Literature DB >> 33370413

Phylogenomics of 8,839 Clostridioides difficile genomes reveals recombination-driven evolution and diversification of toxin A and B.

Michael J Mansfield1,2, Benjamin J-M Tremblay1, Ji Zeng3,4, Xin Wei1, Harold Hodgins1, Jay Worley5,6, Lynn Bry5,7, Min Dong3,4, Andrew C Doxey1.   

Abstract

Clostridioides difficile is the major worldwide cause of antibiotic-associated gastrointestinal infection. A pathogenicity locus (PaLoc) encoding one or two homologous toxins, toxin A (TcdA) and toxin B (TcdB), is essential for C. difficile pathogenicity. However, toxin sequence variation poses major challenges for the development of diagnostic assays, therapeutics, and vaccines. Here, we present a comprehensive phylogenomic analysis of 8,839 C. difficile strains and their toxins including 6,492 genomes that we assembled from the NCBI short read archive. A total of 5,175 tcdA and 8,022 tcdB genes clustered into 7 (A1-A7) and 12 (B1-B12) distinct subtypes, which form the basis of a new method for toxin-based subtyping of C. difficile. We developed a haplotype coloring algorithm to visualize amino acid variation across all toxin sequences, which revealed that TcdB has diversified through extensive homologous recombination throughout its entire sequence, and formed new subtypes through distinct recombination events. In contrast, TcdA varies mainly in the number of repeats in its C-terminal repetitive region, suggesting that recombination-mediated diversification of TcdB provides a selective advantage in C. difficile evolution. The application of toxin subtyping is then validated by classifying 351 C. difficile clinical isolates from Brigham and Women's Hospital in Boston, demonstrating its clinical utility. Subtyping partitions TcdB into binary functional and antigenic groups generated by intragenic recombinations, including two distinct cell-rounding phenotypes, whether recognizing frizzled proteins as receptors, and whether it can be efficiently neutralized by monoclonal antibody bezlotoxumab, the only FDA-approved therapeutic antibody. Our analysis also identifies eight universally conserved surface patches across the TcdB structure, representing ideal targets for developing broad-spectrum therapeutics. Finally, we established an open online database (DiffBase) as a central hub for collection and classification of C. difficile toxins, which will help clinicians decide on therapeutic strategies targeting specific toxin variants, and allow researchers to monitor the ongoing evolution and diversification of C. difficile.

Entities:  

Year:  2020        PMID: 33370413     DOI: 10.1371/journal.ppat.1009181

Source DB:  PubMed          Journal:  PLoS Pathog        ISSN: 1553-7366            Impact factor:   6.823


  9 in total

Review 1.  From signal transduction to protein toxins-a narrative review about milestones on the research route of C. difficile toxins.

Authors:  Klaus Aktories
Journal:  Naunyn Schmiedebergs Arch Pharmacol       Date:  2022-10-07       Impact factor: 3.195

2.  Strain Variation in Clostridioides difficile Cytotoxicity Associated with Genomic Variation at Both Pathogenic and Nonpathogenic Loci.

Authors:  Katie Saund; Ali Pirani; D Borden Lacy; Philip C Hanna; Evan Snitkin
Journal:  mSphere       Date:  2022-05-09       Impact factor: 5.029

3.  Receptor binding mechanisms of Clostridioides difficile toxin B and implications for therapeutics development.

Authors:  Peng Chen; Rongsheng Jin
Journal:  FEBS J       Date:  2021-12-04       Impact factor: 5.622

Review 4.  Clostridioides difficile toxins: mechanisms of action and antitoxin therapeutics.

Authors:  Shannon L Kordus; Audrey K Thomas; D Borden Lacy
Journal:  Nat Rev Microbiol       Date:  2021-11-26       Impact factor: 78.297

5.  Structure of the glucosyltransferase domain of TcdA in complex with RhoA provides insights into substrate recognition.

Authors:  Baohua Chen; Zheng Liu; Kay Perry; Rongsheng Jin
Journal:  Sci Rep       Date:  2022-05-30       Impact factor: 4.996

6.  Whole-Genome Sequencing Reveals the High Nosocomial Transmission and Antimicrobial Resistance of Clostridioides difficile in a Single Center in China, a Four-Year Retrospective Study.

Authors:  Xin Wen; Cong Shen; Jinyu Xia; Lan-Lan Zhong; Zhongwen Wu; Mohamed Abd El-Gawad El-Sayed Ahmed; Nana Long; Furong Ma; Guili Zhang; Wenwei Wu; Jianlve Luo; Yong Xia; Min Dai; Liyan Zhang; Kang Liao; Siyuan Feng; Cha Chen; Yishen Chen; Wenji Luo; Guo-Bao Tian
Journal:  Microbiol Spectr       Date:  2022-01-12

7.  Structural basis for selective modification of Rho and Ras GTPases by Clostridioides difficile toxin B.

Authors:  Zheng Liu; Sicai Zhang; Peng Chen; Songhai Tian; Ji Zeng; Kay Perry; Min Dong; Rongsheng Jin
Journal:  Sci Adv       Date:  2021-10-22       Impact factor: 14.136

8.  Structural basis for CSPG4 as a receptor for TcdB and a therapeutic target in Clostridioides difficile infection.

Authors:  Peng Chen; Ji Zeng; Zheng Liu; Hatim Thaker; Siyu Wang; Songhai Tian; Jie Zhang; Liang Tao; Craig B Gutierrez; Li Xing; Ralf Gerhard; Lan Huang; Min Dong; Rongsheng Jin
Journal:  Nat Commun       Date:  2021-06-18       Impact factor: 14.919

Review 9.  Large Clostridial Toxins: Mechanisms and Roles in Disease.

Authors:  Kathleen E Orrell; Roman A Melnyk
Journal:  Microbiol Mol Biol Rev       Date:  2021-06-02       Impact factor: 13.044

  9 in total

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