Modelling within-host macrophage dynamics in influenza virus infection

Human respiratory disease associated with influenza virus infection is of significant public health concern. Macrophages, as part the front line host innate cellular defence, have been shown to play an important role in controlling viral replication. However, fatal outcomes infection, evidenced patients infected highly pathogenic strains, are often prompt activation and excessive accumulation macrophages. Activated macrophages can produce a large amount pro-inflammatory cytokines, which leads severe symptoms at times death. mechanism for rapid during remains unclear. It has suggested that phenomena may arise from complex interactions between virus. In this work, we develop novel mathematical model study relationship level macrophage load infection. Our combines dynamic essential predicts be negatively correlated when infectivity sufficiently high. We further identify temporary depletion resting response major driver our negative load, providing new insight into mechanisms regulate activation. serves framework dynamics virus-macrophage provides mechanistic explanation existing experimental observations, contributing enhanced understanding