ArticleCurrent microbiology2014
The truncated major pilin subunit Sbp2 of the srtBCD pilus cluster still contributes to Streptococcus suis pathogenesis in the absence of pilus shaft.
Article in Current microbiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- The truncated major pilin subunit SBP2' contributes toApplied and environmental microbiology · 2026Article
- Clinically relevant genomic and phenotypic differences in virulence, antimicrobial resistance, and biofilm-associated tolerance between Streptococcus suis lineages ST1 and ST123.Veterinary research · 2026Article
- Class C sortases of the SrtBCD pilus cluster involved in the virulence of Streptococcus suis in the mouse model.Folia microbiologica · 2026Article
- Genomic analysis and virulence of human Streptococcus suis serotype 14.European journal of clinical microbiology & infectious diseases : official publication of the European Society of Clinical Microbiology · 2025Article
- Identification of the RNA-binding domain-containing protein RbpA that acts as a global regulator of the pathogenicity ofVirulence · 2022Article
- Comparative transcriptomic analysis reveal genes involved in the pathogenicity increase ofVirulence · 2022Article
- Genomic characterization of Streptococcus parasuis, a close relative of Streptococcus suis and also a potential opportunistic zoonotic pathogen.BMC genomics · 2022Article
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Authors and funding
4 authors.
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No grant is acknowledged in the PubMed record.
Abstract
Streptococcus suis serotype 2 (SS2) is an emerging zoonotic agent responsible for a number of infections in pigs and humans. Pili have been proposed as virulence factors in Gram-positive bacteria. However, due to the abolition of pili production, the function of the srtBCD pilus cluster, especially the truncated major pilin subunit Sbp2 (Sbp2', Sbp2″), has not been explored. In this study, isogenic mutants (Δsbp2', Δsbp2″) were constructed by homologous replacement in SS2 strain P1/7. Deletion of sbp2' attenuated the virulence in a zebrafish model as shown by more than an eightfold increase in the LD50 of Δsbp2', compared with that of the parent strain. In addition, the adhesion of Δsbp2' to HEp-2 cell monolayers decreased significantly. Compared with the parent strain, no obvious differences in virulence and adherence efficiency were observed for Δsbp2″. Our data suggest that Sbp2' could be involved in SS2 pathogenesis despite absence of its pilus shaft.
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