Genomic Analysis of Yersinia pestis Strains from Brazil: Search for Virulence Factors and Association with Epidemiological Data.
João Luiz de Lemos Padilha PittaMatheus Filgueira BezerraDiego Leandro Reis da Silva FernandesTessa de BlockAne de Souza NovaesAlzira Maria Paiva de AlmeidaAntonio Mauro RezendePublished in: Pathogens (Basel, Switzerland) (2023)
Yersinia pestis , the etiological agent of the plague, is considered a genetically homogeneous species. Brazil is currently in a period of epidemiological silence but plague antibodies are still detected in sentinel animals, suggesting disease activity in the sylvatic cycle. The present study deployed an in silico approach to analyze virulence factors among 407 Brazilian genomes of Y. pestis belonging to the Fiocruz Collection (1966-1997). The pangenome analysis associated several known virulence factors of Y. pestis in clades according to the presence or absence of genes. Four main strain clades (C, E, G, and H) exhibited the absence of various virulence genes. Notably, clade G displayed the highest number of absent genes, while clade E showed a significant absence of genes related to the T6SS secretion system and clade H predominantly demonstrated the absence of plasmid-related genes. These results suggest attenuation of virulence in these strains over time. The cgMLST analysis associated genomic and epidemiological data highlighting evolutionary patterns related to the isolation years and outbreaks of Y. pestis in Brazil. Thus, the results contribute to the understanding of the genetic diversity and virulence within Y. pestis and the potential for utilizing genomic data in epidemiological investigations.
Keyphrases
- escherichia coli
- pseudomonas aeruginosa
- biofilm formation
- staphylococcus aureus
- antimicrobial resistance
- genome wide
- disease activity
- genetic diversity
- rheumatoid arthritis
- systemic lupus erythematosus
- electronic health record
- bioinformatics analysis
- cystic fibrosis
- big data
- genome wide identification
- candida albicans
- transcription factor
- rheumatoid arthritis patients
- genome wide analysis
- ankylosing spondylitis
- molecular docking