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Article: Antibody-Dependent Cell-Mediated Cytotoxicity Epitopes on the Hemagglutinin Head Region of Pandemic H1N1 Influenza Virus Play Detrimental Roles in H1N1-Infected Mice

TitleAntibody-Dependent Cell-Mediated Cytotoxicity Epitopes on the Hemagglutinin Head Region of Pandemic H1N1 Influenza Virus Play Detrimental Roles in H1N1-Infected Mice
Authors
KeywordsAntibody-dependent cell-mediated cytotoxicity
H1N1 influenza virus
Hemagglutinin
Lung damage
Mice
Issue Date2017
PublisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/immunology
Citation
Frontiers in Immunology, 2017, v. 8, article no. 317, p. 1-11 How to Cite?
AbstractEngaging the antibody-dependent cell-mediated cytotoxicity (ADCC) for killing of virus-infected cells and secretion of antiviral cytokines and chemokines was incorporated as one of the important features in the design of universal influenza vaccines. However, investigation of the ADCC epitopes on the highly immunogenic influenza hemagglutinin (HA) head region has been rarely reported. In this study, we determined the ADCC and antiviral activities of two putative ADCC epitopes, designated E1 and E2, on the HA head of a pandemic H1N1 influenza virus in vitro and in a lethal mouse model. Our data demonstrated that sera from the E1-vaccinated mice could induce high ADCC activities. Importantly, the induction of ADCC response modestly decreased viral load in the lungs of H1N1-infected mice. However, the elevated ADCC significantly increased mouse alveolar damage and mortality than that of the PBS-vaccinated group (P < 0.0001). The phenotype was potentially due to an exaggerated inflammatory cell infiltration triggered by ADCC, as an upregulated release of cytotoxic granules (perforin) was observed in the lung tissue of E1-vaccinated mice after H1N1 influenza virus challenge. Overall, our data suggested that ADCC elicited by certain domains of HA head region might have a detrimental rather than protective effect during influenza virus infection. Thus, future design of universal influenza vaccine shall strike a balance between the induction of protective immunity and potential side effects of ADCC.
Persistent Identifierhttp://hdl.handle.net/10722/246570
ISSN
2023 Impact Factor: 5.7
2023 SCImago Journal Rankings: 1.868
PubMed Central ID
ISI Accession Number ID

 

DC FieldValueLanguage
dc.contributor.authorYe, Z-
dc.contributor.authorYuan, S-
dc.contributor.authorPoon, KM-
dc.contributor.authorWen, L-
dc.contributor.authorYang, D-
dc.contributor.authorSun, Z-
dc.contributor.authorLi, C-
dc.contributor.authorHu, M-
dc.contributor.authorShuai, H-
dc.contributor.authorZhou, J-
dc.contributor.authorZhang, M-
dc.contributor.authorZheng, B-
dc.contributor.authorChu, H-
dc.contributor.authorYuen, KY-
dc.date.accessioned2017-09-18T02:30:48Z-
dc.date.available2017-09-18T02:30:48Z-
dc.date.issued2017-
dc.identifier.citationFrontiers in Immunology, 2017, v. 8, article no. 317, p. 1-11-
dc.identifier.issn1664-3224-
dc.identifier.urihttp://hdl.handle.net/10722/246570-
dc.description.abstractEngaging the antibody-dependent cell-mediated cytotoxicity (ADCC) for killing of virus-infected cells and secretion of antiviral cytokines and chemokines was incorporated as one of the important features in the design of universal influenza vaccines. However, investigation of the ADCC epitopes on the highly immunogenic influenza hemagglutinin (HA) head region has been rarely reported. In this study, we determined the ADCC and antiviral activities of two putative ADCC epitopes, designated E1 and E2, on the HA head of a pandemic H1N1 influenza virus in vitro and in a lethal mouse model. Our data demonstrated that sera from the E1-vaccinated mice could induce high ADCC activities. Importantly, the induction of ADCC response modestly decreased viral load in the lungs of H1N1-infected mice. However, the elevated ADCC significantly increased mouse alveolar damage and mortality than that of the PBS-vaccinated group (P < 0.0001). The phenotype was potentially due to an exaggerated inflammatory cell infiltration triggered by ADCC, as an upregulated release of cytotoxic granules (perforin) was observed in the lung tissue of E1-vaccinated mice after H1N1 influenza virus challenge. Overall, our data suggested that ADCC elicited by certain domains of HA head region might have a detrimental rather than protective effect during influenza virus infection. Thus, future design of universal influenza vaccine shall strike a balance between the induction of protective immunity and potential side effects of ADCC.-
dc.languageeng-
dc.publisherFrontiers Research Foundation. The Journal's web site is located at http://www.frontiersin.org/immunology-
dc.relation.ispartofFrontiers in Immunology-
dc.rightsThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International License.-
dc.subjectAntibody-dependent cell-mediated cytotoxicity-
dc.subjectH1N1 influenza virus-
dc.subjectHemagglutinin-
dc.subjectLung damage-
dc.subjectMice-
dc.titleAntibody-Dependent Cell-Mediated Cytotoxicity Epitopes on the Hemagglutinin Head Region of Pandemic H1N1 Influenza Virus Play Detrimental Roles in H1N1-Infected Mice-
dc.typeArticle-
dc.identifier.emailYe, Z: zwye@hku.hk-
dc.identifier.emailYuan, S: yuansf@hku.hk-
dc.identifier.emailPoon, KM: vinpoon@hku.hk-
dc.identifier.emailWen, LR: wenlei90@hku.hk-
dc.identifier.emailYang, D: dongfang@hku.hk-
dc.identifier.emailLi, C: licun@hku.hk-
dc.identifier.emailZhou, J: jiezhou@hku.hk-
dc.identifier.emailZheng, B: bzheng@hkucc.hku.hk-
dc.identifier.emailChu, H: hinchu@hku.hk-
dc.identifier.emailYuen, KY: kyyuen@hkucc.hku.hk-
dc.identifier.authorityZhou, J=rp01412-
dc.identifier.authorityZhang, M=rp01409-
dc.identifier.authorityZheng, B=rp00353-
dc.identifier.authorityChu, H=rp02125-
dc.identifier.authorityYuen, KY=rp00366-
dc.description.naturepublished_or_final_version-
dc.identifier.doi10.3389/fimmu.2017.00317-
dc.identifier.pmid28377769-
dc.identifier.pmcidPMC5359280-
dc.identifier.scopuseid_2-s2.0-85017191342-
dc.identifier.hkuros276402-
dc.identifier.volume8-
dc.identifier.spagearticle no. 317, p. 1-
dc.identifier.epagearticle no. 317, p. 11-
dc.identifier.isiWOS:000396791900001-
dc.publisher.placeSwitzerland-
dc.identifier.issnl1664-3224-

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