Poor Immunogenicity, Not Vaccine Strain Egg Adaptation, May Explain the Low H3N2 Influenza Vaccine Effectiveness in 2012–2013
Author(s) -
Sarah Cobey,
Sigrid Gouma,
Kaela Parkhouse,
Benjamin S. Chambers,
Hildegund C.J. Ertl,
Kenneth E. Schmader,
Rebecca Halpin,
Xudong Lin,
Timothy B. Stockwell,
Suman R. Das,
Emily Landon,
Vera Tešić,
Ilan Youngster,
Benjamin A. Pinsky,
David E. Wentworth,
Scott E. Hensley,
Yonatan H. Grad
Publication year - 2018
Publication title -
clinical infectious diseases
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.44
H-Index - 336
eISSN - 1537-6591
pISSN - 1058-4838
DOI - 10.1093/cid/ciy097
Subject(s) - immunogenicity , medicine , influenza vaccine , virology , strain (injury) , immunology , vaccination , immune system
Influenza vaccination aims to prevent infection by influenza virus and reduce associated morbidity and mortality; however, vaccine effectiveness (VE) can be modest, especially for subtype A(H3N2). Low VE has been attributed to mismatches between the vaccine and circulating influenza strains and to the vaccine's elicitation of protective immunity in only a subset of the population. The low H3N2 VE in the 2012-2013 season was attributed to egg-adaptive mutations that created antigenic mismatch between the actual vaccine strain (IVR-165) and both the intended vaccine strain (A/Victoria/361/2011) and the predominant circulating strains (clades 3C.2 and 3C.3).
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