Haemophilus Influenzae Genome Evolution During Persistence in The
Haemophilus influenzae genome evolution during PNAS PLUS persistence in the human airways in chronic obstructive pulmonary disease Melinda M. Pettigrewa, Christian P. Ahearnb,c, Janneane F. Gentd, Yong Konge,f,g, Mary C. Gallob,c, James B. Munroh,i, Adonis D’Melloh,i, Sanjay Sethic,j,k, Hervé Tettelinh,i,1, and Timothy F. Murphyb,c,l,1,2 aDepartment of Epidemiology of Microbial Diseases, Yale School of Public Health, New Haven, CT 06510; bDepartment of Microbiology and Immunology, University at Buffalo, The State University of New York, Buffalo, NY 14203; cClinical and Translational Research Center, University at Buffalo, The State University of New York, Buffalo, NY 14203; dDepartment of Environmental Health Sciences, Yale School of Public Health, New Haven, CT 06510; eDepartment of Biostatistics, Yale School of Public Health, New Haven, CT 06510; fDepartment of Molecular Biophysics and Biochemistry, Yale School of Medicine, New Haven, CT 06510; gW.M. Keck Foundation Biotechnology Resource Laboratory, Yale School of Medicine, New Haven, CT 06510; hInstitute for Genome Sciences, University of Maryland School of Medicine, Baltimore, MD 21201; iDepartment of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201; jDivision of Pulmonary, Critical Care and Sleep Medicine, Department of Medicine, University at Buffalo, The State University of New York, Buffalo, NY 14203; kDepartment of Medicine, Veterans Affairs Western New York Healthcare System, Buffalo, NY 14215; and lDivision of Infectious Diseases, Department of Medicine, University at Buffalo, The State University of New York, Buffalo, NY 14203 Edited by Rino Rappuoli, GSK Vaccines, Siena, Italy, and approved February 27, 2018 (received for review November 10, 2017) Nontypeable Haemophilus influenzae (NTHi) exclusively colonize and adaptation cannot be accurately studied in vitro or in animal infect humans and are critical to the pathogenesis of chronic obstruc- models as a result of the unique physiological and immunological tive pulmonary disease (COPD).
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