The antigenic glycoproteins hemagglutinin (HA) and neuraminidase (NA) of influenza A virus subtypes are responsible for viral replication, by binding with sialic acid on host cells and membrane fusion, and cleaving such receptors for virion release respectively. Despite yearly reformulation of seasonal vaccines, continuous evolution of HA and NA has enabled the virus to acquire immune escape and severely hindered the protective effectiveness of antibodies elicited by such medications. This project aims to monitor the evolutionary trajectory by tracking spatiotemporal dynamics of HA and NA and identifying the mutational hotspots within to facilitate vaccine and drug design.