Abstract
How a history of influenza virus infections contributes to protection is not fully understood, but such protection might explain the contrasting age distributions of cases of the two lineages of influenza B, B/Victoria and B/Yamagata. Fitting a statistical model to those distributions using surveillance data from New Zealand, we found they could be explained by historical changes in lineage frequencies combined with cross-protection between strains of the same lineage. We found additional protection against B/Yamagata in people for whom it was their first influenza B infection, similar to the immune imprinting observed in influenza A. While the data were not informative about B/Victoria imprinting, B/Yamagata imprinting could explain the fewer B/Yamagata than B/Victoria cases in cohorts born in the 1990s and the bimodal age distribution of B/Yamagata cases. Longitudinal studies can test if these forms of protection inferred from historical data extend to more recent strains and other populations.
Highlights
How a history of influenza virus infections contributes to protection is not fully understood, but such protection might explain the contrasting age distributions of cases of the two lineages of influenza B, B/Victoria and B/Yamagata
Our model suggests that differences in the age distributions of B/ Victoria and B/Yamagata cases can be explained by historical changes in lineage frequencies combined with cross-protection between strains of the same lineage and additional protection against B/Yamagata in people first infected with it
Imprinting of people born in the late 1980s and early 1990s with B/Yamagata led to fewer B/Yamagata cases in those birth cohorts than in older and younger ones, whose primary influenza B infections were less likely to be B/Yamagata
Summary
How a history of influenza virus infections contributes to protection is not fully understood, but such protection might explain the contrasting age distributions of cases of the two lineages of influenza B, B/Victoria and B/Yamagata. Similar to the different subtypes of influenza A, the two lineages of influenza type B have distinct age distributions of medically attended infections. While the incidence of medically attended infections is highest in children for both lineages, B/ Yamagata appears less common than B/Victoria in teenagers and young adults but the pattern reverses in older age groups. This pattern has been observed in surveillance from the 2000s and 2010s in Oceania[28], East Asia[29], Europe[30,31], and North America[32]. Changes with age in the expression of sialic acid receptors have been proposed to explain the lower mean age of B/ Victoria cases[28], but this explanation does not account for the higher frequency of B/Yamagata cases in middle-aged people
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