency to neutralize infection in ACE2-bearing cells. Our results suggest a novel mechanism by which SARS-CoV can enter target cells and illustrate the potential pitfalls associated with immunization against it. These findings should prompt further investigations into SARS pathogenesis.
CC :	002A05C10
FD :	Coronavirus; Homme; Anticorps; Cysteine endopeptidases; Récepteur FcγR; Syndrome respiratoire aigu sévère
FG :	Coronaviridae; Nidovirales; Virus; Peptidases; Hydrolases; Enzyme; Pathologie de l'appareil respiratoire; Virose; Infection; Pathologie des poumons
ED :	Coronavirus; Human; Antibody; Cysteine endopeptidases; FcγR receptor; Severe acute respiratory syndrome
EG :	Coronaviridae; Nidovirales; Virus; Peptidases; Hydrolases; Enzyme; Respiratory disease; Viral disease; Infection; Lung disease
SD :	Coronavirus; Hombre; Anticuerpo; Cysteine endopeptidases; Receptor FcγR; Síndrome respiratorio agudo severo
LO :	INIST-13592.354000507804940150
ID :	12-0111133

Links to Exploration step

Pascal:12-0111133

Le document en format XML

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<author><name sortKey="Nal, Beatrice" sort="Nal, Beatrice" uniqKey="Nal B" first="Beatrice" last="Nal">Beatrice Nal</name>
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<author><name sortKey="Daeron, Marc" sort="Daeron, Marc" uniqKey="Daeron M" first="Marc" last="Daëron">Marc Daëron</name>
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<author><name sortKey="Bruzzone, Roberto" sort="Bruzzone, Roberto" uniqKey="Bruzzone R" first="Roberto" last="Bruzzone">Roberto Bruzzone</name>
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<series><title level="j" type="main">Journal of virology</title>
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<front><div type="abstract" xml:lang="en">Public health measures successfully contained outbreaks of the severe acute respiratory syndrome coronavirus (SARS-CoV) infection. However, the precursor of the SARS-CoV remains in its natural bat reservoir, and reemergence of a human-adapted SARS-like coronavirus remains a plausible public health concern. Vaccination is a major strategy for containing resurgence of SARS in humans, and a number of vaccine candidates have been tested in experimental animal models. We previously reported that antibody elicited by a SARS-CoV vaccine candidate based on recombinant full-length Spike-protein trimers potentiated infection of human B cell lines despite eliciting in vivo a neutralizing and protective immune response in rodents. These observations prompted us to investigate the mechanisms underlying antibody-dependent enhancement (ADE) of SARS-CoV infection in vitro. We demonstrate here that anti-Spike immune serum, while inhibiting viral entry in a permissive cell line, potentiated infection of immune cells by SARS-CoV Spike-pseudotyped lentiviral particles, as well as replication-competent SARS coronavirus. Antibody-mediated infection was dependent on Fcγ receptor II but did not use the endosomal/lysosomal pathway utilized by angiotensin I converting enzyme 2 (ACE2), the accepted receptor for SARS-CoV. This suggests that ADE of SARS-CoV utilizes a novel cell entry mechanism into immune cells. Different SARS vaccine candidates elicit sera that differ in their capacity to induce ADE in immune cells despite their comparable potency to neutralize infection in ACE2-bearing cells. Our results suggest a novel mechanism by which SARS-CoV can enter target cells and illustrate the potential pitfalls associated with immunization against it. These findings should prompt further investigations into SARS pathogenesis.</div>
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<fC07 i1="08" i2="X" l="ENG"><s0>Viral disease</s0>
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<fC07 i1="08" i2="X" l="SPA"><s0>Virosis</s0>
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<fC07 i1="09" i2="X" l="ENG"><s0>Infection</s0>
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<fC07 i1="09" i2="X" l="SPA"><s0>Infección</s0>
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<fC07 i1="10" i2="X" l="FRE"><s0>Pathologie des poumons</s0>
<s5>16</s5>
</fC07>
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<s5>16</s5>
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<server><NO>PASCAL 12-0111133 INIST</NO>
<ET>Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway</ET>
<AU>JAUME (Martial); YIP (Ming S.); CHEUNG (Chung Y.); LEUNG (Hiu L.); LI (Ping H.); KIEN (Francois); DUTRY (Isabelle); CALLENDRET (Benoit); ESCRIOU (Nicolas); ALTMEYER (Ralf); NAL (Beatrice); DAËRON (Marc); BRUZZONE (Roberto); MALIK PEIRIS (J. S.)</AU>
<AF>HKU-Pasteur Research Centre, 8 Sassoon Road/Hong-Kong (1 aut., 2 aut., 4 aut., 5 aut., 6 aut., 7 aut., 10 aut., 11 aut., 13 aut., 14 aut.); Department of Microbiology, The University of Hong Kong, 21 Sassoon Road/Hong-Kong (3 aut., 7 aut.); Institut Pasteur, Unité de Génétique Moléculaire des Virus à ARN, Département de Virologie, 25 Rue du Docteur Roux/75015 Paris/France (8 aut., 9 aut.); CNRS, UPA3015/75015 Paris/France (8 aut., 9 aut.); Department of Anatomy, The University of Hong Kong, 21 Sassoon Road/Hong-Kong (11 aut.); Institut Pasteur, Département d'lmmunologie, Unité d'Allergologie Moléculaire et Cellulaire, 25 Rue du Docteur Roux/75015 Paris/France (12 aut.); INSERM, Unité 760, 25 Rue du Docteur Roux/75015 Paris/France (12 aut.); Institut Pasteur, Department of Cell Biology and Infection, 25 Rue du Docteur Roux/75015 Paris/France (13 aut.)</AF>
<DT>Publication en série; Niveau analytique</DT>
<SO>Journal of virology; ISSN 0022-538X; Etats-Unis; Da. 2011; Vol. 85; No. 20; Pp. 10582-10597; Bibl. 76 ref.</SO>
<LA>Anglais</LA>
<EA>Public health measures successfully contained outbreaks of the severe acute respiratory syndrome coronavirus (SARS-CoV) infection. However, the precursor of the SARS-CoV remains in its natural bat reservoir, and reemergence of a human-adapted SARS-like coronavirus remains a plausible public health concern. Vaccination is a major strategy for containing resurgence of SARS in humans, and a number of vaccine candidates have been tested in experimental animal models. We previously reported that antibody elicited by a SARS-CoV vaccine candidate based on recombinant full-length Spike-protein trimers potentiated infection of human B cell lines despite eliciting in vivo a neutralizing and protective immune response in rodents. These observations prompted us to investigate the mechanisms underlying antibody-dependent enhancement (ADE) of SARS-CoV infection in vitro. We demonstrate here that anti-Spike immune serum, while inhibiting viral entry in a permissive cell line, potentiated infection of immune cells by SARS-CoV Spike-pseudotyped lentiviral particles, as well as replication-competent SARS coronavirus. Antibody-mediated infection was dependent on Fcγ receptor II but did not use the endosomal/lysosomal pathway utilized by angiotensin I converting enzyme 2 (ACE2), the accepted receptor for SARS-CoV. This suggests that ADE of SARS-CoV utilizes a novel cell entry mechanism into immune cells. Different SARS vaccine candidates elicit sera that differ in their capacity to induce ADE in immune cells despite their comparable potency to neutralize infection in ACE2-bearing cells. Our results suggest a novel mechanism by which SARS-CoV can enter target cells and illustrate the potential pitfalls associated with immunization against it. These findings should prompt further investigations into SARS pathogenesis.</EA>
<CC>002A05C10</CC>
<FD>Coronavirus; Homme; Anticorps; Cysteine endopeptidases; Récepteur FcγR; Syndrome respiratoire aigu sévère</FD>
<FG>Coronaviridae; Nidovirales; Virus; Peptidases; Hydrolases; Enzyme; Pathologie de l'appareil respiratoire; Virose; Infection; Pathologie des poumons</FG>
<ED>Coronavirus; Human; Antibody; Cysteine endopeptidases; FcγR receptor; Severe acute respiratory syndrome</ED>
<EG>Coronaviridae; Nidovirales; Virus; Peptidases; Hydrolases; Enzyme; Respiratory disease; Viral disease; Infection; Lung disease</EG>
<SD>Coronavirus; Hombre; Anticuerpo; Cysteine endopeptidases; Receptor FcγR; Síndrome respiratorio agudo severo</SD>
<LO>INIST-13592.354000507804940150</LO>
<ID>12-0111133</ID>
</server>
</inist>
</record>

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Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway

Anti-Severe Acute Respiratory Syndrome Coronavirus Spike Antibodies Trigger Infection of Human Immune Cells via a pH- and Cysteine Protease-Independent FcγR Pathway

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