Elicitation of immunity in mice after immunization with the S2 subunit of the severe acute respiratory syndrome coronavirus.
Identifieur interne : 002592 ( PubMed/Corpus ); précédent : 002591; suivant : 002593Elicitation of immunity in mice after immunization with the S2 subunit of the severe acute respiratory syndrome coronavirus.
Auteurs : Yingjun Guo ; Shuhan Sun ; Kaiyu Wang ; Shu Zhang ; Weijia Zhu ; Ze ChenSource :
- DNA and cell biology [ 1044-5498 ] ; 2005.
English descriptors
- KwdEn :
- Animals, Antibodies, Viral (blood), COS Cells, Chlorocebus aethiops, Female, Humans, Immunization, Immunoglobulin G (blood), Interferon-gamma (biosynthesis), Interleukin-4 (biosynthesis), Membrane Glycoproteins (genetics), Membrane Glycoproteins (immunology), Mice, Mice, Inbred BALB C, Peptide Fragments (genetics), Peptide Fragments (immunology), Recombinant Proteins (immunology), SARS Virus (immunology), Spike Glycoprotein, Coronavirus, T-Lymphocytes, Cytotoxic (immunology), Vero Cells, Viral Envelope Proteins (genetics), Viral Envelope Proteins (immunology).
- MESH :
- chemical , biosynthesis : Interferon-gamma, Interleukin-4.
- chemical , blood : Antibodies, Viral, Immunoglobulin G.
- chemical , genetics : Membrane Glycoproteins, Peptide Fragments, Viral Envelope Proteins.
- chemical , immunology : Membrane Glycoproteins, Peptide Fragments, Recombinant Proteins, Viral Envelope Proteins.
- immunology : SARS Virus, T-Lymphocytes, Cytotoxic.
- Animals, COS Cells, Chlorocebus aethiops, Female, Humans, Immunization, Mice, Mice, Inbred BALB C, Spike Glycoprotein, Coronavirus, Vero Cells.
Abstract
The S2 domain of the severe acute respiratory syndrome coronavirus (SARS-CoV) spike (S) protein is responsible for fusion between virus and target cell membranes, and is expected to be immungenic. In this study, we investigated the immune responses against the S2 subunit in BALB/c mice, which were vaccinated either with plasmid DNA encoding the S2 domain (residues 681-1120), the recombinant S2 fragment (residues 681-980) in incomplete Freund's adjuvant, or with inactivated SARS-CoV. The increased number of specific cytotoxic cells (CTLs) and the high titer of specific antibody showed stimulation of both arms of the immune system in these groups. The shift in cytokines suggested that Th1-polarized immune response was induced by plasmid pCoVS2, meanwhile the Th2-dominant response was induced by recombinant S2 fragment and inactivated vaccine. However, the titer of neutralizing antibodies was only detectable in mice immunized with inactivated virus, but not with pCoVS2 plasmid. Taken together, the S2 domain could induce specific cellular immune response and a high level of total IgG but little neutralizing antibodies against infection by SARSCoV.
DOI: 10.1089/dna.2005.24.510
PubMed: 16101349
Links to Exploration step
pubmed:16101349Le document en format XML
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<author><name sortKey="Guo, Yingjun" sort="Guo, Yingjun" uniqKey="Guo Y" first="Yingjun" last="Guo">Yingjun Guo</name>
<affiliation><nlm:affiliation>Department of Medical Genetics, The Second Military Medical University, Shanghai, People's Republic of China.</nlm:affiliation>
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<author><name sortKey="Sun, Shuhan" sort="Sun, Shuhan" uniqKey="Sun S" first="Shuhan" last="Sun">Shuhan Sun</name>
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<author><name sortKey="Wang, Kaiyu" sort="Wang, Kaiyu" uniqKey="Wang K" first="Kaiyu" last="Wang">Kaiyu Wang</name>
</author>
<author><name sortKey="Zhang, Shu" sort="Zhang, Shu" uniqKey="Zhang S" first="Shu" last="Zhang">Shu Zhang</name>
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<author><name sortKey="Zhu, Weijia" sort="Zhu, Weijia" uniqKey="Zhu W" first="Weijia" last="Zhu">Weijia Zhu</name>
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<author><name sortKey="Chen, Ze" sort="Chen, Ze" uniqKey="Chen Z" first="Ze" last="Chen">Ze Chen</name>
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<author><name sortKey="Sun, Shuhan" sort="Sun, Shuhan" uniqKey="Sun S" first="Shuhan" last="Sun">Shuhan Sun</name>
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<author><name sortKey="Wang, Kaiyu" sort="Wang, Kaiyu" uniqKey="Wang K" first="Kaiyu" last="Wang">Kaiyu Wang</name>
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<author><name sortKey="Zhang, Shu" sort="Zhang, Shu" uniqKey="Zhang S" first="Shu" last="Zhang">Shu Zhang</name>
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<author><name sortKey="Zhu, Weijia" sort="Zhu, Weijia" uniqKey="Zhu W" first="Weijia" last="Zhu">Weijia Zhu</name>
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<author><name sortKey="Chen, Ze" sort="Chen, Ze" uniqKey="Chen Z" first="Ze" last="Chen">Ze Chen</name>
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<series><title level="j">DNA and cell biology</title>
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<term>Antibodies, Viral (blood)</term>
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<term>Chlorocebus aethiops</term>
<term>Female</term>
<term>Humans</term>
<term>Immunization</term>
<term>Immunoglobulin G (blood)</term>
<term>Interferon-gamma (biosynthesis)</term>
<term>Interleukin-4 (biosynthesis)</term>
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<term>Membrane Glycoproteins (immunology)</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Peptide Fragments (genetics)</term>
<term>Peptide Fragments (immunology)</term>
<term>Recombinant Proteins (immunology)</term>
<term>SARS Virus (immunology)</term>
<term>Spike Glycoprotein, Coronavirus</term>
<term>T-Lymphocytes, Cytotoxic (immunology)</term>
<term>Vero Cells</term>
<term>Viral Envelope Proteins (genetics)</term>
<term>Viral Envelope Proteins (immunology)</term>
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<keywords scheme="MESH" type="chemical" qualifier="biosynthesis" xml:lang="en"><term>Interferon-gamma</term>
<term>Interleukin-4</term>
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<keywords scheme="MESH" type="chemical" qualifier="blood" xml:lang="en"><term>Antibodies, Viral</term>
<term>Immunoglobulin G</term>
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<term>Peptide Fragments</term>
<term>Viral Envelope Proteins</term>
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<keywords scheme="MESH" type="chemical" qualifier="immunology" xml:lang="en"><term>Membrane Glycoproteins</term>
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<term>Viral Envelope Proteins</term>
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<term>COS Cells</term>
<term>Chlorocebus aethiops</term>
<term>Female</term>
<term>Humans</term>
<term>Immunization</term>
<term>Mice</term>
<term>Mice, Inbred BALB C</term>
<term>Spike Glycoprotein, Coronavirus</term>
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<front><div type="abstract" xml:lang="en">The S2 domain of the severe acute respiratory syndrome coronavirus (SARS-CoV) spike (S) protein is responsible for fusion between virus and target cell membranes, and is expected to be immungenic. In this study, we investigated the immune responses against the S2 subunit in BALB/c mice, which were vaccinated either with plasmid DNA encoding the S2 domain (residues 681-1120), the recombinant S2 fragment (residues 681-980) in incomplete Freund's adjuvant, or with inactivated SARS-CoV. The increased number of specific cytotoxic cells (CTLs) and the high titer of specific antibody showed stimulation of both arms of the immune system in these groups. The shift in cytokines suggested that Th1-polarized immune response was induced by plasmid pCoVS2, meanwhile the Th2-dominant response was induced by recombinant S2 fragment and inactivated vaccine. However, the titer of neutralizing antibodies was only detectable in mice immunized with inactivated virus, but not with pCoVS2 plasmid. Taken together, the S2 domain could induce specific cellular immune response and a high level of total IgG but little neutralizing antibodies against infection by SARSCoV.</div>
</front>
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<Abstract><AbstractText>The S2 domain of the severe acute respiratory syndrome coronavirus (SARS-CoV) spike (S) protein is responsible for fusion between virus and target cell membranes, and is expected to be immungenic. In this study, we investigated the immune responses against the S2 subunit in BALB/c mice, which were vaccinated either with plasmid DNA encoding the S2 domain (residues 681-1120), the recombinant S2 fragment (residues 681-980) in incomplete Freund's adjuvant, or with inactivated SARS-CoV. The increased number of specific cytotoxic cells (CTLs) and the high titer of specific antibody showed stimulation of both arms of the immune system in these groups. The shift in cytokines suggested that Th1-polarized immune response was induced by plasmid pCoVS2, meanwhile the Th2-dominant response was induced by recombinant S2 fragment and inactivated vaccine. However, the titer of neutralizing antibodies was only detectable in mice immunized with inactivated virus, but not with pCoVS2 plasmid. Taken together, the S2 domain could induce specific cellular immune response and a high level of total IgG but little neutralizing antibodies against infection by SARSCoV.</AbstractText>
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