Frequency of mutations associated with isoniazid-resistant in clinical Mycobacterium tuberculosis strains by low-cost and density (LCD) DNA microarrays


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نویسندگان: پرویز مهاجری , حدیث صدری

کلمات کلیدی: inhA gene, isoniazid (INH) resistance; katG gene, Mycobacterium tuberculosis (MTB)

نشریه: Annals of Tropical Medicine and Public Health , 5 , 9 ,

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کد مقاله 8992
عنوان فارسی مقاله
عنوان لاتین مقاله Frequency of mutations associated with isoniazid-resistant in clinical Mycobacterium tuberculosis strains by low-cost and density (LCD) DNA microarrays
نوع مقاله مقاله اصیل (پژوهشی، Original)
بالاترین نمایه نامه بین‌المللی ISI
سطح مقاله
IF
عنوان نشریه Annals of Tropical Medicine and Public Health
نوع نشریه خارجی ایندکس شده
شماره نشریه 5
دوره 9
تاریخ انتشار شمسی 1395/06/11
تاریخ انتشار میلادی
آدرس لینک مقاله/ همایش در شبکه اینترنت http://www.atmph.org/article.asp?issn=1755-6783;year=2016;volume=9;issue=5;spage=307;epage=311;aulast=Sadri
DOI 10.4103/1755-6783.190166
آدرس علمی (Affiliation) نویسنده متقاضی Department of Microbiology, School of Medicine, Kermanshah University of Medical Sciences, Kermanshah, Iran

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Background: Isoniazid (INH) is one of the main line drugs used in the treatment of tuberculosis (TB) and the development of resistance against this compound can result in serious problems in the treatment procedures. Resistance to INH is associated with a variety of mutations. Objectives: The aim of the present study is to determine the frequency of major drug resistance mutations across katG and inhA loci of multidrug-resistant (MDR)-MTB isolates using a molecular test. Materials and Methods: 125 Mycobacterium Tuberculosis (MTB) clinical isolates were studied. The Centers for Disease Control and Prevention (CDC) standard conventional proportional method was implied to test drug susceptibility. DNA extraction, katG and InhA amplification, and microarray were performed. Results: From 125 MTB clinical isolates, 34 strains were INH-resistant and 91 strains were INH-sensitive. Of 34 INH-resistant strains, the mutation was identified in 32% KatG 315 (Ser→Thr), in 14% KatG315 (Ser→ Asn), in 52% InhA 15 (C→T), and in 2.9% InhA 17 (G→T). Conclusions: Rapid diagnosis of MDR-TB is essential for the prompt initiation of effective second-line therapy to improve the treatment outcome and limit transmission of this obstinate disease. A range of molecular methods that aid in rapid detection of mutations implicated in MDR-TB have been developed. The sensitivity of the methods is dependent, in principle, on the repertoire of mutations being detected, which is typically limited to mutations in the genes katG and the promoter region of inhA.

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نویسنده نفر چندم مقاله نویسنده مسئول
پرویز مهاجریسومبلي
حدیث صدریاولخير

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