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        <identifier>oai:figshare.com:article/33870202</identifier>
        <datestamp>2026-09-17T03:40:04Z</datestamp>
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          <dc:title>Data Sheet 1_From mutation detection to treatment decisions: CRISPR-enabled diagnostics for drug-resistant tuberculosis.pdf</dc:title>
          <dc:creator>Weijia Yi (24641523)</dc:creator>
          <dc:creator>Fukang Luo (14500750)</dc:creator>
          <dc:creator>Dianping Yi (25000690)</dc:creator>
          <dc:creator>Jing Guo (102972)</dc:creator>
          <dc:creator>Shan Liu (193759)</dc:creator>
          <dc:creator>Qibing Yan (25000693)</dc:creator>
          <dc:creator>Hongzhi Luo (12325703)</dc:creator>
          <dc:subject>Biotechnology</dc:subject>
          <dc:subject>antimicrobial resistance</dc:subject>
          <dc:subject>clinical translation</dc:subject>
          <dc:subject>CRISPR diagnostics</dc:subject>
          <dc:subject>drug-resistant tuberculosis</dc:subject>
          <dc:subject>heteroresistance</dc:subject>
          <dc:subject>mutation-to-drug interpretation</dc:subject>
          <dc:description>&lt;p&gt;Effective management of drug-resistant tuberculosis requires molecular assays that not only detect Mycobacterium tuberculosis but also identify resistance-associated variants, support drug-level interpretation, and indicate when broader confirmatory testing is needed. This narrative review applies a mutation-to-drug-to-decision framework to distinguish assay validity, exact-variant detection, drug-level inference, and decision impact. We synthesize evidence on target accessibility, minority-allele preservation, multiplexing, direct-specimen testing, and sequencing enrichment, emphasizing how these factors shape clinical interpretability. Current evidence remains dominated by analytical studies, isolate-based evaluations, and small direct-specimen investigations, with prospective multicenter treatment-impact validation still lacking. Population-level benchmarks indicate incomplete biological coverage for compact target regions, reaching approximately 92.6% for rpoB RRDR-based rifampicin detection, 85.4% for katG codon 315 plus the inhA promoter for isoniazid, and 84.7%–88.2% for gyrA/gyrB-based fluoroquinolone detection. Allele-specific CRISPR is therefore best suited to rapid rule-in of selected resistance-associated variants, while dispersed or heterogeneous mechanisms require broader molecular or phenotypic assessment. CRISPR should complement WHO-recommended rapid molecular testing and targeted next-generation sequencing rather than replace established molecular or phenotypic methods.&lt;/p&gt;</dc:description>
          <dc:date>2026-09-17T03:40:04Z</dc:date>
          <dc:type>Dataset</dc:type>
          <dc:type>Dataset</dc:type>
          <dc:identifier>10.3389/fbioe.2026.1947704.s001</dc:identifier>
          <dc:relation>https://figshare.com/articles/dataset/Data_Sheet_1_From_mutation_detection_to_treatment_decisions_CRISPR-enabled_diagnostics_for_drug-resistant_tuberculosis_pdf/33870202</dc:relation>
          <dc:rights>CC BY 4.0</dc:rights>
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