Influenza Antigen Engineering Focuses Immune Responses to a Subdominant but Broadly Protective Viral Epitope.


Journal

Cell host & microbe
ISSN: 1934-6069
Titre abrégé: Cell Host Microbe
Pays: United States
ID NLM: 101302316

Informations de publication

Date de publication:
12 Jun 2019
Historique:
received: 31 01 2019
revised: 12 03 2019
accepted: 08 04 2019
pubmed: 21 5 2019
medline: 24 12 2019
entrez: 21 5 2019
Statut: ppublish

Résumé

Viral glycoproteins are under constant immune surveillance by a host's adaptive immune responses. Antigenic variation including glycan introduction or removal is among the mechanisms viruses have evolved to escape host immunity. Understanding how glycosylation affects immunodominance on complex protein antigens may help decipher underlying B cell biology. To determine how B cell responses can be altered by such modifications, we engineered glycans onto the influenza virus hemagglutinin (HA) and characterized the molecular features of the elicited humoral immunity in mice. We found that glycan addition changed the initially diverse antibody repertoire into an epitope-focused, genetically restricted response. Structural analyses showed that one antibody gene family targeted a previously subdominant, occluded epitope at the head interface. Passive transfer of this antibody conferred Fc-dependent protection to influenza virus-challenged mice. These results have potential implications for next-generation viral vaccines aimed at directing B cell responses to preferred epitope(s).

Identifiants

pubmed: 31104946
pii: S1931-3128(19)30206-9
doi: 10.1016/j.chom.2019.04.003
pmc: PMC6748655
mid: NIHMS1529796
pii:
doi:

Substances chimiques

Antibodies, Viral 0
Epitopes 0
Hemagglutinin Glycoproteins, Influenza Virus 0
Polysaccharides 0

Types de publication

Journal Article

Langues

eng

Sous-ensembles de citation

IM

Pagination

827-835.e6

Subventions

Organisme : NINR NIH HHS
ID : R01 NR003126
Pays : United States
Organisme : NIAID NIH HHS
ID : R01 AI128832
Pays : United States
Organisme : NIAID NIH HHS
ID : P01 AI089618
Pays : United States
Organisme : NIAID NIH HHS
ID : UC6 AI058607
Pays : United States
Organisme : NIGMS NIH HHS
ID : P41 GM103403
Pays : United States
Organisme : NCI NIH HHS
ID : P30 CA006516
Pays : United States
Organisme : NIAID NIH HHS
ID : U19 AI117892
Pays : United States

Commentaires et corrections

Type : CommentIn

Informations de copyright

Copyright © 2019 Elsevier Inc. All rights reserved.

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Auteurs

Goran Bajic (G)

Laboratory of Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Max J Maron (MJ)

Ragon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA.

Yu Adachi (Y)

Department of Immunology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.

Taishi Onodera (T)

Department of Immunology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.

Kevin R McCarthy (KR)

Laboratory of Molecular Medicine, Boston Children's Hospital, Harvard Medical School, Boston, MA 02115, USA.

Charles E McGee (CE)

Duke Human Vaccine Institute, Duke University, Durham, NC 27710, USA.

Gregory D Sempowski (GD)

Duke Human Vaccine Institute, Duke University, Durham, NC 27710, USA.

Yoshimasa Takahashi (Y)

Department of Immunology, National Institute of Infectious Diseases, Tokyo 162-8640, Japan.

Garnett Kelsoe (G)

Duke Human Vaccine Institute, Duke University, Durham, NC 27710, USA; Department of Immunology, Duke University, Durham, NC 27710, USA.

Masayuki Kuraoka (M)

Department of Immunology, Duke University, Durham, NC 27710, USA. Electronic address: masayuki.kuraoka@duke.edu.

Aaron G Schmidt (AG)

Ragon Institute of MGH, MIT and Harvard, Cambridge, MA 02139, USA; Department of Microbiology, Harvard Medical School, Boston, MA 02115, USA. Electronic address: aschmidt@crystal.harvard.edu.

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