Decades of research on mammalian immunity to influenza virus infection have thoroughly established the important contributions made by both the innate and adaptive responses in containing the infection, and in eliminating the virus and protecting from reinfection, respectively. While rapid non-specific innate response is functionally distinct from, yet elegantly complementary to, the delayed-but-specific adaptive response, an increasing number of studies have provided evidence suggesting signals generated during the early innate response can have a significant impact on the quality of the later adaptive response, particularly in the context of influenza virus infection. From these findings emerged the notion that certain innate signals can act directly on B cells, and that this can even help activate virus specific B cells independent of T cell help, marking a major shift away from the current two-signal paradigm of lymphocyte activation. Here we review the current understanding of early B cell responses to influenza virus infection and the role of innate signals (particularly IFN-I and TLR7) in shaping this response.