A perspective on potential antibody-dependent enhancement of SARS-CoV-2.
Identifieur interne : 000838 ( Main/Exploration ); précédent : 000837; suivant : 000839A perspective on potential antibody-dependent enhancement of SARS-CoV-2.
Auteurs : Ann M. Arvin [États-Unis] ; Katja Fink [États-Unis, Suisse] ; Michael A. Schmid [États-Unis, Suisse] ; Andrea Cathcart [États-Unis] ; Roberto Spreafico [États-Unis] ; Colin Havenar-Daughton [États-Unis] ; Antonio Lanzavecchia [États-Unis, Suisse] ; Davide Corti [États-Unis, Suisse] ; Herbert W. Virgin [États-Unis]Source :
- Nature [ 1476-4687 ] ; 2020.
Descripteurs français
- KwdFr :
- Animaux (MeSH), Anticorps antiviraux (effets indésirables), Anticorps antiviraux (immunologie), Anticorps antiviraux (usage thérapeutique), Anticorps neutralisants (effets indésirables), Anticorps neutralisants (immunologie), Anticorps neutralisants (usage thérapeutique), Betacoronavirus (immunologie), Betacoronavirus (pathogénicité), Cellules HEK293 (MeSH), Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie), Facilitation dépendante des anticorps (immunologie), Fragments Fab d'immunoglobuline (immunologie), Fragments Fc des immunoglobulines (immunologie), Humains (MeSH), Immunoglobuline G (immunologie), Infections à coronavirus (immunologie), Infections à coronavirus (prévention et contrôle), Infections à coronavirus (virologie), Macaca mulatta (MeSH), Modèles animaux de maladie humaine (MeSH), Orthomyxoviridae (immunologie), Pandémies (MeSH), Pneumopathie virale (immunologie), Pneumopathie virale (virologie), Rats (MeSH), Souris (MeSH), Vaccins antiviraux (effets indésirables), Vaccins antiviraux (immunologie), Virus de la dengue (immunologie), Virus du SRAS (immunologie).
- MESH :
- effets indésirables : Anticorps antiviraux, Anticorps neutralisants, Vaccins antiviraux.
- immunologie : Anticorps antiviraux, Anticorps neutralisants, Betacoronavirus, Coronavirus du syndrome respiratoire du Moyen-Orient, Facilitation dépendante des anticorps, Fragments Fab d'immunoglobuline, Fragments Fc des immunoglobulines, Immunoglobuline G, Infections à coronavirus, Orthomyxoviridae, Pneumopathie virale, Vaccins antiviraux, Virus de la dengue, Virus du SRAS.
- pathogénicité : Betacoronavirus.
- prévention et contrôle : Infections à coronavirus.
- usage thérapeutique : Anticorps antiviraux, Anticorps neutralisants.
- virologie : Infections à coronavirus, Pneumopathie virale.
- Animaux, Cellules HEK293, Humains, Macaca mulatta, Modèles animaux de maladie humaine, Pandémies, Rats, Souris.
English descriptors
- KwdEn :
- Animals (MeSH), Antibodies, Neutralizing (adverse effects), Antibodies, Neutralizing (immunology), Antibodies, Neutralizing (therapeutic use), Antibodies, Viral (adverse effects), Antibodies, Viral (immunology), Antibodies, Viral (therapeutic use), Antibody-Dependent Enhancement (immunology), Betacoronavirus (immunology), Betacoronavirus (pathogenicity), COVID-19 (MeSH), COVID-19 Vaccines (MeSH), Coronavirus Infections (immunology), Coronavirus Infections (prevention & control), Coronavirus Infections (virology), Dengue Virus (immunology), Disease Models, Animal (MeSH), HEK293 Cells (MeSH), Humans (MeSH), Immunoglobulin Fab Fragments (immunology), Immunoglobulin Fc Fragments (immunology), Immunoglobulin G (immunology), Macaca mulatta (MeSH), Mice (MeSH), Middle East Respiratory Syndrome Coronavirus (immunology), Orthomyxoviridae (immunology), Pandemics (MeSH), Pneumonia, Viral (immunology), Pneumonia, Viral (virology), Rats (MeSH), SARS Virus (immunology), SARS-CoV-2 (MeSH), Viral Vaccines (adverse effects), Viral Vaccines (immunology).
- MESH :
- chemical , adverse effects : Antibodies, Neutralizing, Antibodies, Viral, Viral Vaccines.
- chemical , immunology : Antibodies, Neutralizing, Antibodies, Viral, Immunoglobulin Fab Fragments, Immunoglobulin Fc Fragments, Immunoglobulin G, Viral Vaccines.
- chemical , therapeutic use : Antibodies, Neutralizing, Antibodies, Viral.
- immunology : Antibody-Dependent Enhancement, Betacoronavirus, Coronavirus Infections, Dengue Virus, Middle East Respiratory Syndrome Coronavirus, Orthomyxoviridae, Pneumonia, Viral, SARS Virus.
- pathogenicity : Betacoronavirus.
- prevention & control : Coronavirus Infections.
- virology : Coronavirus Infections, Pneumonia, Viral.
- Animals, COVID-19, COVID-19 Vaccines, Disease Models, Animal, HEK293 Cells, Humans, Macaca mulatta, Mice, Pandemics, Rats, SARS-CoV-2.
Abstract
Antibody-dependent enhancement (ADE) of disease is a general concern for the development of vaccines and antibody therapies because the mechanisms that underlie antibody protection against any virus have a theoretical potential to amplify the infection or trigger harmful immunopathology. This possibility requires careful consideration at this critical point in the pandemic of coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here we review observations relevant to the risks of ADE of disease, and their potential implications for SARS-CoV-2 infection. At present, there are no known clinical findings, immunological assays or biomarkers that can differentiate any severe viral infection from immune-enhanced disease, whether by measuring antibodies, T cells or intrinsic host responses. In vitro systems and animal models do not predict the risk of ADE of disease, in part because protective and potentially detrimental antibody-mediated mechanisms are the same and designing animal models depends on understanding how antiviral host responses may become harmful in humans. The implications of our lack of knowledge are twofold. First, comprehensive studies are urgently needed to define clinical correlates of protective immunity against SARS-CoV-2. Second, because ADE of disease cannot be reliably predicted after either vaccination or treatment with antibodies-regardless of what virus is the causative agent-it will be essential to depend on careful analysis of safety in humans as immune interventions for COVID-19 move forward.
DOI: 10.1038/s41586-020-2538-8
PubMed: 32659783
Affiliations:
- Suisse, États-Unis
- Californie, Missouri (État)
- Saint-Louis (Missouri)
- École de médecine (Université Washington de Saint-Louis)
Links toward previous steps (curation, corpus...)
Le document en format XML
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Arvin</name><affiliation wicri:level="2"><nlm:affiliation>Vir Biotechnology, San Francisco, CA, USA. aarvin@vir.bio.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Vir Biotechnology, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation><affiliation wicri:level="2"><nlm:affiliation>Stanford University School of Medicine, Stanford, CA, USA. aarvin@vir.bio.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Stanford University School of Medicine, Stanford, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Fink, Katja" sort="Fink, Katja" uniqKey="Fink K" first="Katja" last="Fink">Katja Fink</name><affiliation wicri:level="2"><nlm:affiliation>Vir Biotechnology, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Vir Biotechnology, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation><affiliation wicri:level="1"><nlm:affiliation>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona</wicri:regionArea><wicri:noRegion>Bellinzona</wicri:noRegion></affiliation></author><author><name sortKey="Schmid, Michael A" sort="Schmid, Michael A" uniqKey="Schmid M" first="Michael A" last="Schmid">Michael A. Schmid</name><affiliation wicri:level="2"><nlm:affiliation>Vir Biotechnology, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Vir Biotechnology, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation><affiliation wicri:level="1"><nlm:affiliation>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona</wicri:regionArea><wicri:noRegion>Bellinzona</wicri:noRegion></affiliation></author><author><name sortKey="Cathcart, Andrea" sort="Cathcart, Andrea" uniqKey="Cathcart A" first="Andrea" last="Cathcart">Andrea Cathcart</name><affiliation wicri:level="2"><nlm:affiliation>Vir Biotechnology, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Vir Biotechnology, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Spreafico, Roberto" sort="Spreafico, Roberto" uniqKey="Spreafico R" first="Roberto" last="Spreafico">Roberto Spreafico</name><affiliation wicri:level="2"><nlm:affiliation>Vir Biotechnology, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Vir Biotechnology, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Havenar Daughton, Colin" sort="Havenar Daughton, Colin" uniqKey="Havenar Daughton C" first="Colin" last="Havenar-Daughton">Colin Havenar-Daughton</name><affiliation wicri:level="2"><nlm:affiliation>Vir Biotechnology, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Vir Biotechnology, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Lanzavecchia, Antonio" sort="Lanzavecchia, Antonio" uniqKey="Lanzavecchia A" first="Antonio" last="Lanzavecchia">Antonio Lanzavecchia</name><affiliation wicri:level="2"><nlm:affiliation>Vir Biotechnology, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Vir Biotechnology, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation><affiliation wicri:level="1"><nlm:affiliation>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona</wicri:regionArea><wicri:noRegion>Bellinzona</wicri:noRegion></affiliation></author><author><name sortKey="Corti, Davide" sort="Corti, Davide" uniqKey="Corti D" first="Davide" last="Corti">Davide Corti</name><affiliation wicri:level="2"><nlm:affiliation>Vir Biotechnology, San Francisco, CA, USA.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Vir Biotechnology, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation><affiliation wicri:level="1"><nlm:affiliation>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona, Switzerland.</nlm:affiliation><country xml:lang="fr">Suisse</country><wicri:regionArea>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona</wicri:regionArea><wicri:noRegion>Bellinzona</wicri:noRegion></affiliation></author><author><name sortKey="Virgin, Herbert W" sort="Virgin, Herbert W" uniqKey="Virgin H" first="Herbert W" last="Virgin">Herbert W. Virgin</name><affiliation wicri:level="2"><nlm:affiliation>Vir Biotechnology, San Francisco, CA, USA. svirgin@vir.bio.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Vir Biotechnology, San Francisco, CA</wicri:regionArea><placeName><region type="state">Californie</region></placeName></affiliation><affiliation wicri:level="4"><nlm:affiliation>Washington University School of Medicine, Saint Louis, MO, USA. svirgin@vir.bio.</nlm:affiliation><country xml:lang="fr">États-Unis</country><wicri:regionArea>Washington University School of Medicine, Saint Louis, MO</wicri:regionArea><placeName><region type="state">Missouri (État)</region><settlement type="city">Saint-Louis (Missouri)</settlement></placeName><orgName type="university">École de médecine (Université Washington de Saint-Louis)</orgName></affiliation></author></analytic><series><title level="j">Nature</title><idno type="eISSN">1476-4687</idno><imprint><date when="2020" type="published">2020</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals (MeSH)</term><term>Antibodies, Neutralizing (adverse effects)</term><term>Antibodies, Neutralizing (immunology)</term><term>Antibodies, Neutralizing (therapeutic use)</term><term>Antibodies, Viral (adverse effects)</term><term>Antibodies, Viral (immunology)</term><term>Antibodies, Viral (therapeutic use)</term><term>Antibody-Dependent Enhancement (immunology)</term><term>Betacoronavirus (immunology)</term><term>Betacoronavirus (pathogenicity)</term><term>COVID-19 (MeSH)</term><term>COVID-19 Vaccines (MeSH)</term><term>Coronavirus Infections (immunology)</term><term>Coronavirus Infections (prevention & control)</term><term>Coronavirus Infections (virology)</term><term>Dengue Virus (immunology)</term><term>Disease Models, Animal (MeSH)</term><term>HEK293 Cells (MeSH)</term><term>Humans (MeSH)</term><term>Immunoglobulin Fab Fragments (immunology)</term><term>Immunoglobulin Fc Fragments (immunology)</term><term>Immunoglobulin G (immunology)</term><term>Macaca mulatta (MeSH)</term><term>Mice (MeSH)</term><term>Middle East Respiratory Syndrome Coronavirus (immunology)</term><term>Orthomyxoviridae (immunology)</term><term>Pandemics (MeSH)</term><term>Pneumonia, Viral (immunology)</term><term>Pneumonia, Viral (virology)</term><term>Rats (MeSH)</term><term>SARS Virus (immunology)</term><term>SARS-CoV-2 (MeSH)</term><term>Viral Vaccines (adverse effects)</term><term>Viral Vaccines (immunology)</term></keywords><keywords scheme="KwdFr" xml:lang="fr"><term>Animaux (MeSH)</term><term>Anticorps antiviraux (effets indésirables)</term><term>Anticorps antiviraux (immunologie)</term><term>Anticorps antiviraux (usage thérapeutique)</term><term>Anticorps neutralisants (effets indésirables)</term><term>Anticorps neutralisants (immunologie)</term><term>Anticorps neutralisants (usage thérapeutique)</term><term>Betacoronavirus (immunologie)</term><term>Betacoronavirus (pathogénicité)</term><term>Cellules HEK293 (MeSH)</term><term>Coronavirus du syndrome respiratoire du Moyen-Orient (immunologie)</term><term>Facilitation dépendante des anticorps (immunologie)</term><term>Fragments Fab d'immunoglobuline (immunologie)</term><term>Fragments Fc des immunoglobulines (immunologie)</term><term>Humains (MeSH)</term><term>Immunoglobuline G (immunologie)</term><term>Infections à coronavirus (immunologie)</term><term>Infections à coronavirus (prévention et contrôle)</term><term>Infections à coronavirus (virologie)</term><term>Macaca mulatta (MeSH)</term><term>Modèles animaux de maladie humaine (MeSH)</term><term>Orthomyxoviridae (immunologie)</term><term>Pandémies (MeSH)</term><term>Pneumopathie virale (immunologie)</term><term>Pneumopathie virale (virologie)</term><term>Rats (MeSH)</term><term>Souris (MeSH)</term><term>Vaccins antiviraux (effets indésirables)</term><term>Vaccins antiviraux (immunologie)</term><term>Virus de la dengue (immunologie)</term><term>Virus du SRAS (immunologie)</term></keywords><keywords scheme="MESH" type="chemical" qualifier="adverse effects" xml:lang="en"><term>Antibodies, Neutralizing</term><term>Antibodies, Viral</term><term>Viral Vaccines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antibodies, Neutralizing</term><term>Antibodies, Viral</term><term>Immunoglobulin Fab Fragments</term><term>Immunoglobulin Fc Fragments</term><term>Immunoglobulin G</term><term>Viral Vaccines</term></keywords><keywords scheme="MESH" type="chemical" qualifier="therapeutic use" xml:lang="en"><term>Antibodies, Neutralizing</term><term>Antibodies, Viral</term></keywords><keywords scheme="MESH" qualifier="effets indésirables" xml:lang="fr"><term>Anticorps antiviraux</term><term>Anticorps neutralisants</term><term>Vaccins antiviraux</term></keywords><keywords scheme="MESH" qualifier="immunologie" xml:lang="fr"><term>Anticorps antiviraux</term><term>Anticorps neutralisants</term><term>Betacoronavirus</term><term>Coronavirus du syndrome respiratoire du Moyen-Orient</term><term>Facilitation dépendante des anticorps</term><term>Fragments Fab d'immunoglobuline</term><term>Fragments Fc des immunoglobulines</term><term>Immunoglobuline G</term><term>Infections à coronavirus</term><term>Orthomyxoviridae</term><term>Pneumopathie virale</term><term>Vaccins antiviraux</term><term>Virus de la dengue</term><term>Virus du SRAS</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Antibody-Dependent Enhancement</term><term>Betacoronavirus</term><term>Coronavirus Infections</term><term>Dengue Virus</term><term>Middle East Respiratory Syndrome Coronavirus</term><term>Orthomyxoviridae</term><term>Pneumonia, Viral</term><term>SARS Virus</term></keywords><keywords scheme="MESH" qualifier="pathogenicity" xml:lang="en"><term>Betacoronavirus</term></keywords><keywords scheme="MESH" qualifier="pathogénicité" xml:lang="fr"><term>Betacoronavirus</term></keywords><keywords scheme="MESH" qualifier="prevention & control" xml:lang="en"><term>Coronavirus Infections</term></keywords><keywords scheme="MESH" qualifier="prévention et contrôle" xml:lang="fr"><term>Infections à coronavirus</term></keywords><keywords scheme="MESH" qualifier="usage thérapeutique" xml:lang="fr"><term>Anticorps antiviraux</term><term>Anticorps neutralisants</term></keywords><keywords scheme="MESH" qualifier="virologie" xml:lang="fr"><term>Infections à coronavirus</term><term>Pneumopathie virale</term></keywords><keywords scheme="MESH" qualifier="virology" xml:lang="en"><term>Coronavirus Infections</term><term>Pneumonia, Viral</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>COVID-19</term><term>COVID-19 Vaccines</term><term>Disease Models, Animal</term><term>HEK293 Cells</term><term>Humans</term><term>Macaca mulatta</term><term>Mice</term><term>Pandemics</term><term>Rats</term><term>SARS-CoV-2</term></keywords><keywords scheme="MESH" xml:lang="fr"><term>Animaux</term><term>Cellules HEK293</term><term>Humains</term><term>Macaca mulatta</term><term>Modèles animaux de maladie humaine</term><term>Pandémies</term><term>Rats</term><term>Souris</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Antibody-dependent enhancement (ADE) of disease is a general concern for the development of vaccines and antibody therapies because the mechanisms that underlie antibody protection against any virus have a theoretical potential to amplify the infection or trigger harmful immunopathology. This possibility requires careful consideration at this critical point in the pandemic of coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here we review observations relevant to the risks of ADE of disease, and their potential implications for SARS-CoV-2 infection. At present, there are no known clinical findings, immunological assays or biomarkers that can differentiate any severe viral infection from immune-enhanced disease, whether by measuring antibodies, T cells or intrinsic host responses. In vitro systems and animal models do not predict the risk of ADE of disease, in part because protective and potentially detrimental antibody-mediated mechanisms are the same and designing animal models depends on understanding how antiviral host responses may become harmful in humans. The implications of our lack of knowledge are twofold. First, comprehensive studies are urgently needed to define clinical correlates of protective immunity against SARS-CoV-2. Second, because ADE of disease cannot be reliably predicted after either vaccination or treatment with antibodies-regardless of what virus is the causative agent-it will be essential to depend on careful analysis of safety in humans as immune interventions for COVID-19 move forward.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">32659783</PMID><DateCompleted><Year>2020</Year><Month>08</Month><Day>27</Day></DateCompleted><DateRevised><Year>2021</Year><Month>01</Month><Day>19</Day></DateRevised><Article PubModel="Print-Electronic"><Journal><ISSN IssnType="Electronic">1476-4687</ISSN><JournalIssue CitedMedium="Internet"><Volume>584</Volume><Issue>7821</Issue><PubDate><Year>2020</Year><Month>08</Month></PubDate></JournalIssue><Title>Nature</Title><ISOAbbreviation>Nature</ISOAbbreviation></Journal><ArticleTitle>A perspective on potential antibody-dependent enhancement of SARS-CoV-2.</ArticleTitle><Pagination><MedlinePgn>353-363</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1038/s41586-020-2538-8</ELocationID><Abstract><AbstractText>Antibody-dependent enhancement (ADE) of disease is a general concern for the development of vaccines and antibody therapies because the mechanisms that underlie antibody protection against any virus have a theoretical potential to amplify the infection or trigger harmful immunopathology. This possibility requires careful consideration at this critical point in the pandemic of coronavirus disease 2019 (COVID-19), which is caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). Here we review observations relevant to the risks of ADE of disease, and their potential implications for SARS-CoV-2 infection. At present, there are no known clinical findings, immunological assays or biomarkers that can differentiate any severe viral infection from immune-enhanced disease, whether by measuring antibodies, T cells or intrinsic host responses. In vitro systems and animal models do not predict the risk of ADE of disease, in part because protective and potentially detrimental antibody-mediated mechanisms are the same and designing animal models depends on understanding how antiviral host responses may become harmful in humans. The implications of our lack of knowledge are twofold. First, comprehensive studies are urgently needed to define clinical correlates of protective immunity against SARS-CoV-2. Second, because ADE of disease cannot be reliably predicted after either vaccination or treatment with antibodies-regardless of what virus is the causative agent-it will be essential to depend on careful analysis of safety in humans as immune interventions for COVID-19 move forward.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Arvin</LastName><ForeName>Ann M</ForeName><Initials>AM</Initials><AffiliationInfo><Affiliation>Vir Biotechnology, San Francisco, CA, USA. aarvin@vir.bio.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Stanford University School of Medicine, Stanford, CA, USA. aarvin@vir.bio.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Fink</LastName><ForeName>Katja</ForeName><Initials>K</Initials><AffiliationInfo><Affiliation>Vir Biotechnology, San Francisco, CA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Schmid</LastName><ForeName>Michael A</ForeName><Initials>MA</Initials><AffiliationInfo><Affiliation>Vir Biotechnology, San Francisco, CA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Cathcart</LastName><ForeName>Andrea</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Vir Biotechnology, San Francisco, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Spreafico</LastName><ForeName>Roberto</ForeName><Initials>R</Initials><AffiliationInfo><Affiliation>Vir Biotechnology, San Francisco, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Havenar-Daughton</LastName><ForeName>Colin</ForeName><Initials>C</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-2880-3927</Identifier><AffiliationInfo><Affiliation>Vir Biotechnology, San Francisco, CA, USA.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lanzavecchia</LastName><ForeName>Antonio</ForeName><Initials>A</Initials><AffiliationInfo><Affiliation>Vir Biotechnology, San Francisco, CA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Corti</LastName><ForeName>Davide</ForeName><Initials>D</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-5797-1364</Identifier><AffiliationInfo><Affiliation>Vir Biotechnology, San Francisco, CA, USA.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Humabs Biomed SA, a subsidiary of Vir Biotechnology, Bellinzona, Switzerland.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Virgin</LastName><ForeName>Herbert W</ForeName><Initials>HW</Initials><Identifier Source="ORCID">http://orcid.org/0000-0001-8580-7628</Identifier><AffiliationInfo><Affiliation>Vir Biotechnology, San Francisco, CA, USA. svirgin@vir.bio.</Affiliation></AffiliationInfo><AffiliationInfo><Affiliation>Washington University School of Medicine, Saint Louis, MO, USA. svirgin@vir.bio.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2020</Year><Month>07</Month><Day>13</Day></ArticleDate></Article><MedlineJournalInfo><Country>England</Country><MedlineTA>Nature</MedlineTA><NlmUniqueID>0410462</NlmUniqueID><ISSNLinking>0028-0836</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D057134">Antibodies, 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PubStatus="entrez"><Year>2020</Year><Month>7</Month><Day>14</Day><Hour>6</Hour><Minute>0</Minute></PubMedPubDate></History><PublicationStatus>ppublish</PublicationStatus><ArticleIdList><ArticleId IdType="pubmed">32659783</ArticleId><ArticleId IdType="doi">10.1038/s41586-020-2538-8</ArticleId><ArticleId IdType="pii">10.1038/s41586-020-2538-8</ArticleId></ArticleIdList><ReferenceList><Reference><Citation>Luke, T. C., Kilbane, E. M., Jackson, J. L. & Hoffman, S. L. Meta-analysis: convalescent blood products for Spanish influenza pneumonia: a future H5N1 treatment? Ann. Intern. Med. 145, 599–609 (2006).</Citation><ArticleIdList><ArticleId IdType="pubmed">16940336</ArticleId></ArticleIdList></Reference><Reference><Citation>Casadevall, A., Dadachova, E. & Pirofski, L. A. Passive antibody therapy for infectious diseases. Nat. Rev. Microbiol. 2, 695–703 (2004).</Citation><ArticleIdList><ArticleId IdType="pubmed">15372080</ArticleId></ArticleIdList></Reference><Reference><Citation>Plotkin, S. A. Correlates of protection induced by vaccination. Clin. Vaccine Immunol. 17, 1055–1065 (2010).</Citation><ArticleIdList><ArticleId IdType="pubmed">2897268</ArticleId><ArticleId IdType="pmcid">2897268</ArticleId></ArticleIdList></Reference><Reference><Citation>VanBlargan, L. A., Goo, L. & Pierson, T. C. Deconstructing the antiviral neutralizing-antibody response: implications for vaccine development and immunity. Microbiol. Mol. Biol. Rev. 80, 989–1010 (2016).</Citation><ArticleIdList><ArticleId IdType="pubmed">27784796</ArticleId><ArticleId IdType="pmcid">5116878</ArticleId></ArticleIdList></Reference><Reference><Citation>Corti, D. & Lanzavecchia, A. Broadly neutralizing antiviral antibodies. Ann. Rev. Immunol. 31, 705–742 (2013).</Citation></Reference><Reference><Citation>Walker, L. M. & Burton, D. R. Passive immunotherapy of viral infections: ‘super-antibodies’ enter the fray. Nat. Rev. Immunol. 18, 297–308 (2018).</Citation><ArticleIdList><ArticleId IdType="pubmed">29379211</ArticleId><ArticleId IdType="pmcid">5918154</ArticleId></ArticleIdList></Reference><Reference><Citation>Lu, L. L., Suscovich, T. J., Fortune, S. M. & Alter, G. Beyond binding: antibody effector functions in infectious diseases. Nat. Rev. Immunol. 18, 46–61 (2018).</Citation><ArticleIdList><ArticleId IdType="pubmed">29063907</ArticleId></ArticleIdList></Reference><Reference><Citation>Bournazos, S. & Ravetch, J. V. Fcγ receptor function and the design of vaccination strategies. Immunity 47, 224–233 (2017).</Citation><ArticleIdList><ArticleId IdType="pubmed">28813656</ArticleId><ArticleId IdType="pmcid">5573140</ArticleId></ArticleIdList></Reference><Reference><Citation>DiLillo, D. J., Tan, G. S., Palese, P. & Ravetch, J. V. Broadly neutralizing hemagglutinin stalk-specific antibodies require FcγR interactions for protection against influenza virus in vivo. Nat. Med. 20, 143–151 (2014).</Citation><ArticleIdList><ArticleId IdType="pubmed">24412922</ArticleId><ArticleId IdType="pmcid">3966466</ArticleId></ArticleIdList></Reference><Reference><Citation>Bournazos, S. et al. Broadly neutralizing anti-HIV-1 antibodies require Fc effector functions for in vivo activity. Cell 158, 1243–1253 (2014).</Citation><ArticleIdList><ArticleId IdType="pubmed">25215485</ArticleId><ArticleId IdType="pmcid">4167398</ArticleId></ArticleIdList></Reference><Reference><Citation>Pyzik, M. et al. The neonatal Fc receptor (FcRn): a misnomer? Front. Immunol. 10, 1540 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">31354709</ArticleId><ArticleId IdType="pmcid">6636548</ArticleId></ArticleIdList></Reference><Reference><Citation>Bergtold, A., Desai, D. D., Gavhane, A. & Clynes, R. Cell surface recycling of internalized antigen permits dendritic cell priming of B cells. Immunity 23, 503–514 (2005).</Citation><ArticleIdList><ArticleId IdType="pubmed">16286018</ArticleId></ArticleIdList></Reference><Reference><Citation>Nishimura, Y. et al. Early antibody therapy can induce long-lasting immunity to SHIV. Nature 543, 559–563 (2017).</Citation><ArticleIdList><ArticleId IdType="pubmed">28289286</ArticleId><ArticleId IdType="pmcid">5458531</ArticleId></ArticleIdList></Reference><Reference><Citation>Gunn, B. M. et al. A Role for Fc function in therapeutic monoclonal antibody-mediated protection against Ebola virus. Cell Host Microbe 24, 221–233.e5 (2018).</Citation><ArticleIdList><ArticleId IdType="pubmed">30092199</ArticleId><ArticleId IdType="pmcid">6298217</ArticleId></ArticleIdList></Reference><Reference><Citation>Graham, B. S. Rapid COVID-19 vaccine development. Science 368, 945–946 (2020).</Citation></Reference><Reference><Citation>Kim, H. W. et al. Respiratory syncytial virus disease in infants despite prior administration of antigenic inactivated vaccine. Am. J. Epidemiol. 89, 422–434 (1969).</Citation><ArticleIdList><ArticleId IdType="pubmed">4305198</ArticleId></ArticleIdList></Reference><Reference><Citation>Kapikian, A. Z., Mitchell, R. H., Chanock, R. M., Shvedoff, R. A. & Stewart, C. E. An epidemiologic study of altered clinical reactivity to respiratory syncytial (RS) virus infection in children previously vaccinated with an inactivated RS virus vaccine. Am. J. Epidemiol. 89, 405–421 (1969).</Citation><ArticleIdList><ArticleId IdType="pubmed">4305197</ArticleId></ArticleIdList></Reference><Reference><Citation>Polack, F. P., Hoffman, S. J., Crujeiras, G. & Griffin, D. E. A role for nonprotective complement-fixing antibodies with low avidity for measles virus in atypical measles. Nat. Med. 9, 1209–1213 (2003).</Citation><ArticleIdList><ArticleId IdType="pubmed">12925847</ArticleId></ArticleIdList></Reference><Reference><Citation>Simmons, C. P., Farrar, J. J., Nguyen, V. & Wills, B. Dengue. N. Engl. J. Med. 366, 1423–1432 (2012).</Citation></Reference><Reference><Citation>Katzelnick, L. C. et al. Antibody-dependent enhancement of severe dengue disease in humans. Science 358, 929–932 (2017).</Citation><ArticleIdList><ArticleId IdType="pubmed">29097492</ArticleId><ArticleId IdType="pmcid">5858873</ArticleId></ArticleIdList></Reference><Reference><Citation>Guzman, M. G., Alvarez, M. & Halstead, S. B. Secondary infection as a risk factor for dengue hemorrhagic fever/dengue shock syndrome: an historical perspective and role of antibody-dependent enhancement of infection. Arch. Virol. 158, 1445–1459 (2013).</Citation><ArticleIdList><ArticleId IdType="pubmed">23471635</ArticleId></ArticleIdList></Reference><Reference><Citation>Iwasaki, A. & Yang, Y. The potential danger of suboptimal antibody responses in COVID-19. Nat. Rev. Immunol. 20, 339–341 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32317716</ArticleId></ArticleIdList></Reference><Reference><Citation>Dekkers, G. et al. Affinity of human IgG subclasses to mouse Fc gamma receptors. MAbs 9, 767–773 (2017).</Citation><ArticleIdList><ArticleId IdType="pubmed">28463043</ArticleId><ArticleId IdType="pmcid">5524164</ArticleId></ArticleIdList></Reference><Reference><Citation>Crowley, A. R. & Ackerman, M. E. Mind the gap: how interspecies variability in IgG and its receptors may complicate comparisons of human and non-human primate effector function. Front. Immunol. 10, 697 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">31024542</ArticleId><ArticleId IdType="pmcid">6463756</ArticleId></ArticleIdList></Reference><Reference><Citation>Fulginiti, V. A. et al. Respiratory virus immunization. A field trial of two inactivated respiratory virus vaccines; an aqueous trivalent parainfluenza virus vaccine and an alum-precipitated respiratory syncytial virus vaccine. Am. J. Epidemiol. 89, 435–448 (1969).</Citation><ArticleIdList><ArticleId IdType="pubmed">4305199</ArticleId></ArticleIdList></Reference><Reference><Citation>Chin, J., Magoffin, R. L., Shearer, L. A., Schieble, J. H. & Lennette, E. H. Field evaluation of a respiratory syncytial virus vaccine and a trivalent parainfluenza virus vaccine in a pediatric population. Am. J. Epidemiol. 89, 449–463 (1969).</Citation><ArticleIdList><ArticleId IdType="pubmed">4305200</ArticleId></ArticleIdList></Reference><Reference><Citation>Murphy, B. R. et al. Dissociation between serum neutralizing and glycoprotein antibody responses of infants and children who received inactivated respiratory syncytial virus vaccine. J. Clin. Microbiol. 24, 197–202 (1986).</Citation><ArticleIdList><ArticleId IdType="pubmed">3755730</ArticleId><ArticleId IdType="pmcid">268874</ArticleId></ArticleIdList></Reference><Reference><Citation>Polack, F. P. et al. A role for immune complexes in enhanced respiratory syncytial virus disease. J. Exp. Med. 196, 859–865 (2002).</Citation><ArticleIdList><ArticleId IdType="pubmed">12235218</ArticleId><ArticleId IdType="pmcid">2194058</ArticleId></ArticleIdList></Reference><Reference><Citation>Atkinson, J. P. et al. The human complement system: basic concepts and clinical relevance. Clin. Immunol. https://doi.org/10.1016/B978-0-7020-6896-6.00021-1 (2019).</Citation></Reference><Reference><Citation>Kim, H. W. et al. Cell-mediated immunity to respiratory syncytial virus induced by inactivated vaccine or by infection. Pediatr. Res. 10, 75–78 (1976).</Citation><ArticleIdList><ArticleId IdType="pubmed">1246465</ArticleId></ArticleIdList></Reference><Reference><Citation>van Erp, E. A., Luytjes, W., Ferwerda, G. & van Kasteren, P. B. Fc-mediated antibody effector functions during respiratory syncytial virus infection and disease. Front. Immunol. 10, 548 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">30967872</ArticleId><ArticleId IdType="pmcid">6438959</ArticleId></ArticleIdList></Reference><Reference><Citation>Delgado, M. F. et al. Lack of antibody affinity maturation due to poor Toll-like receptor stimulation leads to enhanced respiratory syncytial virus disease. Nat. Med. 15, 34–41 (2009).</Citation><ArticleIdList><ArticleId IdType="pubmed">19079256</ArticleId></ArticleIdList></Reference><Reference><Citation>Ruckwardt, T. J., Morabito, K. M. & Graham, B. S. Immunological lessons from respiratory syncytial virus vaccine development. Immunity 51, 429–442 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">31533056</ArticleId></ArticleIdList></Reference><Reference><Citation>Aranda, S. S. & Polack, F. P. Prevention of pediatric respiratory syncytial virus lower respiratory tract illness: perspectives for the next decade. Front. Immunol. 10, 1006 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">31134078</ArticleId><ArticleId IdType="pmcid">6524688</ArticleId></ArticleIdList></Reference><Reference><Citation>Regeneron to discontinue development of Suptavumab for respiratory syncytial virus. https://investor.regeneron.com/news-releases/news-release-details/regeneron-discontinue-development-suptavumab-respiratory (2017).</Citation></Reference><Reference><Citation>Domachowske, J. B. et al. Safety, tolerability and pharmacokinetics of MEDI8897, an extended half-life single-dose respiratory syncytial virus prefusion F-targeting monoclonal antibody administered as a single dose to healthy preterm infants. Pediatr. Infect. Dis. J. 37, 886–892 (2018).</Citation><ArticleIdList><ArticleId IdType="pubmed">29373476</ArticleId><ArticleId IdType="pmcid">6133204</ArticleId></ArticleIdList></Reference><Reference><Citation>Ng, S. et al. Novel correlates of protection against pandemic H1N1 influenza A virus infection. Nat. Med. 25, 962–967 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">31160818</ArticleId><ArticleId IdType="pmcid">6608747</ArticleId></ArticleIdList></Reference><Reference><Citation>Skowronski, D. M. et al. Association between the 2008–09 seasonal influenza vaccine and pandemic H1N1 illness during spring–summer 2009: four observational studies from Canada. PLoS Med. 7, e1000258 (2010).</Citation><ArticleIdList><ArticleId IdType="pubmed">20386731</ArticleId><ArticleId IdType="pmcid">2850386</ArticleId></ArticleIdList></Reference><Reference><Citation>Wu, J. T. et al. The infection attack rate and severity of 2009 pandemic H1N1 influenza in Hong Kong. Clin. Infect. Dis. 51, 1184–1191 (2010).</Citation><ArticleIdList><ArticleId IdType="pubmed">20964521</ArticleId><ArticleId IdType="pmcid">3034199</ArticleId></ArticleIdList></Reference><Reference><Citation>Lansbury, L. E. et al. Effectiveness of 2009 pandemic influenza A(H1N1) vaccines: a systematic review and meta-analysis. Vaccine 35, 1996–2006 (2017).</Citation><ArticleIdList><ArticleId IdType="pubmed">28302409</ArticleId></ArticleIdList></Reference><Reference><Citation>Osterholm, M. T., Kelley, N. S., Sommer, A. & Belongia, E. A. Efficacy and effectiveness of influenza vaccines: a systematic review and meta-analysis. Lancet Infect. Dis. 12, 36–44 (2012).</Citation><ArticleIdList><ArticleId IdType="pubmed">22032844</ArticleId></ArticleIdList></Reference><Reference><Citation>Monsalvo, A. C. et al. Severe pandemic 2009 H1N1 influenza disease due to pathogenic immune complexes. Nat. Med. 17, 195–199 (2011).</Citation><ArticleIdList><ArticleId IdType="pubmed">21131958</ArticleId></ArticleIdList></Reference><Reference><Citation>Co, M. D. T. et al. Relationship of preexisting influenza hemagglutination inhibition, complement-dependent lytic, and antibody-dependent cellular cytotoxicity antibodies to the development of clinical illness in a prospective study of A(H1N1)pdm09 influenza in children. Viral Immunol. 27, 375–382 (2014).</Citation><ArticleIdList><ArticleId IdType="pubmed">25141276</ArticleId><ArticleId IdType="pmcid">4183906</ArticleId></ArticleIdList></Reference><Reference><Citation>Khurana, S. et al. Vaccine-induced anti-HA2 antibodies promote virus fusion and enhance influenza virus respiratory disease. Sci. Transl. Med. 5, 200ra114 (2013).</Citation><ArticleIdList><ArticleId IdType="pubmed">23986398</ArticleId></ArticleIdList></Reference><Reference><Citation>Winarski, K. L. et al. Antibody-dependent enhancement of influenza disease promoted by increase in hemagglutinin stem flexibility and virus fusion kinetics. Proc. Natl Acad. Sci. USA 116, 15194–15199 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">31296560</ArticleId></ArticleIdList></Reference><Reference><Citation>Beltramello, M. et al. The human immune response to dengue virus is dominated by highly cross-reactive antibodies endowed with neutralizing and enhancing activity. Cell Host Microbe 8, 271–283 (2010).</Citation><ArticleIdList><ArticleId IdType="pubmed">20833378</ArticleId></ArticleIdList></Reference><Reference><Citation>de Alwis, R. et al. Dengue viruses are enhanced by distinct populations of serotype cross-reactive antibodies in human immune sera. PLoS Pathog. 10, e1004386 (2014).</Citation><ArticleIdList><ArticleId IdType="pubmed">25275316</ArticleId><ArticleId IdType="pmcid">4183589</ArticleId></ArticleIdList></Reference><Reference><Citation>Thomas, S. J. & Yoon, I.-K. A review of Dengvaxia®: development to deployment. Hum. Vaccin. Immunother. 15, 2295–2314 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">31589551</ArticleId><ArticleId IdType="pmcid">6816420</ArticleId></ArticleIdList></Reference><Reference><Citation>WHO Report. Dengue vaccine: WHO position paper, September 2018 – Recommendations. Vaccine 37, 4848–4849 (2019).</Citation></Reference><Reference><Citation>Rodriguez-Barraquer, I. et al. Impact of preexisting dengue immunity on Zika virus emergence in a dengue endemic region. Science 363, 607–610 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">30733412</ArticleId></ArticleIdList></Reference><Reference><Citation>Chan, K. R. et al. Cross-reactive antibodies enhance live attenuated virus infection for increased immunogenicity. Nat. Microbiol. 1, 16164 (2016).</Citation><ArticleIdList><ArticleId IdType="pubmed">27642668</ArticleId><ArticleId IdType="pmcid">7097525</ArticleId></ArticleIdList></Reference><Reference><Citation>Browne, S. K., Beeler, J. A. & Roberts, J. N. Summary of the vaccines and related biological products advisory committee meeting held to consider evaluation of vaccine candidates for the prevention of respiratory syncytial virus disease in RSV-naïve infants. Vaccine 38, 101–106 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">31706809</ArticleId></ArticleIdList></Reference><Reference><Citation>Hoffmann, M. et al. SARS-CoV-2 cell entry depends on ACE2 and TMPRSS2 and is blocked by a clinically proven protease inhibitor. Cell 181, 271–280.e8 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32142651</ArticleId><ArticleId IdType="pmcid">32142651</ArticleId></ArticleIdList></Reference><Reference><Citation>Walls, A. C. et al. Structure, function, and antigenicity of the SARS-CoV-2 spike glycoprotein. Cell 181, 281–292.e6 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">7102599</ArticleId><ArticleId IdType="pmcid">7102599</ArticleId></ArticleIdList></Reference><Reference><Citation>Wrapp, D. et al. Cryo-EM structure of the 2019-nCoV spike in the prefusion conformation. Science 367, 1260–1263 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32075877</ArticleId><ArticleId IdType="pmcid">7164637</ArticleId></ArticleIdList></Reference><Reference><Citation>Muus, C. et al. Integrated analyses of single-cell atlases reveal age, gender, and smoking status associations with cell type-specific expression of mediators of SARS-CoV-2 viral entry and highlights inflammatory programs in putative target cells. Preprint at https://www.biorxiv.org/content/10.1101/2020.04.19.049254v2 (2020).</Citation></Reference><Reference><Citation>Sungnak, W. et al. SARS-CoV-2 entry factors are highly expressed in nasal epithelial cells together with innate immune genes. Nat. Med. 26, 681–687 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32327758</ArticleId></ArticleIdList></Reference><Reference><Citation>Ziegler, C. et al. SARS-CoV-2 receptor ACE2 is an interferon-stimulated gene in human airway epithelial cells and is enriched in specific cell subsets across tissues. Cell 181, 1016–1035.e19 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32413319</ArticleId><ArticleId IdType="pmcid">7252096</ArticleId></ArticleIdList></Reference><Reference><Citation>Wellcome Sanger Institute, Human Cell Atlas & Chan Zuckerberg Initiative. COVID-19 Cell Atlas, https://www.covid19cellatlas.org/</Citation></Reference><Reference><Citation>Chan Zuckerberg Biohub & Stanford University. Lung Cell Atlas, https://hlca.ds.czbiohub.org/</Citation></Reference><Reference><Citation>Ng, K. et al. Pre-existing and de novo humoral immunity to SARS-CoV-2 in humans. Preprint at https://www.biorxiv.org/content/10.1101/2020.05.14.095414v1 (2020).</Citation></Reference><Reference><Citation>Braun, J. et al. Presence of SARS-CoV-2 reactive T cells in COVID-19 patients and healthy donors. Preprint at https://www.medrxiv.org/content/10.1101/2020.04.17.20061440v1 (2020). Detection of anti-S protein CD4 <sup>+</sup> T cells in 83% patients with COVID-19 with reactivity to epitopes in both N- and C-terminal domains, and in 34% of healthy unexposed donors, indicating cross-reactive T cell immunity against SARS-CoV-2 attributable to previous coronavirus infections, with epitopes predominantly in the C-terminal domain that has higher homology to other coronaviruses.</Citation></Reference><Reference><Citation>Grifoni, A. et al. Targets of T cell responses to SARS-CoV-2 coronavirus in humans with COVID-19 disease and unexposed individuals. Cell 181, 1489–1501.e15 (2020). Extensive analysis of CD4 and CD8 T cell responses to epitopes of S-, M- and N proteins as well as non-structural proteins of SARS-CoV-2 in convalescent patients with COVID-19 and detection of cross-reactive CD4 <sup>+</sup> T cells that recognized SAR-CoV-2 epitopes in 40–60% of unexposed donors.</Citation><ArticleIdList><ArticleId IdType="pubmed">32473127</ArticleId><ArticleId IdType="pmcid">7237901</ArticleId></ArticleIdList></Reference><Reference><Citation>van der Hoek, L., Pyrc, K. & Berkhout, B. Human coronavirus NL63, a new respiratory virus. FEMS Microbiol. Rev. 30, 760–773 (2006).</Citation><ArticleIdList><ArticleId IdType="pubmed">16911043</ArticleId></ArticleIdList></Reference><Reference><Citation>Callow, K. A., Parry, H. F., Sergeant, M. & Tyrrell, D. A. J. The time course of the immune response to experimental coronavirus infection of man. Epidemiol. Infect. 105, 435–446 (1990).</Citation><ArticleIdList><ArticleId IdType="pubmed">2170159</ArticleId><ArticleId IdType="pmcid">2271881</ArticleId></ArticleIdList></Reference><Reference><Citation>Reed, S. E. The behaviour of recent isolates of human respiratory coronavirus in vitro and in volunteers: evidence of heterogeneity among 229E-related strains. J. Med. Virol. 13, 179–192 (1984).</Citation><ArticleIdList><ArticleId IdType="pubmed">6319590</ArticleId><ArticleId IdType="pmcid">7166702</ArticleId></ArticleIdList></Reference><Reference><Citation>Chan, K. H. et al. Serological responses in patients with severe acute respiratory syndrome coronavirus infection and cross-reactivity with human coronaviruses 229E, OC43, and NL63. Clin. Diagn. Lab. Immunol. 12, 1317–1321 (2005).</Citation><ArticleIdList><ArticleId IdType="pubmed">16275947</ArticleId><ArticleId IdType="pmcid">1287763</ArticleId></ArticleIdList></Reference><Reference><Citation>Kissler, S. M., Tedijanto, C., Goldstein, E., Grad, Y. H. & Lipsitch, M. Projecting the transmission dynamics of SARS-CoV-2 through the postpandemic period. Science 368, 860–868 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32291278</ArticleId></ArticleIdList></Reference><Reference><Citation>Pinto, D. et al. Cross-neutralization of SARS-CoV-2 by a human monoclonal SARS-CoV antibody. Nature 583, 290–295 (2020).</Citation></Reference><Reference><Citation>Okba, N. M. A. et al. Severe acute respiratory syndrome coronavirus 2−specific antibody responses in coronavirus disease patients. Emerging Infect. Dis. 26, 1478–1488 (2020).</Citation><ArticleIdList><ArticleId IdType="pmcid">7323511</ArticleId></ArticleIdList></Reference><Reference><Citation>Lv, H. et al. Cross-reactive antibody response between SARS-CoV-2 and SARS-CoV infections. Cell Reports 31, 107725 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32426212</ArticleId><ArticleId IdType="pmcid">7231734</ArticleId></ArticleIdList></Reference><Reference><Citation>Guo, X. et al. Long-term persistence of IgG antibodies in SARS-CoV infected healthcare workers. Preprint at https://www.medrxiv.org/content/10.1101/2020.02.12.20021386v1 (2020).</Citation></Reference><Reference><Citation>Lavezzo, E. et al. Suppression of COVID-19 outbreak in the municipality of Vo, Italy. Nature https://doi.org/10.1038/s41586-020-2488-1 (2020).</Citation></Reference><Reference><Citation>Yeh, K.-M. et al. Experience of using convalescent plasma for severe acute respiratory syndrome among healthcare workers in a Taiwan hospital. J. Antimicrob. Chemother. 56, 919–922 (2005).</Citation><ArticleIdList><ArticleId IdType="pubmed">16183666</ArticleId><ArticleId IdType="pmcid">7110092</ArticleId></ArticleIdList></Reference><Reference><Citation>Cheng, Y. et al. Use of convalescent plasma therapy in SARS patients in Hong Kong. Eur. J. Clin. Microbiol. Infect. Dis. 24, 44–46 (2005).</Citation></Reference><Reference><Citation>Mair-Jenkins, J. et al. The effectiveness of convalescent plasma and hyperimmune immunoglobulin for the treatment of severe acute respiratory infections of viral etiology: a systematic review and exploratory meta-analysis. J. Infect. Dis. 211, 80–90 (2015).</Citation><ArticleIdList><ArticleId IdType="pubmed">25030060</ArticleId></ArticleIdList></Reference><Reference><Citation>Ko, J.-H. et al. Challenges of convalescent plasma infusion therapy in Middle East respiratory coronavirus infection: a single centre experience. Antivir. Ther. 23, 617–622 (2018).</Citation><ArticleIdList><ArticleId IdType="pubmed">29923831</ArticleId></ArticleIdList></Reference><Reference><Citation>Duan, K. et al. Effectiveness of convalescent plasma therapy in severe COVID-19 patients. Proc. Natl Acad. Sci. USA 117, 9490–9496 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32253318</ArticleId></ArticleIdList></Reference><Reference><Citation>Shen, C. et al. Treatment of 5 critically ill patients with COVID-19 with convalescent plasma. J. Am. Med. Assoc. 323, 1582–1589 (2020).</Citation></Reference><Reference><Citation>Li, L. et al. Effect of convalescent plasma therapy on time to clinical improvement in patients with severe and life-threatening COVID-19: a randomized clinical trial. J. Am. Med. Assoc. https://doi.org/10.1001/jama.2020.10044 (2020).</Citation></Reference><Reference><Citation>Joyner, M. J. & Wright, R. S. Safety update: COVID-19 convalescent plasma in 20,000 hospitalized patients. Mayo Clin. Proc. https://doi.org/10.1016/j.mayocp.2020.06.028 (2020). Major US-wide study of the administration of convalescent plasma to patients with COVID-19 with severe respiratory disease, followed by observation for seven days post-infusion with no evidence of disease progression associated with passive-antibody therapy.</Citation></Reference><Reference><Citation>Chen, L., Xiong, J., Bao, L. & Shi, Y. Convalescent plasma as a potential therapy for COVID-19. Lancet Infect. Dis. 20, 398–400 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32113510</ArticleId><ArticleId IdType="pmcid">7128218</ArticleId></ArticleIdList></Reference><Reference><Citation>de Alwis, R., Chen, S., Gan, E. S. & Ooi, E. E. Impact of immune enhancement on COVID-19 polyclonal hyperimmune globulin therapy and vaccine development. EBioMedicine 55, 102768 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32344202</ArticleId><ArticleId IdType="pmcid">7161485</ArticleId></ArticleIdList></Reference><Reference><Citation>Galeotti, C., Kaveri, S. V. & Bayry, J. IVIG-mediated effector functions in autoimmune and inflammatory diseases. Int. Immunol. 29, 491–498 (2017).</Citation><ArticleIdList><ArticleId IdType="pubmed">28666326</ArticleId></ArticleIdList></Reference><Reference><Citation>Zandman-Goddard, G., Levy, Y. & Shoenfeld, Y. Intravenous immunoglobulin therapy and systemic lupus erythematosus. Clin. Rev. Allergy Immunol. 29, 219–228 (2005).</Citation><ArticleIdList><ArticleId IdType="pubmed">16391397</ArticleId></ArticleIdList></Reference><Reference><Citation>Lee, N. et al. Anti-SARS-CoV IgG response in relation to disease severity of severe acute respiratory syndrome. J. Clin. Virol. 35, 179–184 (2006).</Citation><ArticleIdList><ArticleId IdType="pubmed">16112612</ArticleId></ArticleIdList></Reference><Reference><Citation>Zhang, L. et al. Antibody responses against SARS coronavirus are correlated with disease outcome of infected individuals. J. Med. Virol. 78, 1–8 (2006).</Citation><ArticleIdList><ArticleId IdType="pubmed">16299724</ArticleId></ArticleIdList></Reference><Reference><Citation>Ho, M.-S. et al. Neutralizing antibody response and SARS severity. Emerg. Infect. Dis. 11, 1730–1737 (2005).</Citation><ArticleIdList><ArticleId IdType="pubmed">16318725</ArticleId><ArticleId IdType="pmcid">3367364</ArticleId></ArticleIdList></Reference><Reference><Citation>Liu, L. et al. Anti-spike IgG causes severe acute lung injury by skewing macrophage responses during acute SARS-CoV infection. JCI Insight 4, e123158 (2019).</Citation><ArticleIdList><ArticleId IdType="pmcid">6478436</ArticleId></ArticleIdList></Reference><Reference><Citation>Huang, A. et al. A systematic review of antibody mediated immunity to coronaviruses: antibody kinetics, correlates of protection, and association of antibody responses with severity of disease. Preprint at https://www.medrxiv.org/content/10.1101/2020.04.14.20065771v1 (2020). Meta-analysis of reports of antibody responses to SARS-CoV, MERS-CoV and initial reports of SARS-CoV-2 in infected patients, describing inconclusive evidence for a relationship between antibody titres and disease severity.</Citation></Reference><Reference><Citation>Martines, R. B. et al. Pathology and pathogenesis of SARS-CoV-2 associated with fatal coronavirus disease, United States. Emerg. Infect. Dis. https://doi.org/10.3201/eid2609.202095 (2020).</Citation></Reference><Reference><Citation>Ramcharan, T. et al. Paediatric inflammatory multisystem syndrome: temporally associated with SARS-CoV-2 (PIMS-TS): cardiac features, management and short-term outcomes at a UK tertiary paediatric hospital. Pediatr. Cardiol. https://doi.org/10.1007/s00246-020-02391-2 (2020).</Citation></Reference><Reference><Citation>Yang, Z.-Y. et al. pH-dependent entry of severe acute respiratory syndrome coronavirus is mediated by the spike glycoprotein and enhanced by dendritic cell transfer through DC-SIGN. J. Virol. 78, 5642–5650 (2004).</Citation><ArticleIdList><ArticleId IdType="pubmed">15140961</ArticleId><ArticleId IdType="pmcid">415834</ArticleId></ArticleIdList></Reference><Reference><Citation>Quinlan, B. D. et al. The SARS-CoV-2 receptor-binding domain elicits a potent neutralizing response without antibody-dependent enhancement. Preprint at https://www.biorxiv.org/content/10.1101/2020.04.10.036418v1 (2020).</Citation></Reference><Reference><Citation>Yip, M. S. et al. Antibody-dependent enhancement of SARS coronavirus infection and its role in the pathogenesis of SARS. Hong Kong Med. J. 22, 25–31 (2016).</Citation><ArticleIdList><ArticleId IdType="pubmed">27390007</ArticleId></ArticleIdList></Reference><Reference><Citation>Yip, M. S. et al. Antibody-dependent infection of human macrophages by severe acute respiratory syndrome coronavirus. Virol. J. 11, 82 (2014).</Citation><ArticleIdList><ArticleId IdType="pubmed">24885320</ArticleId><ArticleId IdType="pmcid">4018502</ArticleId></ArticleIdList></Reference><Reference><Citation>Wang, S.-F. et al. Antibody-dependent SARS coronavirus infection is mediated by antibodies against spike proteins. Biochem. Biophys. Res. Commun. 451, 208–214 (2014).</Citation><ArticleIdList><ArticleId IdType="pubmed">25073113</ArticleId><ArticleId IdType="pmcid">7092860</ArticleId></ArticleIdList></Reference><Reference><Citation>Jaume, M. et al. Anti-severe acute respiratory syndrome coronavirus spike antibodies trigger infection of human immune cells via a pH- and cysteine protease-independent FcγR pathway. J. Virol. 85, 10582–10597 (2011).</Citation><ArticleIdList><ArticleId IdType="pubmed">21775467</ArticleId><ArticleId IdType="pmcid">3187504</ArticleId></ArticleIdList></Reference><Reference><Citation>Wan, Y. et al. Molecular mechanism for antibody-dependent enhancement of coronavirus entry. J. Virol. 94, e02015–e02019 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">31826992</ArticleId><ArticleId IdType="pmcid">7022351</ArticleId></ArticleIdList></Reference><Reference><Citation>Yilla, M. et al. SARS-coronavirus replication in human peripheral monocytes/macrophages. Virus Res. 107, 93–101 (2005).</Citation><ArticleIdList><ArticleId IdType="pubmed">15567038</ArticleId></ArticleIdList></Reference><Reference><Citation>Lau, Y. L., Peiris, J. S. M. & Law, H. K. W. Role of dendritic cells in SARS coronavirus infection. Hong Kong Med. J. 18, 28–30 (2012).</Citation><ArticleIdList><ArticleId IdType="pubmed">22865220</ArticleId></ArticleIdList></Reference><Reference><Citation>Tynell, J. et al. Middle East respiratory syndrome coronavirus shows poor replication but significant induction of antiviral responses in human monocyte-derived macrophages and dendritic cells. J. Gen. Virol. 97, 344–355 (2016).</Citation><ArticleIdList><ArticleId IdType="pubmed">26602089</ArticleId><ArticleId IdType="pmcid">4804640</ArticleId></ArticleIdList></Reference><Reference><Citation>Hui, K. P. Y. et al. Tropism, replication competence, and innate immune responses of the coronavirus SARS-CoV-2 in human respiratory tract and conjunctiva: an analysis in ex-vivo and in-vitro cultures. Lancet Respir. Med. 8, 687–695 (2020).</Citation></Reference><Reference><Citation>Zhou, J. et al. Active replication of Middle East respiratory syndrome coronavirus and aberrant induction of inflammatory cytokines and chemokines in human macrophages: implications for pathogenesis. J. Infect. Dis. 209, 1331–1342 (2014).</Citation><ArticleIdList><ArticleId IdType="pubmed">24065148</ArticleId></ArticleIdList></Reference><Reference><Citation>ter Meulen, J. et al. Human monoclonal antibody as prophylaxis for SARS coronavirus infection in ferrets. Lancet 363, 2139–2141 (2004).</Citation><ArticleIdList><ArticleId IdType="pubmed">15220038</ArticleId><ArticleId IdType="pmcid">7112500</ArticleId></ArticleIdList></Reference><Reference><Citation>Czub, M., Weingartl, H., Czub, S., He, R. & Cao, J. Evaluation of modified vaccinia virus Ankara based recombinant SARS vaccine in ferrets. Vaccine 23, 2273–2279 (2005).</Citation><ArticleIdList><ArticleId IdType="pubmed">15755610</ArticleId><ArticleId IdType="pmcid">7115540</ArticleId></ArticleIdList></Reference><Reference><Citation>Corti, D. et al. Prophylactic and postexposure efficacy of a potent human monoclonal antibody against MERS coronavirus. Proc. Natl Acad. Sci. USA 112, 10473–10478 (2015).</Citation><ArticleIdList><ArticleId IdType="pubmed">26216974</ArticleId></ArticleIdList></Reference><Reference><Citation>Rockx, B. et al. Structural basis for potent cross-neutralizing human monoclonal antibody protection against lethal human and zoonotic severe acute respiratory syndrome coronavirus challenge. J. Virol. 82, 3220–3235 (2008).</Citation><ArticleIdList><ArticleId IdType="pubmed">18199635</ArticleId><ArticleId IdType="pmcid">2268459</ArticleId></ArticleIdList></Reference><Reference><Citation>Smith, P., DiLillo, D. J., Bournazos, S., Li, F. & Ravetch, J. V. Mouse model recapitulating human Fcγ receptor structural and functional diversity. Proc. Natl Acad. Sci. USA 109, 6181–6186 (2012).</Citation><ArticleIdList><ArticleId IdType="pubmed">22474370</ArticleId></ArticleIdList></Reference><Reference><Citation>Subbarao, K. et al. Prior infection and passive transfer of neutralizing antibody prevent replication of severe acute respiratory syndrome coronavirus in the respiratory tract of mice. J. Virol. 78, 3572–3577 (2004).</Citation><ArticleIdList><ArticleId IdType="pubmed">15016880</ArticleId><ArticleId IdType="pmcid">371090</ArticleId></ArticleIdList></Reference><Reference><Citation>Yasui, F. et al. Phagocytic cells contribute to the antibody-mediated elimination of pulmonary-infected SARS coronavirus. Virology 454–455, 157–168 (2014).</Citation><ArticleIdList><ArticleId IdType="pubmed">24725942</ArticleId></ArticleIdList></Reference><Reference><Citation>Fett, C., DeDiego, M. L., Regla-Nava, J. A., Enjuanes, L. & Perlman, S. Complete protection against severe acute respiratory syndrome coronavirus-mediated lethal respiratory disease in aged mice by immunization with a mouse-adapted virus lacking E protein. J. Virol. 87, 6551–6559 (2013).</Citation><ArticleIdList><ArticleId IdType="pubmed">23576515</ArticleId><ArticleId IdType="pmcid">3676143</ArticleId></ArticleIdList></Reference><Reference><Citation>Bolles, M. et al. A double-inactivated severe acute respiratory syndrome coronavirus vaccine provides incomplete protection in mice and induces increased eosinophilic proinflammatory pulmonary response upon challenge. J. Virol. 85, 12201–12215 (2011).</Citation><ArticleIdList><ArticleId IdType="pubmed">21937658</ArticleId><ArticleId IdType="pmcid">3209347</ArticleId></ArticleIdList></Reference><Reference><Citation>Hotez, P. J., Corry, D. B. & Bottazzi, M. E. COVID-19 vaccine design: the Janus face of immune enhancement. Nat. Rev. Immunol. 20, 347–348 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32346094</ArticleId></ArticleIdList></Reference><Reference><Citation>Tseng, C.-T. et al. Immunization with SARS coronavirus vaccines leads to pulmonary immunopathology on challenge with the SARS virus. PLoS ONE 7, e35421 (2012).</Citation><ArticleIdList><ArticleId IdType="pubmed">22536382</ArticleId><ArticleId IdType="pmcid">3335060</ArticleId></ArticleIdList></Reference><Reference><Citation>Corbett, K. S. et al. SARS-CoV-2 mRNA vaccine development enabled by prototype pathogen preparedness. Preprint at https://www.biorxiv.org/content/10.1101/2020.06.11.145920v1 (2020).</Citation></Reference><Reference><Citation>Zost, S. J. et al. Potently neutralizing human antibodies that block SARS-CoV-2 receptor binding and protect animals. Preprint at https://www.biorxiv.org/content/10.1101/2020.05.22.111005v1 (2020). Protection of mice against SARS-CoV-2 by human mAbs targeting distinct epitopes of the S protein, some of which had synergistic effects in vitro, without evidence of ADE of disease in the animal model.</Citation></Reference><Reference><Citation>Rogers, T. F. et al. Isolation of potent SARS-CoV-2 neutralizing antibodies and protection from disease in a small animal model. Science https://doi.org/10.1126/science.abc7520 (2020). Protective effects of neutralizing mAbs against RBD and non-RBD epitopes of SARS-CoV-2 S protein without evidence of ADE of disease in a Syrian hamster model.</Citation></Reference><Reference><Citation>Kam, Y. W. et al. Antibodies against trimeric S glycoprotein protect hamsters against SARS-CoV challenge despite their capacity to mediate FcγRII-dependent entry into B cells in vitro. Vaccine 25, 729–740 (2007).</Citation><ArticleIdList><ArticleId IdType="pubmed">17049691</ArticleId></ArticleIdList></Reference><Reference><Citation>Pedersen, N. C. An update on feline infectious peritonitis: virology and immunopathogenesis. Vet. J. 201, 123–132 (2014).</Citation><ArticleIdList><ArticleId IdType="pubmed">24837550</ArticleId><ArticleId IdType="pmcid">7110662</ArticleId></ArticleIdList></Reference><Reference><Citation>Rockx, B. et al. Comparative pathogenesis of COVID-19, MERS, and SARS in a nonhuman primate model. Science 368, 1012–1015 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32303590</ArticleId><ArticleId IdType="pmcid">7164679</ArticleId></ArticleIdList></Reference><Reference><Citation>Munster, V. et al. Respiratory disease and virus shedding in rhesus macaques inoculated with SARS-CoV-2. Preprint at https://www.biorxiv.org/content/10.1101/2020.03.21.001628v1 (2020).</Citation></Reference><Reference><Citation>Chandrashekar, A. et al. SARS-CoV-2 infection protects against rechallenge in rhesus macaques. Science https://doi.org/10.1126/science.abc4776 (2020). Infection of rhesus macaques with SARS-CoV-2 and a comprehensive analysis of antibody neutralizing and Fc-mediated effector function showing multi-factorial correlation with protection against re-challenge.</Citation></Reference><Reference><Citation>Zhou, J. et al. Immunogenicity, safety, and protective efficacy of an inactivated SARS-associated coronavirus vaccine in rhesus monkeys. Vaccine 23, 3202–3209 (2005).</Citation><ArticleIdList><ArticleId IdType="pubmed">15837221</ArticleId><ArticleId IdType="pmcid">7115379</ArticleId></ArticleIdList></Reference><Reference><Citation>Wang, Q. et al. Immunodominant SARS coronavirus epitopes in humans elicited both enhancing and neutralizing effects on infection in non-human primates. ACS Infect. Dis. 2, 361–376 (2016).</Citation></Reference><Reference><Citation>Chen, Z. et al. Recombinant modified vaccinia virus Ankara expressing the spike glycoprotein of severe acute respiratory syndrome coronavirus induces protective neutralizing antibodies primarily targeting the receptor binding region. J. Virol. 79, 2678–2688 (2005).</Citation><ArticleIdList><ArticleId IdType="pubmed">15708987</ArticleId><ArticleId IdType="pmcid">548443</ArticleId></ArticleIdList></Reference><Reference><Citation>Qin, E. et al. Immunogenicity and protective efficacy in monkeys of purified inactivated Vero-cell SARS vaccine. Vaccine 24, 1028–1034 (2006).</Citation><ArticleIdList><ArticleId IdType="pubmed">16388880</ArticleId></ArticleIdList></Reference><Reference><Citation>Clay, C. et al. Primary severe acute respiratory syndrome coronavirus infection limits replication but not lung inflammation upon homologous rechallenge. J. Virol. 86, 4234–4244 (2012).</Citation><ArticleIdList><ArticleId IdType="pubmed">22345460</ArticleId><ArticleId IdType="pmcid">3318632</ArticleId></ArticleIdList></Reference><Reference><Citation>Muthumani, K. et al. A synthetic consensus anti-spike protein DNA vaccine induces protective immunity against Middle East respiratory syndrome coronavirus in nonhuman primates. Sci. Transl. Med. 7, 301ra132 (2015).</Citation><ArticleIdList><ArticleId IdType="pubmed">26290414</ArticleId><ArticleId IdType="pmcid">4573558</ArticleId></ArticleIdList></Reference><Reference><Citation>Lan, J. et al. Recombinant receptor binding domain protein induces partial protective immunity in rhesus macaques against Middle East respiratory syndrome coronavirus challenge. EBioMedicine 2, 1438–1446 (2015).</Citation><ArticleIdList><ArticleId IdType="pubmed">26629538</ArticleId><ArticleId IdType="pmcid">4634622</ArticleId></ArticleIdList></Reference><Reference><Citation>van Doremalen, N. et al. A single dose of ChAdOx1 MERS provides protective immunity in rhesus macaques. Sci. Adv. 6, eaba8399 (2020).</Citation><ArticleIdList><ArticleId IdType="pubmed">32577525</ArticleId><ArticleId IdType="pmcid">7286676</ArticleId></ArticleIdList></Reference><Reference><Citation>Gao, Q. et al. Rapid development of an inactivated vaccine candidate for SARS-CoV-2. Science 369, 77–81 (2020). Protection of rhesus macaques against SARS-CoV-2 challenge after immunization with purified inactivated SARS-CoV-2 virus without evidence of ADE of disease.</Citation></Reference><Reference><Citation>Yu, J. et al. DNA vaccine protection against SARS-CoV-2 in rhesus macaques. Science https://doi.org/10.1126/science.abc6284 (2020). Immunization of rhesus macaques with DNA vaccines expressing forms of the SARS-CoV-2 S protein resulted in reduced infection following challenge after administration of full-length S protein without evidence of ADE of disease.</Citation><ArticleIdList><ArticleId IdType="doi">10.1126/science.abc6284</ArticleId><ArticleId IdType="pubmed">33335017</ArticleId><ArticleId IdType="pmcid">7574914</ArticleId></ArticleIdList></Reference><Reference><Citation>Miyoshi-Akiyama, T. et al. Fully human monoclonal antibody directed to proteolytic cleavage site in severe acute respiratory syndrome (SARS) coronavirus S protein neutralizes the virus in a rhesus macaque SARS model. J. Infect. Dis. 203, 1574–1581 (2011).</Citation><ArticleIdList><ArticleId IdType="pubmed">21592986</ArticleId><ArticleId IdType="pmcid">7107252</ArticleId></ArticleIdList></Reference><Reference><Citation>Johnson, R. F. et al. 3B11-N, a monoclonal antibody against MERS-CoV, reduces lung pathology in rhesus monkeys following intratracheal inoculation of MERS-CoV Jordan-n3/2012. Virology 490, 49–58 (2016).</Citation><ArticleIdList><ArticleId IdType="pubmed">26828465</ArticleId><ArticleId IdType="pmcid">4769911</ArticleId></ArticleIdList></Reference><Reference><Citation>de Wit, E. et al. Prophylactic and therapeutic efficacy of mAb treatment against MERS-CoV in common marmosets. Antiviral Res. 156, 64–71 (2018).</Citation><ArticleIdList><ArticleId IdType="pubmed">29885377</ArticleId><ArticleId IdType="pmcid">7113689</ArticleId></ArticleIdList></Reference><Reference><Citation>de Wit, E. et al. Prophylactic efficacy of a human monoclonal antibody against MERS-CoV in the common marmoset. Antiviral Res. 163, 70–74 (2019).</Citation><ArticleIdList><ArticleId IdType="pubmed">30684561</ArticleId><ArticleId IdType="pmcid">7113761</ArticleId></ArticleIdList></Reference><Reference><Citation>Chen, Z. et al. Human neutralizing monoclonal antibody inhibition of Middle East respiratory syndrome coronavirus replication in the common marmoset. J. Infect. Dis. 215, 1807–1815 (2017).</Citation><ArticleIdList><ArticleId IdType="pubmed">28472421</ArticleId><ArticleId IdType="pmcid">7107363</ArticleId></ArticleIdList></Reference><Reference><Citation>Lam, J. H. et al. Dengue vaccine-induced CD8<sup>+</sup> T cell immunity confers protection in the context of enhancing, interfering maternal antibodies. JCI Insight 2, e94500 (2017).</Citation><ArticleIdList><ArticleId IdType="pmcid">5752305</ArticleId></ArticleIdList></Reference></ReferenceList></PubmedData></pubmed><affiliations><list><country><li>Suisse</li><li>États-Unis</li></country><region><li>Californie</li><li>Missouri (État)</li></region><settlement><li>Saint-Louis (Missouri)</li></settlement><orgName><li>École de médecine (Université Washington de Saint-Louis)</li></orgName></list><tree><country name="États-Unis"><region name="Californie"><name sortKey="Arvin, Ann M" sort="Arvin, Ann M" uniqKey="Arvin A" first="Ann M" last="Arvin">Ann M. Arvin</name></region><name sortKey="Arvin, Ann M" sort="Arvin, Ann M" uniqKey="Arvin A" first="Ann M" last="Arvin">Ann M. Arvin</name><name sortKey="Cathcart, Andrea" sort="Cathcart, Andrea" uniqKey="Cathcart A" first="Andrea" last="Cathcart">Andrea Cathcart</name><name sortKey="Corti, Davide" sort="Corti, Davide" uniqKey="Corti D" first="Davide" last="Corti">Davide Corti</name><name sortKey="Fink, Katja" sort="Fink, Katja" uniqKey="Fink K" first="Katja" last="Fink">Katja Fink</name><name sortKey="Havenar Daughton, Colin" sort="Havenar Daughton, Colin" uniqKey="Havenar Daughton C" first="Colin" last="Havenar-Daughton">Colin Havenar-Daughton</name><name sortKey="Lanzavecchia, Antonio" sort="Lanzavecchia, Antonio" uniqKey="Lanzavecchia A" first="Antonio" last="Lanzavecchia">Antonio Lanzavecchia</name><name sortKey="Schmid, Michael A" sort="Schmid, Michael A" uniqKey="Schmid M" first="Michael A" last="Schmid">Michael A. Schmid</name><name sortKey="Spreafico, Roberto" sort="Spreafico, Roberto" uniqKey="Spreafico R" first="Roberto" last="Spreafico">Roberto Spreafico</name><name sortKey="Virgin, Herbert W" sort="Virgin, Herbert W" uniqKey="Virgin H" first="Herbert W" last="Virgin">Herbert W. Virgin</name><name sortKey="Virgin, Herbert W" sort="Virgin, Herbert W" uniqKey="Virgin H" first="Herbert W" last="Virgin">Herbert W. Virgin</name></country><country name="Suisse"><noRegion><name sortKey="Fink, Katja" sort="Fink, Katja" uniqKey="Fink K" first="Katja" last="Fink">Katja Fink</name></noRegion><name sortKey="Corti, Davide" sort="Corti, Davide" uniqKey="Corti D" first="Davide" last="Corti">Davide Corti</name><name sortKey="Lanzavecchia, Antonio" sort="Lanzavecchia, Antonio" uniqKey="Lanzavecchia A" first="Antonio" last="Lanzavecchia">Antonio Lanzavecchia</name><name sortKey="Schmid, Michael A" sort="Schmid, Michael A" uniqKey="Schmid M" first="Michael A" last="Schmid">Michael A. 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