Abstract
Two lineages of influenza B virus currently co-circulate and have distinct antigenicity, termed Victoria and Yamagata after the B/Victoria/2/87 and B/Yamagata/16/88 strains, respectively. We analyzed antibody titer dynamics following PCR-confirmed influenza B virus infection in a longitudinal community-based cohort study conducted in Hong Kong from 2009–2014 to assess patterns in changes in antibody titers to B/Victoria and B/Yamagata viruses following infections with each lineage. Among 62 PCR-confirmed cases, almost half had undetectable hemagglutination inhibition (HAI) antibody titers to the lineage of infection both pre-infection and post-infection. Among those infected with influenza B/Victoria who showed an HAI titer response after infection, we found strong rises to the lineage of infection, positive but smaller cross-lineage HAI titer boosts, a small dependence of HAI titer boosts on pre-infection titers, and a shorter half-life of HAI titers in adults. Our study is limited by the low HAI sensitivity for non-ether-treated IBV antigen and the incapacity of performing other assays with higher sensitivity, as well as the mismatch between the B/Yamagata lineage circulating strain and the assay strain in one of the study seasons.
Highlights
Influenza B virus infections are responsible for a considerable fraction of all influenza-associated morbidity and mortality [1]
A number of studies have noted distinct patterns in age distributions of infections with influenza B/Victoria and B/Yamagata virus strains, with viruses of both lineages being most commonly identified in children, but influenza B/Yamagata virus infections more frequently identified in adults and older adults [3, 4]
Pooled nose and throat swabs were tested by reverse transcription polymerase chain reaction (PCR) for influenza A and B, and the lineage of influenza B positives was determined with lineage-specific primers [7, 8]
Summary
Influenza B virus infections are responsible for a considerable fraction of all influenza-associated morbidity and mortality [1]. Two lineages of influenza B virus with distinct antigenicity, termed Victoria and Yamagata after the B/Victoria/2/87 and B/Yamagata/16/88 strains, respectively. They have been co-circulating globally since at least 2001 [1, 2]. A number of studies have noted distinct patterns in age distributions of infections with influenza B/Victoria and B/Yamagata virus strains, with viruses of both lineages being most commonly identified in children, but influenza B/Yamagata virus infections more frequently identified in adults and older adults [3, 4]. One of the possible explanations for this pattern is “imprinting”, where immune responses to recent infections are affected by primary infection in childhood [5]. We examined changes in serum antibody titers against influenza B
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