Seasonal influenza in humans is predominantly caused by influenza A virus (IAV) and influenza B virus (IBV), but they differ markedly in host range, evolutionary dynamics, and pandemic potential. Such phenotypic divergence reflects the distinct molecular strategies employed by the two viruses at key stages of their life cycles. Hemagglutinin (HA) of IAV possesses prominent structural plasticity, which endows it with the capacity to recognize both avian-type α2,3-linked and human-type α2,6-linked sialic acid receptors, and the function of IAV polymerase is highly dependent on host acidic nuclear phosphoprotein 32 (ANP32) family proteins. Moreover, IAV utilizes multiple pleiotropic virulence factors, such as the nonstructural protein 1 (NS1), to modulate host immune responses and inflammatory processes, thereby contributing to viral fitness, host adaptation, and pandemic potential. In contrast, the HA of IBV preferentially binds to human-type (α2,6-linked) sialic acid receptors and exhibits a more restricted receptor-binding profile.While IBV polymerase is well adapted to human ANP32A and ANP32B, yet shows poor compatibility with avian ANP32 proteins. Additionally, the immunomodulatory machinery is relatively streamlined, engaging host cell death pathways in a more limited manner that may contribute to generally less extensive inflammatory responses in many experimental and clinical settings. As a result, IBV transmission is largely confined to humans, with a narrow host range and a predominantly seasonal epidemic pattern. In this review, we systematically compare IAV and IBV with respect to four core pathogenic processes, namely viral entry, genome replication efficiency and host factor dependence, immune evasion, and the regulation of host cell death pathways, to explain how these mechanisms collectively shape differences in host range, evolutionary dynamics, and pandemic potential. We particularly emphasize the capacity of IAV to achieve efficient replication in a wide range of host species, a trait that facilitates its multi-host circulation and viral gene reassortment. These insights establish a theoretical framework for enhancing influenza surveillance and guiding the development of next-generation influenza vaccines and antiviral therapeutics.