| Literature DB >> 29358649 |
Francesc Coll1, Jody Phelan1, Grant A Hill-Cawthorne2,3, Mridul B Nair2, Kim Mallard1, Shahjahan Ali2, Abdallah M Abdallah2, Saad Alghamdi4, Mona Alsomali2, Abdallah O Ahmed5, Stephanie Portelli1,6, Yaa Oppong1, Adriana Alves7, Theolis Barbosa Bessa8, Susana Campino1, Maxine Caws9,10, Anirvan Chatterjee11, Amelia C Crampin12,13, Keertan Dheda14, Nicholas Furnham1, Judith R Glynn12,13, Louis Grandjean15, Dang Minh Ha10, Rumina Hasan16, Zahra Hasan16, Martin L Hibberd1, Moses Joloba17, Edward C Jones-López18, Tomoshige Matsumoto19, Anabela Miranda7, David J Moore1,15, Nora Mocillo20, Stefan Panaiotov21, Julian Parkhill22, Carlos Penha23, João Perdigão24, Isabel Portugal24, Zineb Rchiad2, Jaime Robledo25, Patricia Sheen14, Nashwa Talaat Shesha26, Frik A Sirgel27, Christophe Sola28, Erivelton Oliveira Sousa8,29, Elizabeth M Streicher27, Paul Van Helden27, Miguel Viveiros30, Robert M Warren27, Ruth McNerney31,32, Arnab Pain33,34, Taane G Clark35,36.
Abstract
To characterize the genetic determinants of resistance to antituberculosis drugs, we performed a genome-wide association study (GWAS) of 6,465 Mycobacterium tuberculosis clinical isolates from more than 30 countries. A GWAS approach within a mixed-regression framework was followed by a phylogenetics-based test for independent mutations. In addition to mutations in established and recently described resistance-associated genes, novel mutations were discovered for resistance to cycloserine, ethionamide and para-aminosalicylic acid. The capacity to detect mutations associated with resistance to ethionamide, pyrazinamide, capreomycin, cycloserine and para-aminosalicylic acid was enhanced by inclusion of insertions and deletions. Odds ratios for mutations within candidate genes were found to reflect levels of resistance. New epistatic relationships between candidate drug-resistance-associated genes were identified. Findings also suggest the involvement of efflux pumps (drrA and Rv2688c) in the emergence of resistance. This study will inform the design of new diagnostic tests and expedite the investigation of resistance and compensatory epistatic mechanisms.Entities:
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Year: 2018 PMID: 29358649 DOI: 10.1038/s41588-017-0029-0
Source DB: PubMed Journal: Nat Genet ISSN: 1061-4036 Impact factor: 38.330