Publications by authors named "P Palittapongarnpim"

Mycobacterium tuberculosis Complex (MTBC), the etiological agent of tuberculosis (TB), demonstrates considerable genotypic diversity with distinct geographic distributions and variable virulence profiles. The pe-ppe gene family is especially noteworthy for its extensive variability and roles in host immune response modulation and virulence enhancement. We sequenced an Mtb genotype L2.

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Article Synopsis
  • Tuberculosis caused by Mycobacterium tuberculosis (Mtb) remains a major global health concern, and this study introduces a new method to identify large genetic insertions and deletions (indels) that have been overlooked.
  • The analysis of 1,960 Mtb clinical isolates shows that harmful genetic variants are rarely found in essential survival genes, while Mtb genomes contain many partially harmful mutations.
  • The research also links specific genetic variations, including indels in various genes, to patient outcomes and antibiotic resistance, offering insights that could improve tuberculosis treatment and prediction of risks.
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(MTB) presents a global health issue. Various genotypes of MTB have different geographic distributions. The majority of MTB in Thailand belong to lineages 1 and 2.

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serovar Kentucky ST198 is a major health threat due to its resistance to ciprofloxacin and several other drugs, including third-generation cephalosporins. Many drug-resistant genes have been identified in the genomic island 1 variant K (SGI1-K). In this study, we investigated the antimicrobial resistance (AMR) profile and genotypic relatedness of two isolates of ciprofloxacin-resistant (CIP) .

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is considered by many to be the deadliest microbe, with the estimated annual cases numbering more than 10 million. The bacteria, including , are classified into nine major lineages and hundreds of sublineages, each with different geographical distributions and levels of virulence. The phylogeographic patterns can be a result of recent and early human migrations as well as coevolution between the bacteria and various human populations, which may explain why many studies on human genetic factors contributing to tuberculosis have not been replicable in different areas.

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