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• The mortality burden of influenza has been substantial in Shanghai, especially among the elderly. • Excessive mortality associated with influenza B virus is dominated by B(Yamagata) lineage. • The evidence for sex differences in influenza-associated mortality for respiratory and circulatory diseases is limited. Few studies have explored the different lineages of influenza B viruses, which cause excessive fatalities. This study aimed to estimate age- and sex-specific excessive mortality associated with influenza subtypes/lineages in Shanghai, during 2010–2015. We used quasi-Poisson regression models to fit weekly numbers of deaths from various causes by adjusting long-term trend, seasonal trend, and absolute humidity as confounding factors. The mortality burden associated with influenza subtypes/lineages was estimated by age and sex. The average influenza-associated excessive mortality rate in deaths coded as all-cause was 27.66 (95%CI: 22.30–33.88) per 100,000 person-years. The excessive deaths from six underlying causes in people aged ≥65 years weight heavily. Compared to influenza B(Victoria) lineage, influenza B(Yamagata) lineage had more effect on the influenza-associated disease burden, particularly in patients with respiratory and circulatory diseases. There was no statistical significance of sex in the mortality burden associated with influenza. Disproportionate mortality associated with influenza B virus is dominated by B(Yamagata) lineage in Shanghai, and the evidence for sex differences in the influenza-associated mortality burden for respiratory and circulatory diseases is limited. Improving the vaccination of the elderly and strengthening laboratory-based surveillance of influenza B lineages in Shanghai are needed to reduce this influenza's disease burden. [ABSTRACT FROM AUTHOR]

Influenza B virus (IBV) belongs to the Orthomyxoviridae family and generally causes sporadic epidemics but is occasionally deadly to individuals. The current research mainly focuses on clinical and pathological characteristics of IBV. However, to better prevent or treat the disease, one must determine the strategies developed by IBV to invade and disrupt cellular proteins and approach to replicate itself, to suppress antiviral innate immunity, and understand how the host responds to IBV infection. The B/Shanghai/PD114/2018 virus was able to infect alveolar epithelial cells (A549) cells, with good potential for replication. To identify host cellular responses against IBV infection, differentially expressed genes (DEGs) were obtained using RNA sequencing. The GO and KEGG pathway term enrichment analyses with the DEGs were performed, and we found that the DEGs were primary involved in metabolic processes and cellular function, which may be related to the host response, including the innate immune response against the virus. Our transcriptome analysis results demonstrated robust induction of interferon and interferon-stimulated gene expression by IBV in human cells during the early stages of infection, providing a foundation for further studies focused on antiviral drug development and interactions between the virus and host. [ABSTRACT FROM AUTHOR]