Toll-like receptor 7 (TLR7) triggers innate and adaptive antiviral immune responses through its capacity to recognize single-stranded RNA. TLR7 loss-of-function mutants have been described as associated with life threatening pneumonia in severe COVID-19 patients. Whereas it is clear that TLR7-driven innate induction of type I IFN appears central to control SARS-CoV2 virus spreading during the first few days of infection, the impact of TLR7-deficiency on adaptive B cell immunity is less clear. In the present study, we examined the role of TLR7 in the adaptive B cells response to various pathogen-like antigens (PLAs). We used inactivated SARS-CoV2 and a PLA-based COVID-19 vaccine candidate designed to mimic SARS-CoV2 with encapsulated bacterial ssRNA as TLR7 ligands and conjugated with the RBD of the SARS-CoV2 Spike protein. Upon repeated immunization with inactivated SARS-CoV2 or PLA COVID-19 vaccine, our data show that Tlr7-deficiency abolished the germinal center (GC) dependent production of RBD-specific class-switched IgG2b and IgG2c, and neutralizing antibodies to SARS-CoV2. In an adoptive transfer model, we also provide evidence for a non-redundant role for B cell-intrinsic TLR7 in the promotion of RBD-specific IgG2b/IgG2c and memory B cells. Together, these data demonstrate that the induction of GC reaction and class-switch recombination to the Myd88-dependent IgG2b/IgG2c in response to SARS-CoV2 or PLAs is strictly dependent on cell-intrinsic activation of TLR7 in B cells.