Pathogenic Mechanisms of Panton-Valentine Leukocidin in Staphylococcus aureus Infections

Summary

Panton-Valentine leukocidin (PVL) is a bicomponent, pore-forming toxin produced by certain strains of Staphylococcus aureus that targets polymorphonuclear leukocytes, particularly neutrophils. Its two subunits, LukS-PV and LukF-PV, assemble in the host cell membrane to create transmembrane pores, leading to rapid ion flux, cellular swelling and cytolysis. At sublytic concentrations, PVL triggers neutrophil activation and the release of pro-inflammatory mediators, including interleukins and tumour necrosis factor, which amplify local tissue inflammation and contribute to necrosis. The genes encoding PVL are carried on mobile bacteriophages and can transfer between strains, promoting the emergence of virulent lineages in both community and hospital settings. Clinically, PVL-positive S. aureus is associated with severe skin and soft tissue infections, necrotising pneumonia and osteomyelitis, frequently in otherwise healthy individuals. The interplay between rapid neutrophil lysis and exaggerated inflammatory signalling underlies the aggressive tissue damage observed in PVL-mediated disease. Rapid detection of pvl genes and strategies to inhibit toxin activity are therefore central to improving patient outcomes and curbing the global spread of these hypervirulent clones.

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Pathogenic Mechanisms of Panton-Valentine Leukocidin in Staphylococcus aureus Infections publication trend

The graph below shows the total number of articles in pathogenic mechanisms of panton-valentine leukocidin in staphylococcus aureus infections across all publications each year (not limited to Nature Index journals).

Technical terms

Pore-forming toxin: A protein that inserts into host cell membranes to create pores, causing ionic imbalance and cell death.

LukS-PV and LukF-PV: The two polypeptide components that oligomerise to form the functional PVL pore complex.

Bacteriophage: A virus that infects bacteria and can carry genes—such as lukSF-PV—between bacterial hosts.

Exotoxin suppression: A therapeutic strategy aiming to reduce toxin synthesis by inhibiting bacterial protein production, often via specific antibiotics.

References

  1. Does Adjunctive Clindamycin Have a Role in Staphylococcus aureus Bacteremia? A Protocol for the Adjunctive Treatment Domain of the Staphylococcus aureus Network Adaptive Platform (SNAP) Randomized Controlled Trial. Clinical Infectious Diseases (2024).
  2. Detection of Staphylococcus aureus virulence gene pvl based on CRISPR strip. Frontiers in Immunology (2024).
  3. Staphylococcal Panton-Valentine Leukocidin Induces Pro-Inflammatory Cytokine Production and Nuclear Factor-Kappa B Activation in Neutrophils. PLOS ONE (2012).
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