Research on the Genetic Polymorphism and Function of with Premature Stop Codons in .

is a Gram-positive bacterial species that causes listeriosis, a major foodborne disease worldwide. The virulence factor facilitates the invasion of into intestinal epithelial cells expressing E-cadherin receptors. Naturally occurring premature stop codon (PMSC) mutations in have been shown to result in the production of truncated proteins associated with attenuated virulence. Moreover, different strains contain distinct variants. In this study, we first characterized in 546 strains isolated from various foods in Shanghai. The results showed that 36.1% (95% Confidence Interval: 32.0~40.2%) of the food isolates harbored with PMSC, which was found to be associated with clonal complex (CC) types, with the highest proportions observed in CC9 and CC121. To investigate the function of , we first used the dominant CC87 isolated from patients as the test strain and constructed an strain via homologous recombination. Resistance tests and virulence tests showed that while did not affect the resistance of , it significantly influenced cell adhesion and invasiveness. To further explore the function of , we performed virulence tests on five CC-type strains carrying with PMSC and their corresponding strains with intact . We found that the virulence of strains carrying or with PMSC was associated with their CC type. Our preliminary results showed that premature termination of did not significantly affect the adhesion and invasion abilities of low-virulence CC-type strains in Caco-2 cells, but substantially promoted those of high-virulence strains such as CC8 and CC7. In summary, this study preliminarily evaluated the effects of integrity and PMSC mutation variation on the virulence of , providing a foundation for further research on -related pathogenic mechanisms.