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Staphylococcus aureus ( S. aureus ) is a significant human pathogen known for its ability to form biofilms, which increase its resistance to antibiotics and immune defenses. This review delves into the mechanisms of biofilm formation in S. aureus , emphasizing the critical roles of various virulence factors. During the initial attachment phase, surface proteins such as protein A, fibronectin-binding proteins (FnBPs), and clumping factors (ClfA and ClfB) are anchored by sortase A (SrtA), facilitating adherence to host tissues and surfaces. Biofilm maturation is driven by polysaccharide intercellular adhesin (PIA), while the extracellular polymeric substance (EPS) matrix—comprising polysaccharides, extracellular DNA, proteins, and lipids—reinforces biofilm stability and defense mechanisms. Regulatory systems such as MgrA, ClpP, and the SaeR/SaeS two-component system dynamically modulate the expression of virulence and biofilm-associated genes, enabling bacterial adaptation to environmental stressors. Additionally, toxins such as alpha-hemolysin (Hla) and enzymes such as coagulase (Coa) and von Willebrand factor-binding protein (vWbp) play pivotal roles in immune evasion and biofilm protection. This review also explores emerging therapeutic strategies that target these virulence factors, highlighting their potential in treating persistent S. aureus infections. Understanding the intricate interplay between virulence factors and biofilm formation provides valuable insights for developing of more effective therapeutic interventions.
Wang et al. (Thu,) studied this question.