Frontiers in Immunology· 2026Q1
SEVI fibrils are induced by bacterial surface molecules and exert antimicrobial activity against ESKAPE pathogens
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- 2026year
Short summary
Semen-derived enhancer of viral infection (SEVI) fibrils, formed from a peptide naturally present in seminal plasma, exhibit direct, dose-dependent antibacterial activity against ESKAPE pathogens and urogenital bacteria at physiologically relevant concentrations.
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Key points
- SEVI fibrils exhibit direct, dose-dependent antibacterial activity against ESKAPE pathogens and urogenital bacteria.
- Bacterial surface molecules (lipopolysaccharides, lipoteichoic acid) induce SEVI fibril formation.
- Antibacterial activity is dependent on the fibrillar structure of SEVI, as disruption abolishes the effect.
- Mechanistic studies suggest SEVI induces a stress response in bacteria, including intracellular polyphosphate accumulation, rather than significant membrane disruption.
AI-generated from the title and abstract; the full text is not read.
Abstract
Abstract The semen-derived enhancer of viral infection (SEVI) is an amyloid fibril formed by the self-assembly of the PAP248-286 peptide, a cleavage product of prostatic acid phosphatase, which is naturally present in human seminal plasma. Beyond its previously described role in HIV transmission, findings highlight a physiological function for SEVI in innate immunity. As many amyloids display antimicrobial effects, we tested SEVI fibrils for antibacterial activity against microbial ESKAPE pathogens and urogenital bacteria, including Pseudomonas aeruginosa, Klebsiella quasipneumoniae, Escherichia coli, Acinetobacter baumannii, Staphylococcus aureus, Streptococcus agalactiae and Listeria monocytogenes . SEVI exhibited direct dose-dependent antibacterial effects in radial diffusion and survival assays, with activity observed at physiologically relevant concentrations. Bacterial surface molecules such as lipopolysaccharides and lipoteichoic acid induced the formation of SEVI fibrils, as confirmed by kinetic assays. Preincubation with epigallocatechin gallate, a fibril disruptor, abolished SEVI’s antibacterial activity, pointing to the importance of its fibrillar structure. Mechanistic studies and electron microscopy revealed limited bacterial membrane disruption and the intracellular accumulation of polyphosphate granules in P. aeruginosa , indicating a stress response. In conclusion, SEVI exerts a potent antibacterial activity against pathogens found in the urogenital tract, indicating a potential physiological role in vaginal mucosal immunity.
The authors' abstract, as published at the source. Frontiers in Immunology, 2026 · DOI ↗
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MicrobiologyImmunology and Microbiology