Artículo
en Inglés
| BVSDIP, FIOCRUZ | ID: dip-3282
The 7th cholerapandemic reached Latin America in 1991, spreading from Peru to virtually all Latin American countries.During the late epidemic period, a strain that failed to ferment sucrose dominated choleraoutbreaks in the NorthernBrazilian Amazon region. In order to understand the genomic characteristics and the determinants of this altered sucrose fermenting phenotype, the genome of the strain IEC224 was sequenced. This paperreports a broad genomic study of this strain, showing its correlation with the major epidemic lineage. The potentially mobile genomic regions are shown to possess GC content deviation, and harbor the main V. choleravirulencegenes. A novel bioinformatic approach was appliedin order to identify the putative functions of hypothetical proteins, and was compared with the automatic annotation by RAST. The genome of a large bacteriophage was found to be integrated to the IEC224s alanine aminopeptidasegene. The presence of this phage is shown to be a common characteristic of the El Tor strains from the Latin American epidemic, aswell as its putative ancestor from Angola. The defective sucrose fermenting phenotype is shown to be due to a single nucleotide insertion in the V. cholerae sucrose-specific transportationgene. This frame-shift mutation truncated a membrane protein, altering its structural pore-like conformation. Further, the identification of a common bacteriophage reinforces both the monophyletic and African-Origin hypotheses for the main causative agent of the 1991 Latin Americacholeraepidemics.(AU)