Magnitude of Phenotypic and MTBDRplus Line Probe Assay First-Line Anti-Tuberculosis Drug Resistance Among Tuberculosis Patients; Northwest Ethiopia

Background. This study aims to evaluate GenoType MTBDRplusand GenoType MTBDRslfor their ability to detect drug-resistant tuberculosis in a Chinese population.Methods. We collected 112Mycobacteria tuberculosisstrains from Jiangsu province, China. The conventional DST and line probe assay were used to detect drug resistance to rifampicin (RFP), isoniazid (INH), ofloxacin (OFX), kanamycin (Km), and ethambutol (EMB).Results. The sensitivity and specificity were 100% and 50% for RFP and 86.11% and 47.06% for INH, respectively. The most common mutations observed in MTBDRpluswererpoBWT8 omission + MUT3 presence,katGWT omission + MUT1 presence, andinhAWT1 omission + MUT1 presence. For drug resistance to OFX, Km, and EMB, the sensitivity of MTBDRslwas 94.74%, 62.50%, and 58.82%, respectively, while the specificity was 92.59%, 98.81%, and 91.67%, respectively. The most common mutations weregyrAWT3 omission + MUT3C presence,rrsMUT1 presence,embBWT omission + MUT1B presence, andembBWT omission + MUT1A presence. Sequencing analysis found several uncommon mutations.Conclusion. In combination with DST, application of the GenoType MTBDRplusand GenoType MTBDRslassays might be a useful additional tool to allow for the rapid and safe diagnosis of drug resistance to RFP and OFX.

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Direct Detection of Mycobacterium tuberculosis Complex DNA and Rifampin Resistance in Clinical Specimens from Tuberculosis Patients by Line Probe Assay

Journal of Clinical Microbiology ◽

10.1128/jcm.01332-06 ◽

2006 ◽

Vol 44 (12) ◽

pp. 4384-4388 ◽

Cited By ~ 35

Author(s):

H. Traore ◽

A. van Deun ◽

I. C. Shamputa ◽

L. Rigouts ◽

F. Portaels

Keyword(s):

Mycobacterium Tuberculosis ◽

Mycobacterium Tuberculosis Complex ◽

Direct Detection ◽

Line Probe Assay ◽

Tuberculosis Complex ◽

Tuberculosis Patients ◽

Clinical Specimens ◽

Rifampin Resistance ◽

Probe Assay

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Comparative Evaluation of Three Human Immunodeficiency Virus Genotyping Systems: the HIV-GenotypR Method, the HIV PRT GeneChip Assay, and the HIV-1 RT Line Probe Assay

Journal of Clinical Microbiology ◽

10.1128/jcm.38.8.3022-3028.2000 ◽

2000 ◽

Vol 38 (8) ◽

pp. 3022-3028 ◽

Cited By ~ 50

Author(s):

John W. Wilson ◽

Pamela Bean ◽

Terry Robins ◽

Frank Graziano ◽

David H. Persing

Keyword(s):

Human Immunodeficiency Virus ◽

Drug Resistance ◽

Resistance Mutation ◽

Wild Type Virus ◽

Line Probe Assay ◽

Treatment Regimens ◽

Immunodeficiency Virus ◽

Treatment Naïve ◽

Probe Assay ◽

Hiv 1

Evaluation of drug resistance by human immunodeficiency virus (HIV) genotyping has proven to be useful for the selection of drug combinations with maximum antiretroviral activity. We compared three genotyping methods for identification of mutations known to confer drug resistance in the reverse transcriptase (RT) and protease genes of HIV type 1 (HIV-1). The HIV-GenotypR method (GenotypR; Specialty Laboratories, Inc., Santa Monica, Calif.) with the ABI 377 DNA sequencer (Applied Biosystems Inc.), the HIV PRT GeneChip assay (GeneChip; Affymetrix, Santa Clara, Calif.), and the HIV-1 RT Line Probe Assay (LiPA; Innogenetics, Alpharetta, Ga.) were used to genotype plasma samples from HIV-infected patients attending the University of Wisconsin Hospitals and Clinics and the Mayo Clinic. At the time of analysis, patients were failing combination therapy (n= 18) or were treatment naive (n = 6). Forty codons of the RT and protease genes were analyzed by GenotypR and GeneChip for resistance-associated mutations. LiPA analyzed seven RT codons for mutations. Each sample was genotyped by all three assays, and each assay was subjected to pairwise comparisons. At least 92% of the codons tested (by the three assays) in paired comparisons were concordant. GenotypR and GeneChip demonstrated 96.6% concordance over the 40 codons tested. GenotypR identified slightly more mutations than GeneChip and LiPA; GeneChip identified all primary mutations that corresponded to failing treatment regimens. Each assay identified at least 84% of the mutations identified by the other assays. Mutations that were discordant between the assays mainly comprised secondary mutations and natural polymorphisms. The assays had better concordance for mutations that corresponded to current failing regimens, present in the more predominant viral quasispecies. In the treatment-naive patients, GenotypR, GeneChip, and LiPA mainly identified wild-type virus. Only the LiPA identified K70R, a possible transmitted zidovudine resistance mutation, in the RT gene of a treatment-naive patient. We conclude that although discrepancies in results exist between assays, each assay showed a similar capacity to identify potentially clinically relevant mutations related to patient treatment regimens.

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