Laufer Center Seminar - Hwan Kim
Hwan Kim, Ph.D
Associate Professor
Department of Microbiology and Immunology
Stony Brook University
August 28, 2026 at 12:30 PM
Laufer Center Lecture Hall 101
Title: Disarming Staphylococcus aureus virulence
Abstract: Staphylococcus aureus has successfully evolved to exploit and neutralize host immunity, enabling its transition from harmlessly colonizing anterior nares to causing severe, deep-tissue infections. Strikingly, prior S. aureus infections often fail to elicit protective immunity, leaving individuals vulnerable to recurrent infections. Making matters worse, the rapid rise and spread of antibiotic-resistant S. aureus continue to threaten public health. To address this, extensive research has identified virulence factors, elucidated their underlying molecular mechanisms, and explored vaccine and immune-therapeutic strategies. Unfortunately, all clinical vaccine trials targeting individual or combined antigens have failed to meet primary endpoints.
Among these virulence factors, Staphylococcal protein A (SpA) is a predominant, conserved surface-anchored polypeptide that engages host immunoglobulins and B cell receptors, thereby impairing antibody-mediated recognition and modulating B cell-dependent adaptive immunity. Notably, neutralizing SpA during infection significantly reduces S. aureus burden and triggers broad-spectrum anti-S. aureus responses in murine models.
While SpA neutralization offers a promising therapeutic platform, additional strategies are necessary to overcome antibiotic resistance and perturb multifactorial virulence mechanisms. Many virulence determinants use distinct biochemical interactions involving allosteric (distal) sites to induce structural changes at the active site. In collaboration with the Laufer Center, we employ newly developed computational modeling to identify small molecules that bind allosteric and active sites to neutralize critical biochemical functions of S. aureus virulence determinants. Further, we aim to evaluate the potential of these inhibitors to synergize with existing antibiotics and preclinical vaccines.
