Abstract
Globally, tuberculosis (TB) remains a prevalent threat to public health. In 2019, TB affected 10 million people and caused 1.4 million deaths. The major challenge for controlling this infectious disease is the emergence and spread of drug-resistant Mycobacterium tuberculosis, the causative agent of TB. The antibiotic streptomycin is not a current first-line anti-TB drug. However, WHO recommends its use in patients infected with a streptomycin-sensitive strain. Several mutations in the M. tuberculosis rpsL, rrs and gidB genes have proved association with streptomycin resistance. In this study, we performed a molecular analysis of these genes in clinical isolates to determine the prevalence of known or novel mutations. Here, we describe the genetic analysis outcome. Furthermore, a biocomputational analysis of the MtGidB L101F variant, the product of a novel mutation detected in gidB during molecular analysis, is also reported as a theoretical approach to study the apparent genotype-phenotype association.
Highlights
Tuberculosis (TB) is among the top 10 causes of death and the leading disease caused by a single infectious agent, Mycobacterium tuberculosis, ranking above
Given that Str interacts with such a nucleoside, an impaired GidB function would affect the G518 methylation status of M. tuberculosis 16S
G13R is within the N-terminal domain, and L101F is in the SAM-dependent methyltransferase (SAM-MTase) domain, within the SAM-interacting region [25,36,37]
Summary
Tuberculosis (TB) is among the top 10 causes of death and the leading disease caused by a single infectious agent, Mycobacterium tuberculosis, ranking above. Mutations in the M. tuberculosis rpsL, rrs and gidB genes, respectively, encoding the ribosomal protein S12, 16S rRNA and glucose-inhibited division protein B, have been associated with Str resistance [13,17,18,19,20,21]. Given that Str interacts with such a nucleoside, an impaired GidB function would affect the G518 methylation status of M. tuberculosis 16S rRNA, interfering with drug binding and, producing the observed StrR phenotype [21,25,26,27,28]. A biocomputational analysis was used as a theoretical approach to study the apparent genotype-phenotype association observed in two StrR isolates containing the 301c>t mutation in gidB, which produces the non-synonymous substitution L101F in the gene product
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