Bibliographic citations
Carlos, C., Diaz, A. (2022). Ocurrencia de mutaciones en el gen pncA y mutaciones en otros genes (rpsA, panD y clpC1) asociados a la resistencia a la pirazinamida en Mycobacterium tuberculosis a través del análisis de 3016 genomas de aislados clínicos de Lima y Callao [Universidad Peruana Cayetano Heredia]. https://hdl.handle.net/20.500.12866/13487
Carlos, C., Diaz, A. Ocurrencia de mutaciones en el gen pncA y mutaciones en otros genes (rpsA, panD y clpC1) asociados a la resistencia a la pirazinamida en Mycobacterium tuberculosis a través del análisis de 3016 genomas de aislados clínicos de Lima y Callao []. PE: Universidad Peruana Cayetano Heredia; 2022. https://hdl.handle.net/20.500.12866/13487
@misc{renati/685984,
title = "Ocurrencia de mutaciones en el gen pncA y mutaciones en otros genes (rpsA, panD y clpC1) asociados a la resistencia a la pirazinamida en Mycobacterium tuberculosis a través del análisis de 3016 genomas de aislados clínicos de Lima y Callao",
author = "Diaz Lostao, Analucia",
publisher = "Universidad Peruana Cayetano Heredia",
year = "2022"
}
Tuberculosis is a disease caused by the bacillus Mycobacterium tuberculosis, which mainly affects the lungs. Pyrazinamide (PZA) is one of the most widely used antibiotics to combat it since it eliminates latent bacilli, however, the number of PZA-resistant strains is increasing. Its main resistance mechanism is related to a wide variety of mutations in the pncA gene, which encodes the enzyme pyrazinamidase (PZAse), necessary for drug activation. In addition, mutations have been found in other genes associated with the mechanism of action of PZA, such as rpsA, panD or clpC1, but the exclusive presence of mutations in these genes in resistant strains to PZA is almost nonexistent. Therefore, the presence of these mutations together with mutations in the pncA gene in resistant strains could explain the level of resistance to PZA in combination with the reduction of PZAse activity. Thus, the present study aims to determine the association between mutations in the pncA gene and mutations in other genes that explain resistance to PZA in M. tuberculosis. For this, 3016 genomes of clinical isolates from Peru were analyzed and the statistical significance of these comparisons was verified using the test of proportions and chi square. We show that there is an association between resistant strains and mutations in the rpsA and clpC1 genes, which could explain PZA resistance in M. tuberculosis through an additive effect.
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