Background Staphylococcus aureus is a common gram-positive bacterium that is the
causative agent for several human diseases, including sepsis. A key virulence mechanism is
pathogen binding to host fibrinogen through the c-terminal region of the γ-chain. Previous
work demonstrated that Fgg Δ5 mice expressing mutant fibrinogen γ Δ5 lacking a S. aureus
binding motif had significantly improved survival following S. aureus septicemia. Fibrinogen
γ′ is a human splice variant that represents about 10-15% of the total fibrinogen in plasma …