Chronic viral infections such as HIV and Hepatitis C result in poor humoral immune responses, characterised by the delayed generation of neutralising antibodies and dysregulation of memory B cell formation. Little is known regarding the mechanisms dictating the fundamental changes that result in dysfunctional B cell memory during chronic viral infection. Understanding these factors will be key for developing effective vaccines. We used an in vivo mouse model utilising acute and chronic strains of lymphocytic choriomeningitis virus (LCMV) in conjunction with a B cell tetramer specific for the LCMV nucleoprotein to examine antigen-specific memory B cell subset formation following infection. We performed phenotypic analysis of genetically modified mouse strains, BrdU-labelling studies and single cell RNA-sequencing to examine memory B cell formation, phenotype and function in response to acute vs. chronic LCMV infection. We found that memory B cells generated during chronic viral infection are highly proliferative, unlike classical memory B cells. Single-cell RNA-seq identified key genes downregulated in memory B cells generated in chronic infection including CD21, which promotes enhanced B cell responses to antigen, CD23, which binds C3 (complement)-coated immune complexes to mediate selection of B cells, CD55, which protects host cells from complement-mediated damage, and GILZ, a lack of which is associated with immune complex glomerulonephritis. To examine the role of excess immune complexes in the formation of effective B cell memory, we utilised mice in which B cell-intrinsic T-bet, which regulates antibody production to viral infection, was ablated. T-bet deletion resulted in increased expression of classical memory B cell markers, decreased circulating LCMV-specific immune complexes and reduced viremia. Understanding the factors driving altered humoral immune memory formation and the roles of memory B cells formed in the context of chronic viral infection is integral for improving therapeutics.