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 : 002151 ( Main/Exploration ); précédent : 002150; suivant : 002152Anti-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 [République populaire de Chine] ; Ming S. Yip ; Chung Y. Cheung ; Hiu L. Leung ; Ping H. Li ; Francois Kien ; Isabelle Dutry ; Benoît Callendret ; Nicolas Escriou ; Ralf Altmeyer ; Beatrice Nal ; Marc Daëron ; Roberto Bruzzone ; J S Malik PeirisSource :
- Journal of virology [ 1098-5514 ] ; 2011.
Descripteurs français
- KwdFr :
- Animaux, Anticorps antiviraux (métabolisme), Anticorps neutralisants (métabolisme), Cellules cultivées, Concentration en ions d'hydrogène, Cysteine proteases, Facilitation dépendante des anticorps, Glycoprotéine de spicule des coronavirus, Glycoprotéines membranaires (métabolisme), Humains, Lymphocytes (virologie), Protéines de l'enveloppe virale (métabolisme), Pénétration virale, Récepteurs du fragment Fc des IgG (métabolisme), Souris, Souris de lignée BALB C, Virus du SRAS (immunologie), Virus du SRAS (pathogénicité).
- MESH :
- immunologie : Virus du SRAS.
- métabolisme : Anticorps antiviraux, Anticorps neutralisants, Glycoprotéines membranaires, Protéines de l'enveloppe virale, Récepteurs du fragment Fc des IgG.
- pathogénicité : Virus du SRAS.
- virologie : Lymphocytes.
- Animaux, Cellules cultivées, Concentration en ions d'hydrogène, Cysteine proteases, Facilitation dépendante des anticorps, Glycoprotéine de spicule des coronavirus, Humains, Pénétration virale, Souris, Souris de lignée BALB C.
English descriptors
- KwdEn :
- Animals, Antibodies, Neutralizing (metabolism), Antibodies, Viral (metabolism), Antibody-Dependent Enhancement, Cells, Cultured, Chlorocebus aethiops, Cysteine Proteases, Humans, Hydrogen-Ion Concentration, Lymphocytes (virology), Membrane Glycoproteins (metabolism), Mice, Mice, Inbred BALB C, Receptors, IgG (metabolism), SARS Virus (immunology), SARS Virus (pathogenicity), Spike Glycoprotein, Coronavirus, Viral Envelope Proteins (metabolism), Virus Internalization.
- MESH :
- chemical , metabolism : Antibodies, Neutralizing, Antibodies, Viral, Membrane Glycoproteins, Receptors, IgG, Viral Envelope Proteins.
- immunology : SARS Virus.
- pathogenicity : SARS Virus.
- virology : Lymphocytes.
- Animals, Antibody-Dependent Enhancement, Cells, Cultured, Chlorocebus aethiops, Cysteine Proteases, Humans, Hydrogen-Ion Concentration, Mice, Mice, Inbred BALB C, Spike Glycoprotein, Coronavirus, Virus Internalization.
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.
Url:
DOI: 10.1128/JVI.00671-11
PubMed: 21775467
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream PubMed, to step Corpus: 001492
- to stream PubMed, to step Curation: 001492
- to stream PubMed, to step Checkpoint: 001530
- to stream Ncbi, to step Merge: 002363
- to stream Ncbi, to step Curation: 002363
- to stream Ncbi, to step Checkpoint: 002363
- to stream Hal, to step Corpus: 000016
- to stream Hal, to step Curation: 000016
- to stream Hal, to step Checkpoint: 000123
- to stream Main, to step Merge: 002178
- to stream Main, to step Curation: 002151
Le document en format XML
<record><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH- and cysteine protease-independent FcγR pathway.</title><author><name sortKey="Jaume, Martial" sort="Jaume, Martial" uniqKey="Jaume M" first="Martial" last="Jaume">Martial Jaume</name><affiliation wicri:level="1"><nlm:affiliation>HKU-Pasteur Research Centre, Dexter H. C. Man Building, 8 Sassoon Road, Pokfulam, Hong Kong SAR, China. breizh@hku.hk</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>HKU-Pasteur Research Centre, Dexter H. C. Man Building, 8 Sassoon Road, Pokfulam, Hong Kong SAR</wicri:regionArea><wicri:noRegion>Hong Kong SAR</wicri:noRegion></affiliation></author><author><name sortKey="Yip, Ming S" sort="Yip, Ming S" uniqKey="Yip M" first="Ming S" last="Yip">Ming S. Yip</name></author><author><name sortKey="Cheung, Chung Y" sort="Cheung, Chung Y" uniqKey="Cheung C" first="Chung Y" last="Cheung">Chung Y. Cheung</name></author><author><name sortKey="Leung, Hiu L" sort="Leung, Hiu L" uniqKey="Leung H" first="Hiu L" last="Leung">Hiu L. Leung</name></author><author><name sortKey="Li, Ping H" sort="Li, Ping H" uniqKey="Li P" first="Ping H" last="Li">Ping H. Li</name></author><author><name sortKey="Kien, Francois" sort="Kien, Francois" uniqKey="Kien F" first="Francois" last="Kien">Francois Kien</name></author><author><name sortKey="Dutry, Isabelle" sort="Dutry, Isabelle" uniqKey="Dutry I" first="Isabelle" last="Dutry">Isabelle Dutry</name></author><author><name sortKey="Callendret, Benoit" sort="Callendret, Benoit" uniqKey="Callendret B" first="Benoît" last="Callendret">Benoît Callendret</name></author><author><name sortKey="Escriou, Nicolas" sort="Escriou, Nicolas" uniqKey="Escriou N" first="Nicolas" last="Escriou">Nicolas Escriou</name></author><author><name sortKey="Altmeyer, Ralf" sort="Altmeyer, Ralf" uniqKey="Altmeyer R" first="Ralf" last="Altmeyer">Ralf Altmeyer</name></author><author><name sortKey="Nal, Beatrice" sort="Nal, Beatrice" uniqKey="Nal B" first="Beatrice" last="Nal">Beatrice Nal</name></author><author><name sortKey="Daeron, Marc" sort="Daeron, Marc" uniqKey="Daeron M" first="Marc" last="Daëron">Marc Daëron</name></author><author><name sortKey="Bruzzone, Roberto" sort="Bruzzone, Roberto" uniqKey="Bruzzone R" first="Roberto" last="Bruzzone">Roberto Bruzzone</name></author><author><name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J S Malik" last="Peiris">J S Malik Peiris</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="2011">2011</date><idno type="RBID">pubmed:21775467</idno><idno type="pmid">21775467</idno><idno type="doi">10.1128/JVI.00671-11</idno><idno type="wicri:Area/PubMed/Corpus">001492</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Corpus" wicri:corpus="PubMed">001492</idno><idno type="wicri:Area/PubMed/Curation">001492</idno><idno type="wicri:explorRef" wicri:stream="PubMed" wicri:step="Curation">001492</idno><idno type="wicri:Area/PubMed/Checkpoint">001530</idno><idno type="wicri:explorRef" wicri:stream="Checkpoint" wicri:step="PubMed">001530</idno><idno type="wicri:Area/Ncbi/Merge">002363</idno><idno type="wicri:Area/Ncbi/Curation">002363</idno><idno type="wicri:Area/Ncbi/Checkpoint">002363</idno><idno type="wicri:source">HAL</idno><idno type="RBID">Hal:pasteur-00612415</idno><idno type="url">https://hal-riip.archives-ouvertes.fr/pasteur-00612415</idno><idno type="wicri:Area/Hal/Corpus">000016</idno><idno type="wicri:Area/Hal/Curation">000016</idno><idno type="wicri:Area/Hal/Checkpoint">000123</idno><idno type="wicri:explorRef" wicri:stream="Hal" wicri:step="Checkpoint">000123</idno><idno type="wicri:doubleKey">0022-538X:2011:Jaume M:anti:sars:cov</idno><idno type="wicri:Area/Main/Merge">002178</idno><idno type="wicri:Area/Main/Curation">002151</idno><idno type="wicri:Area/Main/Exploration">002151</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH- and cysteine protease-independent FcγR pathway.</title><author><name sortKey="Jaume, Martial" sort="Jaume, Martial" uniqKey="Jaume M" first="Martial" last="Jaume">Martial Jaume</name><affiliation wicri:level="1"><nlm:affiliation>HKU-Pasteur Research Centre, Dexter H. C. Man Building, 8 Sassoon Road, Pokfulam, Hong Kong SAR, China. breizh@hku.hk</nlm:affiliation><country xml:lang="fr">République populaire de Chine</country><wicri:regionArea>HKU-Pasteur Research Centre, Dexter H. C. Man Building, 8 Sassoon Road, Pokfulam, Hong Kong SAR</wicri:regionArea><wicri:noRegion>Hong Kong SAR</wicri:noRegion></affiliation></author><author><name sortKey="Yip, Ming S" sort="Yip, Ming S" uniqKey="Yip M" first="Ming S" last="Yip">Ming S. Yip</name></author><author><name sortKey="Cheung, Chung Y" sort="Cheung, Chung Y" uniqKey="Cheung C" first="Chung Y" last="Cheung">Chung Y. Cheung</name></author><author><name sortKey="Leung, Hiu L" sort="Leung, Hiu L" uniqKey="Leung H" first="Hiu L" last="Leung">Hiu L. Leung</name></author><author><name sortKey="Li, Ping H" sort="Li, Ping H" uniqKey="Li P" first="Ping H" last="Li">Ping H. Li</name></author><author><name sortKey="Kien, Francois" sort="Kien, Francois" uniqKey="Kien F" first="Francois" last="Kien">Francois Kien</name></author><author><name sortKey="Dutry, Isabelle" sort="Dutry, Isabelle" uniqKey="Dutry I" first="Isabelle" last="Dutry">Isabelle Dutry</name></author><author><name sortKey="Callendret, Benoit" sort="Callendret, Benoit" uniqKey="Callendret B" first="Benoît" last="Callendret">Benoît Callendret</name></author><author><name sortKey="Escriou, Nicolas" sort="Escriou, Nicolas" uniqKey="Escriou N" first="Nicolas" last="Escriou">Nicolas Escriou</name></author><author><name sortKey="Altmeyer, Ralf" sort="Altmeyer, Ralf" uniqKey="Altmeyer R" first="Ralf" last="Altmeyer">Ralf Altmeyer</name></author><author><name sortKey="Nal, Beatrice" sort="Nal, Beatrice" uniqKey="Nal B" first="Beatrice" last="Nal">Beatrice Nal</name></author><author><name sortKey="Daeron, Marc" sort="Daeron, Marc" uniqKey="Daeron M" first="Marc" last="Daëron">Marc Daëron</name></author><author><name sortKey="Bruzzone, Roberto" sort="Bruzzone, Roberto" uniqKey="Bruzzone R" first="Roberto" last="Bruzzone">Roberto Bruzzone</name></author><author><name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J S Malik" last="Peiris">J S Malik Peiris</name></author></analytic><series><title level="j">Journal of virology</title><idno type="eISSN">1098-5514</idno><imprint><date when="2011" type="published">2011</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Neutralizing (metabolism)</term><term>Antibodies, Viral (metabolism)</term><term>Antibody-Dependent Enhancement</term><term>Cells, Cultured</term><term>Chlorocebus aethiops</term><term>Cysteine Proteases</term><term>Humans</term><term>Hydrogen-Ion Concentration</term><term>Lymphocytes (virology)</term><term>Membrane Glycoproteins (metabolism)</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Receptors, IgG (metabolism)</term><term>SARS Virus (immunology)</term><term>SARS Virus (pathogenicity)</term><term>Spike Glycoprotein, Coronavirus</term><term>Viral Envelope Proteins (metabolism)</term><term>Virus Internalization</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux</term><term>Anticorps antiviraux (métabolisme)</term><term>Anticorps neutralisants (métabolisme)</term><term>Cellules cultivées</term><term>Concentration en ions d'hydrogène</term><term>Cysteine proteases</term><term>Facilitation dépendante des anticorps</term><term>Glycoprotéine de spicule des coronavirus</term><term>Glycoprotéines membranaires (métabolisme)</term><term>Humains</term><term>Lymphocytes (virologie)</term><term>Protéines de l'enveloppe virale (métabolisme)</term><term>Pénétration virale</term><term>Récepteurs du fragment Fc des IgG (métabolisme)</term><term>Souris</term><term>Souris de lignée BALB C</term><term>Virus du SRAS (immunologie)</term><term>Virus du SRAS (pathogénicité)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="metabolism" xml:lang="en"><term>Antibodies, Neutralizing</term><term>Antibodies, Viral</term><term>Membrane Glycoproteins</term><term>Receptors, IgG</term><term>Viral Envelope Proteins</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="métabolisme" xml:lang="fr"><term>Anticorps antiviraux</term><term>Anticorps neutralisants</term><term>Glycoprotéines membranaires</term><term>Protéines de l'enveloppe virale</term><term>Récepteurs du fragment Fc des IgG</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Lymphocytes</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Lymphocytes</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Antibody-Dependent Enhancement</term><term>Cells, Cultured</term><term>Chlorocebus aethiops</term><term>Cysteine Proteases</term><term>Humans</term><term>Hydrogen-Ion Concentration</term><term>Mice</term><term>Mice, Inbred BALB C</term><term>Spike Glycoprotein, Coronavirus</term><term>Virus Internalization</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules cultivées</term><term>Concentration en ions d'hydrogène</term><term>Cysteine proteases</term><term>Facilitation dépendante des anticorps</term><term>Glycoprotéine de spicule des coronavirus</term><term>Humains</term><term>Pénétration virale</term><term>Souris</term><term>Souris de lignée BALB C</term></keywords></textClass></profileDesc></teiHeader><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></front></TEI><affiliations><list><country><li>République populaire de Chine</li></country></list><tree><noCountry><name sortKey="Altmeyer, Ralf" sort="Altmeyer, Ralf" uniqKey="Altmeyer R" first="Ralf" last="Altmeyer">Ralf Altmeyer</name><name sortKey="Bruzzone, Roberto" sort="Bruzzone, Roberto" uniqKey="Bruzzone R" first="Roberto" last="Bruzzone">Roberto Bruzzone</name><name sortKey="Callendret, Benoit" sort="Callendret, Benoit" uniqKey="Callendret B" first="Benoît" last="Callendret">Benoît Callendret</name><name sortKey="Cheung, Chung Y" sort="Cheung, Chung Y" uniqKey="Cheung C" first="Chung Y" last="Cheung">Chung Y. Cheung</name><name sortKey="Daeron, Marc" sort="Daeron, Marc" uniqKey="Daeron M" first="Marc" last="Daëron">Marc Daëron</name><name sortKey="Dutry, Isabelle" sort="Dutry, Isabelle" uniqKey="Dutry I" first="Isabelle" last="Dutry">Isabelle Dutry</name><name sortKey="Escriou, Nicolas" sort="Escriou, Nicolas" uniqKey="Escriou N" first="Nicolas" last="Escriou">Nicolas Escriou</name><name sortKey="Kien, Francois" sort="Kien, Francois" uniqKey="Kien F" first="Francois" last="Kien">Francois Kien</name><name sortKey="Leung, Hiu L" sort="Leung, Hiu L" uniqKey="Leung H" first="Hiu L" last="Leung">Hiu L. Leung</name><name sortKey="Li, Ping H" sort="Li, Ping H" uniqKey="Li P" first="Ping H" last="Li">Ping H. Li</name><name sortKey="Nal, Beatrice" sort="Nal, Beatrice" uniqKey="Nal B" first="Beatrice" last="Nal">Beatrice Nal</name><name sortKey="Peiris, J S Malik" sort="Peiris, J S Malik" uniqKey="Peiris J" first="J S Malik" last="Peiris">J S Malik Peiris</name><name sortKey="Yip, Ming S" sort="Yip, Ming S" uniqKey="Yip M" first="Ming S" last="Yip">Ming S. Yip</name></noCountry><country name="République populaire de Chine"><noRegion><name sortKey="Jaume, Martial" sort="Jaume, Martial" uniqKey="Jaume M" first="Martial" last="Jaume">Martial Jaume</name></noRegion></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Sante/explor/SrasV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 002151 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 002151 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Sante
|area= SrasV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= pubmed:21775467
|texte= Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH- and cysteine protease-independent FcγR pathway.
}}
Pour générer des pages wiki
HfdIndexSelect -h $EXPLOR_AREA/Data/Main/Exploration/RBID.i -Sk "pubmed:21775467" \
| HfdSelect -Kh $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd \
| NlmPubMed2Wicri -a SrasV1
| This area was generated with Dilib version V0.6.33. |  |