M
Midori Kato-Maeda
Researcher at University of California, San Francisco
Publications - 87
Citations - 6504
Midori Kato-Maeda is an academic researcher from University of California, San Francisco. The author has contributed to research in topics: Mycobacterium tuberculosis & Tuberculosis. The author has an hindex of 30, co-authored 82 publications receiving 5773 citations. Previous affiliations of Midori Kato-Maeda include San Francisco General Hospital & Stanford University.
Papers
More filters
Journal ArticleDOI
Variable host-pathogen compatibility in Mycobacterium tuberculosis.
Sebastien Gagneux,Kathryn DeRiemer,Tran Van,Midori Kato-Maeda,Bouke C. de Jong,Sujatha Narayanan,Mark P. Nicol,Stefan Niemann,Kristin Kremer,M. Cristina Gutierrez,Markus Hilty,Philip C. Hopewell,Peter M. Small +12 more
TL;DR: It is demonstrated that the global population structure of M. tuberculosis is defined by six phylogeographical lineages, each associated with specific, sympatric human populations, and in an urban cosmopolitan environment, mycobacterial lineages were much more likely to spread in sympatrics than in allopatric patient populations.
Journal ArticleDOI
Out-of-Africa migration and Neolithic coexpansion of Mycobacterium tuberculosis with modern humans
Iñaki Comas,Mireia Coscolla,Mireia Coscolla,Tao Luo,Sonia Borrell,Sonia Borrell,Kathryn E. Holt,Midori Kato-Maeda,Julian Parkhill,Bijaya Malla,Bijaya Malla,Stefan Berg,Guy E. Thwaites,Dorothy Yeboah-Manu,Graham H. Bothamley,Jian Mei,Lan-Hai Wei,Stephen D. Bentley,Simon R. Harris,Stefan Niemann,Roland Diel,Abraham Aseffa,Qian Gao,Douglas B. Young,Douglas B. Young,Sebastien Gagneux,Sebastien Gagneux +26 more
TL;DR: Coalescent analyses indicate that MTBC emerged about 70,000 years ago, accompanied migrations of anatomically modern humans out of Africa and expanded as a consequence of increases in human population density during the Neolithic period, consistent with MTBC displaying characteristics indicative of adaptation to both low and high host densities.
Journal ArticleDOI
Whole-genome sequencing of rifampicin-resistant Mycobacterium tuberculosis strains identifies compensatory mutations in RNA polymerase genes.
Iñaki Comas,Sonia Borrell,Sonia Borrell,Andreas Roetzer,Graham Rose,Bijaya Malla,Bijaya Malla,Midori Kato-Maeda,James E. Galagan,James E. Galagan,Stefan Niemann,Sebastien Gagneux,Sebastien Gagneux +12 more
TL;DR: These findings support a role for compensatory evolution in the global epidemics of MDR TB and show that M. tuberculosis strains harboring these compensatory mutations showed a high competitive fitness in vitro and were associated with high fitness in vivo.
Journal ArticleDOI
Genomic analysis identifies targets of convergent positive selection in drug-resistant Mycobacterium tuberculosis
Maha R. Farhat,B. Jesse Shapiro,Karen J. Kieser,Razvan Sultana,Karen R. Jacobson,Karen R. Jacobson,Thomas C. Victor,Robin M. Warren,Elizabeth M. Streicher,Alistair Calver,Alexander Sloutsky,Devinder Kaur,Jamie E. Posey,Bonnie B. Plikaytis,Marco R. Oggioni,Jennifer L. Gardy,James C. Johnston,Mabel Rodrigues,Patrick Tang,Midori Kato-Maeda,Mark L. Borowsky,Bhavana Muddukrishna,Barry N. Kreiswirth,Natalia Kurepina,James E. Galagan,Sebastien Gagneux,Sebastien Gagneux,Bruce W. Birren,Eric J. Rubin,Eric S. Lander,Pardis C. Sabeti,Megan Murray +31 more
TL;DR: Functional genetic analysis of mutations in one gene, ponA1, demonstrated an in vitro growth advantage in the presence of the drug rifampicin, and evidence of positive selection in an additional 39 genomic regions in resistant isolates was found.
Journal ArticleDOI
Functional and evolutionary genomics of Mycobacterium tuberculosis: Insights from genomic deletions in 100 strains
Anthony G. Tsolaki,Aaron E. Hirsh,Kathryn DeRiemer,Jose Antonio Enciso,Melissa Z. Wong,Margaret Hannan,Yves Olivier L Goguet De La Salmoniere,Kumiko Aman,Midori Kato-Maeda,Peter M. Small +9 more
TL;DR: To better understand genome function and evolution in Mycobacterium tuberculosis, the genomes of 100 epidemiologically well characterized clinical isolates were interrogated by DNA microarrays and sequencing and 224 genes were found to be partially or completely deleted.