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Pre-existing immunity to influenza is dependent on a number of factors and can vary greatly within and across influenza subtypes. In this study, volunteers (aged 18–85 years) were vaccinated with split, inactivated FluzoneTM in four consecutive influenza seasons from 2013 to 2016. The impact of repeat vaccination on breadth and durability of functional antibodies was assessed for total IgG and IgA anti-hemagglutinin (HA) binding antibodies and hemagglutination-inhibition (HAI) activity against both influenza B lineages. Many subjects were able to maintain high seroprotective titers to the vaccine strains in subsequent years, which resulted in low vaccine-induced seroconversion rates. This was especially evident in younger subjects who typically had higher titers and maintained these titers into the following season. In contrast, the HAI titers in elderly subjects were generally lower and more likely to decline prior to the start of the next influenza season. Immunological recall or ‘back-boosting’ to antigenically related viruses was associated with seroconversion. Overall, influenza vaccination in both younger and older people elicited broadly reactive immune responses within a lineage, as well as cross-reactive immune responses between lineages. This study exemplified the impact that age and influenza exposure history have on determining an individual’s ability to respond to future influenza infections.

We used national sentinel surveillance data in China for 2005–2016 to examine the lineage-specific epidemiology of influenza B. Influenza B viruses circulated every year with relatively lower activity than influenza A. B/Yamagata was more frequently detected in adults than in children.

Influenza B viruses (IBV) are an important cause of morbidity and mortality during interpandemic periods in the human population. Two phylogenetically distinct IBV lineages, B/Yamagata and B/Victoria, co-circulate worldwide and they present challenges for vaccine strain selection. Until the present study, there was little information regarding the pattern of the circulating strains of IBV in Uruguay. A subset of positive influenza B samples from influenza-like illness (ILI) outpatients and severe acute respiratory illness (SARI) inpatients detected in sentinel hospitals in Uruguay during 2012–2019 were selected. The sequencing of the hemagglutinin (HA) and neuraminidase (NA) genes showed substitutions at the amino acid level. Phylogenetic analysis reveals the co-circulation of both lineages in almost all seasonal epidemics in Uruguay, and allows recognizing a lineage-level vaccine mismatch in approximately one-third of the seasons studied. The epidemiological results show that the proportion of IBV found in ILI was significantly higher than the observed in SARI cases across different groups of age (9.7% ILI, 3.2% SARI) and patients between 5–14 years constituted the majority (33%) of all influenza B infection (p < 0.05). Interestingly, we found that individuals >25 years were particularly vulnerable to Yamagata lineage infections.

Victoria and Yamagata lineages of influenza B viruses are globally circulating in seasonal epidemics. Madin−Darby canine kidney (MDCK) cells are permissive for viral isolation and vaccine manufacture. Nevertheless, the interplay between influenza B viruses and host microRNAs has not been investigated in this cell line. Therefore, the present study aims at high-throughput analysis of canine microRNA profile upon infection of influenza B viruses. Briefly, MDCK cells were infected with Victoria or Yamagata lineage at MOI of 0.01. After being harvested at 6, 12 and 24 h post infection, microRNAs were subjected to high-throughput sequencing based on MiSeq platform (Illumina). The results demonstrated that five microRNAs including cfa-miR-197, cfa-miR-215, cfa-miR361, cfa-miR-1841, and cfa-miR-1842 were overexpressed in both Victoria and Yamagata lineage infections. Interestingly, computational prediction showed that karyopherin alpha 6 (KPNA6) was targeted by cfa-miR-197 and cfa-miR-215. Moreover, the binding sites of both microRNAs were assessed by 3′-UTR reporter assay. The results showed that only cfa-miR-197 could bind to the target sites of KPNA6, leading to suppressing luciferase activity. Additionally, silencing of KPNA6 was confirmed by overexpression of cfa-miR-197. This study provides canine microRNA responses to seasonal influenza B viruses, suggesting that virus-mediated microRNAs might play crucial roles in host gene regulation.