Enhanced inflammation in New Zealand white rabbits when MERS-CoV reinfection occurs in the absence of neutralizing antibody.
Identifieur interne : 000B95 ( PubMed/Corpus ); précédent : 000B94; suivant : 000B96Enhanced inflammation in New Zealand white rabbits when MERS-CoV reinfection occurs in the absence of neutralizing antibody.
Auteurs : Katherine V. Houser ; Andrew J. Broadbent ; Lisa Gretebeck ; Leatrice Vogel ; Elaine W. Lamirande ; Troy Sutton ; Kevin W. Bock ; Mahnaz Minai ; Marlene Orandle ; Ian N. Moore ; Kanta SubbaraoSource :
- PLoS pathogens [ 1553-7374 ] ; 2017.
English descriptors
- KwdEn :
- Animals, Antibodies, Neutralizing (immunology), Antibodies, Viral (immunology), Coronavirus Infections (immunology), Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Immunohistochemistry, Inflammation (immunology), Middle East Respiratory Syndrome Coronavirus (immunology), Neutralization Tests, Polymerase Chain Reaction, Rabbits.
- MESH :
- chemical , immunology : Antibodies, Neutralizing, Antibodies, Viral.
- immunology : Coronavirus Infections, Inflammation, Middle East Respiratory Syndrome Coronavirus.
- Animals, Disease Models, Animal, Enzyme-Linked Immunosorbent Assay, Fluorescent Antibody Technique, Immunohistochemistry, Neutralization Tests, Polymerase Chain Reaction, Rabbits.
Abstract
The Middle East respiratory syndrome coronavirus (MERS-CoV) is a zoonotic betacoronavirus that was first detected in humans in 2012 as a cause of severe acute respiratory disease. As of July 28, 2017, there have been 2,040 confirmed cases with 712 reported deaths. While many infections have been fatal, there have also been a large number of mild or asymptomatic cases discovered through monitoring and contact tracing. New Zealand white rabbits are a possible model for asymptomatic infection with MERS-CoV. In order to discover more about non-lethal infections and to learn whether a single infection with MERS-CoV would protect against reinfection, we inoculated rabbits with MERS-CoV and monitored the antibody and inflammatory response. Following intranasal infection, rabbits developed a transient dose-dependent pulmonary infection with moderately high levels of viral RNA, viral antigen, and perivascular inflammation in multiple lung lobes that was not associated with clinical signs. The rabbits developed antibodies against viral proteins that lacked neutralizing activity and the animals were not protected from reinfection. In fact, reinfection resulted in enhanced pulmonary inflammation, without an associated increase in viral RNA titers. Interestingly, passive transfer of serum from previously infected rabbits to naïve rabbits was associated with enhanced inflammation upon infection. We further found this inflammation was accompanied by increased recruitment of complement proteins compared to primary infection. However, reinfection elicited neutralizing antibodies that protected rabbits from subsequent viral challenge. Our data from the rabbit model suggests that people exposed to MERS-CoV who fail to develop a neutralizing antibody response, or persons whose neutralizing antibody titers have waned, may be at risk for severe lung disease on re-exposure to MERS-CoV.
DOI: 10.1371/journal.ppat.1006565
PubMed: 28817732
Links to Exploration step
pubmed:28817732Le document en format XML
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Bock</name><affiliation><nlm:affiliation>Comparative Medicine Branch, Infectious Disease Pathogenesis Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Minai, Mahnaz" sort="Minai, Mahnaz" uniqKey="Minai M" first="Mahnaz" last="Minai">Mahnaz Minai</name><affiliation><nlm:affiliation>Comparative Medicine Branch, Infectious Disease Pathogenesis Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Orandle, Marlene" sort="Orandle, Marlene" uniqKey="Orandle M" first="Marlene" last="Orandle">Marlene Orandle</name><affiliation><nlm:affiliation>Comparative Medicine Branch, Infectious Disease Pathogenesis Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Moore, Ian N" sort="Moore, Ian N" uniqKey="Moore I" first="Ian N" last="Moore">Ian N. Moore</name><affiliation><nlm:affiliation>Comparative Medicine Branch, Infectious Disease Pathogenesis Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</nlm:affiliation></affiliation></author><author><name sortKey="Subbarao, Kanta" sort="Subbarao, Kanta" uniqKey="Subbarao K" first="Kanta" last="Subbarao">Kanta Subbarao</name><affiliation><nlm:affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</nlm:affiliation></affiliation></author></analytic><series><title level="j">PLoS pathogens</title><idno type="eISSN">1553-7374</idno><imprint><date when="2017" type="published">2017</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animals</term><term>Antibodies, Neutralizing (immunology)</term><term>Antibodies, Viral (immunology)</term><term>Coronavirus Infections (immunology)</term><term>Disease Models, Animal</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Fluorescent Antibody Technique</term><term>Immunohistochemistry</term><term>Inflammation (immunology)</term><term>Middle East Respiratory Syndrome Coronavirus (immunology)</term><term>Neutralization Tests</term><term>Polymerase Chain Reaction</term><term>Rabbits</term></keywords><keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Antibodies, Neutralizing</term><term>Antibodies, Viral</term></keywords><keywords scheme="MESH" qualifier="immunology" xml:lang="en"><term>Coronavirus Infections</term><term>Inflammation</term><term>Middle East Respiratory Syndrome Coronavirus</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Animals</term><term>Disease Models, Animal</term><term>Enzyme-Linked Immunosorbent Assay</term><term>Fluorescent Antibody Technique</term><term>Immunohistochemistry</term><term>Neutralization Tests</term><term>Polymerase Chain Reaction</term><term>Rabbits</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The Middle East respiratory syndrome coronavirus (MERS-CoV) is a zoonotic betacoronavirus that was first detected in humans in 2012 as a cause of severe acute respiratory disease. As of July 28, 2017, there have been 2,040 confirmed cases with 712 reported deaths. While many infections have been fatal, there have also been a large number of mild or asymptomatic cases discovered through monitoring and contact tracing. New Zealand white rabbits are a possible model for asymptomatic infection with MERS-CoV. In order to discover more about non-lethal infections and to learn whether a single infection with MERS-CoV would protect against reinfection, we inoculated rabbits with MERS-CoV and monitored the antibody and inflammatory response. Following intranasal infection, rabbits developed a transient dose-dependent pulmonary infection with moderately high levels of viral RNA, viral antigen, and perivascular inflammation in multiple lung lobes that was not associated with clinical signs. The rabbits developed antibodies against viral proteins that lacked neutralizing activity and the animals were not protected from reinfection. In fact, reinfection resulted in enhanced pulmonary inflammation, without an associated increase in viral RNA titers. Interestingly, passive transfer of serum from previously infected rabbits to naïve rabbits was associated with enhanced inflammation upon infection. We further found this inflammation was accompanied by increased recruitment of complement proteins compared to primary infection. However, reinfection elicited neutralizing antibodies that protected rabbits from subsequent viral challenge. Our data from the rabbit model suggests that people exposed to MERS-CoV who fail to develop a neutralizing antibody response, or persons whose neutralizing antibody titers have waned, may be at risk for severe lung disease on re-exposure to MERS-CoV.</div></front></TEI><pubmed><MedlineCitation Status="MEDLINE" Owner="NLM"><PMID Version="1">28817732</PMID><DateCompleted><Year>2017</Year><Month>10</Month><Day>02</Day></DateCompleted><DateRevised><Year>2018</Year><Month>11</Month><Day>13</Day></DateRevised><Article PubModel="Electronic-eCollection"><Journal><ISSN IssnType="Electronic">1553-7374</ISSN><JournalIssue CitedMedium="Internet"><Volume>13</Volume><Issue>8</Issue><PubDate><Year>2017</Year><Month>Aug</Month></PubDate></JournalIssue><Title>PLoS pathogens</Title><ISOAbbreviation>PLoS Pathog.</ISOAbbreviation></Journal><ArticleTitle>Enhanced inflammation in New Zealand white rabbits when MERS-CoV reinfection occurs in the absence of neutralizing antibody.</ArticleTitle><Pagination><MedlinePgn>e1006565</MedlinePgn></Pagination><ELocationID EIdType="doi" ValidYN="Y">10.1371/journal.ppat.1006565</ELocationID><Abstract><AbstractText>The Middle East respiratory syndrome coronavirus (MERS-CoV) is a zoonotic betacoronavirus that was first detected in humans in 2012 as a cause of severe acute respiratory disease. As of July 28, 2017, there have been 2,040 confirmed cases with 712 reported deaths. While many infections have been fatal, there have also been a large number of mild or asymptomatic cases discovered through monitoring and contact tracing. New Zealand white rabbits are a possible model for asymptomatic infection with MERS-CoV. In order to discover more about non-lethal infections and to learn whether a single infection with MERS-CoV would protect against reinfection, we inoculated rabbits with MERS-CoV and monitored the antibody and inflammatory response. Following intranasal infection, rabbits developed a transient dose-dependent pulmonary infection with moderately high levels of viral RNA, viral antigen, and perivascular inflammation in multiple lung lobes that was not associated with clinical signs. The rabbits developed antibodies against viral proteins that lacked neutralizing activity and the animals were not protected from reinfection. In fact, reinfection resulted in enhanced pulmonary inflammation, without an associated increase in viral RNA titers. Interestingly, passive transfer of serum from previously infected rabbits to naïve rabbits was associated with enhanced inflammation upon infection. We further found this inflammation was accompanied by increased recruitment of complement proteins compared to primary infection. However, reinfection elicited neutralizing antibodies that protected rabbits from subsequent viral challenge. Our data from the rabbit model suggests that people exposed to MERS-CoV who fail to develop a neutralizing antibody response, or persons whose neutralizing antibody titers have waned, may be at risk for severe lung disease on re-exposure to MERS-CoV.</AbstractText></Abstract><AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Houser</LastName><ForeName>Katherine V</ForeName><Initials>KV</Initials><AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Broadbent</LastName><ForeName>Andrew J</ForeName><Initials>AJ</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-4716-1835</Identifier><AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Gretebeck</LastName><ForeName>Lisa</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Vogel</LastName><ForeName>Leatrice</ForeName><Initials>L</Initials><AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Lamirande</LastName><ForeName>Elaine W</ForeName><Initials>EW</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-3597-7319</Identifier><AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Sutton</LastName><ForeName>Troy</ForeName><Initials>T</Initials><AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Bock</LastName><ForeName>Kevin W</ForeName><Initials>KW</Initials><Identifier Source="ORCID">http://orcid.org/0000-0001-9454-0937</Identifier><AffiliationInfo><Affiliation>Comparative Medicine Branch, Infectious Disease Pathogenesis Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Minai</LastName><ForeName>Mahnaz</ForeName><Initials>M</Initials><Identifier Source="ORCID">http://orcid.org/0000-0002-3642-8063</Identifier><AffiliationInfo><Affiliation>Comparative Medicine Branch, Infectious Disease Pathogenesis Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Orandle</LastName><ForeName>Marlene</ForeName><Initials>M</Initials><AffiliationInfo><Affiliation>Comparative Medicine Branch, Infectious Disease Pathogenesis Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Moore</LastName><ForeName>Ian N</ForeName><Initials>IN</Initials><AffiliationInfo><Affiliation>Comparative Medicine Branch, Infectious Disease Pathogenesis Section, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author><Author ValidYN="Y"><LastName>Subbarao</LastName><ForeName>Kanta</ForeName><Initials>K</Initials><Identifier Source="ORCID">http://orcid.org/0000-0003-1713-3056</Identifier><AffiliationInfo><Affiliation>Laboratory of Infectious Diseases, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, MD, United States of America.</Affiliation></AffiliationInfo></Author></AuthorList><Language>eng</Language><PublicationTypeList><PublicationType UI="D016428">Journal Article</PublicationType></PublicationTypeList><ArticleDate DateType="Electronic"><Year>2017</Year><Month>08</Month><Day>17</Day></ArticleDate></Article><MedlineJournalInfo><Country>United States</Country><MedlineTA>PLoS Pathog</MedlineTA><NlmUniqueID>101238921</NlmUniqueID><ISSNLinking>1553-7366</ISSNLinking></MedlineJournalInfo><ChemicalList><Chemical><RegistryNumber>0</RegistryNumber><NameOfSubstance UI="D057134">Antibodies, 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