The Experts below are selected from a list of 501 Experts worldwide ranked by ideXlab platform

Xuan Zhuang - One of the best experts on this subject based on the ideXlab platform.

  • A comprehensive description and evolutionary analysis of 22 grouper (Perciformes, Epinephelidae) mitochondrial genomes with emphasis on two novel genome organizations. PloS One. 2013; 8(8):e73561. doi: 10.1371/journal.pone.0073561 PMID: 23951357
    2016
    Co-Authors: Xuan Zhuang, Xiang Zhang, Shaoxiong Ding
    Abstract:

    Groupers of the family Epinephelidae are a diverse and economically valuable group of reef fishes. To investigate the evolution of their mitochondrial genomes we characterized and compared these genomes among 22 species, 17 newly sequenced. Among these fishes we identified three distinct genome organizations, two of them never previously reported in vertebrates. In 19 of these species, mitochondrial genomes followed the typical vertebrate canonical organization with 13 protein-coding genes, 22 tRNAs, two rRNAs, and a non-coding control region. Differing from this, members of genus Variola have an extra tRNA-Ile between tRNA-Val and 16S rRNA. Evidence suggests that this evolved from tRNA-Val via a duplication event due to Slipped Strand Mispairing during replication. Additionally, Cephalopholis argus has an extra tRNA-Asp in the midst of the control region, likely resulting from long-range duplication of the canonical tRNA-Asp through illicit priming of mitochondrial replication by tRNAs. Along with their gene contents, we characterized the regulatory elements of these mitochondrial genomes ’ control regions, including putative termination-associated sequences and conserved sequence blocks. Looking at the mitochondrial genomic constituents, rRNA and tRNA are the most conserved, followed by protein-coding genes, and non-coding regions are the most divergent. Divergence rates vary among the protein-coding genes, and the three cytochrome oxidase subunits (COI, II, III) are the most conserved, while NADH dehydrogenase subunit 6 (ND6) and the AT

  • a comprehensive description and evolutionary analysis of 22 grouper perciformes epinephelidae mitochondrial genomes with emphasis on two novel genome organizations
    PLOS ONE, 2013
    Co-Authors: Xuan Zhuang, Xiang Zhang, Shaoxiong Ding
    Abstract:

    Groupers of the family Epinephelidae are a diverse and economically valuable group of reef fishes. To investigate the evolution of their mitochondrial genomes we characterized and compared these genomes among 22 species, 17 newly sequenced. Among these fishes we identified three distinct genome organizations, two of them never previously reported in vertebrates. In 19 of these species, mitochondrial genomes followed the typical vertebrate canonical organization with 13 protein-coding genes, 22 tRNAs, two rRNAs, and a non-coding control region. Differing from this, members of genus Variola have an extra tRNA-Ile between tRNA-Val and 16S rRNA. Evidence suggests that this evolved from tRNA-Val via a duplication event due to Slipped Strand Mispairing during replication. Additionally, Cephalopholisargus has an extra tRNA-Asp in the midst of the control region, likely resulting from long-range duplication of the canonical tRNA-Asp through illicit priming of mitochondrial replication by tRNAs. Along with their gene contents, we characterized the regulatory elements of these mitochondrial genomes' control regions, including putative termination-associated sequences and conserved sequence blocks. Looking at the mitochondrial genomic constituents, rRNA and tRNA are the most conserved, followed by protein-coding genes, and non-coding regions are the most divergent. Divergence rates vary among the protein-coding genes, and the three cytochrome oxidase subunits (COI, II, III) are the most conserved, while NADH dehydrogenase subunit 6 (ND6) and the ATP synthase subunit 8 (ATP8) are the most divergent. We then tested the phylogenetic utility of this new mt genome data using 12 protein-coding genes of 48 species from the suborder Percoidei. From this, we provide further support for the elevation of the subfamily Epinephelinae to family Epinephelidae, the resurrection of the genus Hyporthodus, and the combination of the monotypic genera Anyperodon and Cromileptes to genus Epinephelus, and Aethaloperca to genus Cephalopholis.

Timothy F Murphy - One of the best experts on this subject based on the ideXlab platform.

  • persistence of moraxella catarrhalis in chronic obstructive pulmonary disease and regulation of the hag mid adhesin
    The Journal of Infectious Diseases, 2019
    Co-Authors: Timothy F Murphy, Melinda M Pettigrew, Aimee L Brauer, Eric R Lafontaine, Herve Tettelin
    Abstract:

    BACKGROUND Persistence of bacterial pathogens in the airways has profound consequences on the course and pathogenesis of chronic obstructive pulmonary disease (COPD). Patients with COPD continuously acquire and clear strains of Moraxella catarrhalis, a major pathogen in COPD. Some strains are cleared quickly and some persist for months to years. The mechanism of the variability in duration of persistence is unknown. METHODS Guided by genome sequences of selected strains, we studied the expression of Hag/MID, hag/mid gene sequences, adherence to human cells, and autoaggregation in longitudinally collected strains of M. catarrhalis from adults with COPD. RESULTS Twenty-eight of 30 cleared strains of M. catarrhalis expressed Hag/MID whereas 17 of 30 persistent strains expressed Hag/MID upon acquisition by patients. All persistent strains ceased expression of Hag/MID during persistence. Expression of Hag/MID in human airways was regulated by Slipped-Strand Mispairing. Virulence-associated phenotypes (adherence to human respiratory epithelial cells and autoaggregation) paralleled Hag/MID expression in airway isolates. CONCLUSIONS Most strains of M. catarrhalis express Hag/MID upon acquisition by adults with COPD and all persistent strains shut off expression during persistence. These observations suggest that Hag/MID is important for initial colonization by M. catarrhalis and that cessation of expression facilitates persistence in COPD airways.

  • changes in iga protease expression are conferred by changes in genomes during persistent infection by nontypeable haemophilus influenzae in chronic obstructive pulmonary disease
    Infection and Immunity, 2018
    Co-Authors: Mary C Gallo, Charmaine Kirkham, Samantha Eng, Remon S Bebawee, Yong Kong, Melinda M Pettigrew, Herve Tettelin, Timothy F Murphy
    Abstract:

    ABSTRACT Nontypeable Haemophilus influenzae (NTHi) is an exclusively human pathobiont that plays a critical role in the course and pathogenesis of chronic obstructive pulmonary disease (COPD). NTHi causes acute exacerbations of COPD and also causes persistent infection of the lower airways. NTHi expresses four IgA protease variants (A1, A2, B1, and B2) that play different roles in virulence. Expression of IgA proteases varies among NTHi strains, but little is known about the frequency and mechanisms by which NTHi modulates IgA protease expression during infection in COPD. To assess expression of IgA protease during natural infection in COPD, we studied IgA protease expression by 101 persistent strains (median duration of persistence, 161 days; range, 2 to 1,422 days) collected longitudinally from patients enrolled in a 20-year study of COPD upon initial acquisition and immediately before clearance from the host. Upon acquisition, 89 (88%) expressed IgA protease. A total of 16 of 101 (16%) strains of NTHi altered expression of IgA protease during persistence. Indels and Slipped-Strand Mispairing of mononucleotide repeats conferred changes in expression of igaA1, igaA2, and igaB1. Strains with igaB2 underwent frequent changes in expression of IgA protease B2 during persistence, mediated by Slipped-Strand Mispairing of a 7-nucleotide repeat, TCAAAAT, within the open reading frame of igaB2. We conclude that changes in iga gene sequences result in changes in expression of IgA proteases by NTHi during persistent infection in the respiratory tract of patients with COPD.

  • haemophilus influenzae genome evolution during persistence in the human airways in chronic obstructive pulmonary disease
    Proceedings of the National Academy of Sciences of the United States of America, 2018
    Co-Authors: Melinda M Pettigrew, Mary C Gallo, Yong Kong, Herve Tettelin, Christian P Ahearn, Janneane F Gent, James B Munro, Adonis Dmello, Sanjay Sethi, Timothy F Murphy
    Abstract:

    Nontypeable Haemophilus influenzae (NTHi) exclusively colonize and infect humans and are critical to the pathogenesis of chronic obstructive pulmonary disease (COPD). In vitro and animal models do not accurately capture the complex environments encountered by NTHi during human infection. We conducted whole-genome sequencing of 269 longitudinally collected cleared and persistent NTHi from a 15-y prospective study of adults with COPD. Genome sequences were used to elucidate the phylogeny of NTHi isolates, identify genomic changes that occur with persistence in the human airways, and evaluate the effect of selective pressure on 12 candidate vaccine antigens. Strains persisted in individuals with COPD for as long as 1,422 d. Slipped-Strand Mispairing, mediated by changes in simple sequence repeats in multiple genes during persistence, regulates expression of critical virulence functions, including adherence, nutrient uptake, and modification of surface molecules, and is a major mechanism for survival in the hostile environment of the human airways. A subset of strains underwent a large 400-kb inversion during persistence. NTHi does not undergo significant gene gain or loss during persistence, in contrast to other persistent respiratory tract pathogens. Amino acid sequence changes occurred in 8 of 12 candidate vaccine antigens during persistence, an observation with important implications for vaccine development. These results indicate that NTHi alters its genome during persistence by regulation of critical virulence functions primarily by Slipped-Strand Mispairing, advancing our understanding of how a bacterial pathogen that plays a critical role in COPD adapts to survival in the human respiratory tract.

Shaoxiong Ding - One of the best experts on this subject based on the ideXlab platform.

  • A comprehensive description and evolutionary analysis of 22 grouper (Perciformes, Epinephelidae) mitochondrial genomes with emphasis on two novel genome organizations. PloS One. 2013; 8(8):e73561. doi: 10.1371/journal.pone.0073561 PMID: 23951357
    2016
    Co-Authors: Xuan Zhuang, Xiang Zhang, Shaoxiong Ding
    Abstract:

    Groupers of the family Epinephelidae are a diverse and economically valuable group of reef fishes. To investigate the evolution of their mitochondrial genomes we characterized and compared these genomes among 22 species, 17 newly sequenced. Among these fishes we identified three distinct genome organizations, two of them never previously reported in vertebrates. In 19 of these species, mitochondrial genomes followed the typical vertebrate canonical organization with 13 protein-coding genes, 22 tRNAs, two rRNAs, and a non-coding control region. Differing from this, members of genus Variola have an extra tRNA-Ile between tRNA-Val and 16S rRNA. Evidence suggests that this evolved from tRNA-Val via a duplication event due to Slipped Strand Mispairing during replication. Additionally, Cephalopholis argus has an extra tRNA-Asp in the midst of the control region, likely resulting from long-range duplication of the canonical tRNA-Asp through illicit priming of mitochondrial replication by tRNAs. Along with their gene contents, we characterized the regulatory elements of these mitochondrial genomes ’ control regions, including putative termination-associated sequences and conserved sequence blocks. Looking at the mitochondrial genomic constituents, rRNA and tRNA are the most conserved, followed by protein-coding genes, and non-coding regions are the most divergent. Divergence rates vary among the protein-coding genes, and the three cytochrome oxidase subunits (COI, II, III) are the most conserved, while NADH dehydrogenase subunit 6 (ND6) and the AT

  • a comprehensive description and evolutionary analysis of 22 grouper perciformes epinephelidae mitochondrial genomes with emphasis on two novel genome organizations
    PLOS ONE, 2013
    Co-Authors: Xuan Zhuang, Xiang Zhang, Shaoxiong Ding
    Abstract:

    Groupers of the family Epinephelidae are a diverse and economically valuable group of reef fishes. To investigate the evolution of their mitochondrial genomes we characterized and compared these genomes among 22 species, 17 newly sequenced. Among these fishes we identified three distinct genome organizations, two of them never previously reported in vertebrates. In 19 of these species, mitochondrial genomes followed the typical vertebrate canonical organization with 13 protein-coding genes, 22 tRNAs, two rRNAs, and a non-coding control region. Differing from this, members of genus Variola have an extra tRNA-Ile between tRNA-Val and 16S rRNA. Evidence suggests that this evolved from tRNA-Val via a duplication event due to Slipped Strand Mispairing during replication. Additionally, Cephalopholisargus has an extra tRNA-Asp in the midst of the control region, likely resulting from long-range duplication of the canonical tRNA-Asp through illicit priming of mitochondrial replication by tRNAs. Along with their gene contents, we characterized the regulatory elements of these mitochondrial genomes' control regions, including putative termination-associated sequences and conserved sequence blocks. Looking at the mitochondrial genomic constituents, rRNA and tRNA are the most conserved, followed by protein-coding genes, and non-coding regions are the most divergent. Divergence rates vary among the protein-coding genes, and the three cytochrome oxidase subunits (COI, II, III) are the most conserved, while NADH dehydrogenase subunit 6 (ND6) and the ATP synthase subunit 8 (ATP8) are the most divergent. We then tested the phylogenetic utility of this new mt genome data using 12 protein-coding genes of 48 species from the suborder Percoidei. From this, we provide further support for the elevation of the subfamily Epinephelinae to family Epinephelidae, the resurrection of the genus Hyporthodus, and the combination of the monotypic genera Anyperodon and Cromileptes to genus Epinephelus, and Aethaloperca to genus Cephalopholis.

Herve Tettelin - One of the best experts on this subject based on the ideXlab platform.

  • persistence of moraxella catarrhalis in chronic obstructive pulmonary disease and regulation of the hag mid adhesin
    The Journal of Infectious Diseases, 2019
    Co-Authors: Timothy F Murphy, Melinda M Pettigrew, Aimee L Brauer, Eric R Lafontaine, Herve Tettelin
    Abstract:

    BACKGROUND Persistence of bacterial pathogens in the airways has profound consequences on the course and pathogenesis of chronic obstructive pulmonary disease (COPD). Patients with COPD continuously acquire and clear strains of Moraxella catarrhalis, a major pathogen in COPD. Some strains are cleared quickly and some persist for months to years. The mechanism of the variability in duration of persistence is unknown. METHODS Guided by genome sequences of selected strains, we studied the expression of Hag/MID, hag/mid gene sequences, adherence to human cells, and autoaggregation in longitudinally collected strains of M. catarrhalis from adults with COPD. RESULTS Twenty-eight of 30 cleared strains of M. catarrhalis expressed Hag/MID whereas 17 of 30 persistent strains expressed Hag/MID upon acquisition by patients. All persistent strains ceased expression of Hag/MID during persistence. Expression of Hag/MID in human airways was regulated by Slipped-Strand Mispairing. Virulence-associated phenotypes (adherence to human respiratory epithelial cells and autoaggregation) paralleled Hag/MID expression in airway isolates. CONCLUSIONS Most strains of M. catarrhalis express Hag/MID upon acquisition by adults with COPD and all persistent strains shut off expression during persistence. These observations suggest that Hag/MID is important for initial colonization by M. catarrhalis and that cessation of expression facilitates persistence in COPD airways.

  • changes in iga protease expression are conferred by changes in genomes during persistent infection by nontypeable haemophilus influenzae in chronic obstructive pulmonary disease
    Infection and Immunity, 2018
    Co-Authors: Mary C Gallo, Charmaine Kirkham, Samantha Eng, Remon S Bebawee, Yong Kong, Melinda M Pettigrew, Herve Tettelin, Timothy F Murphy
    Abstract:

    ABSTRACT Nontypeable Haemophilus influenzae (NTHi) is an exclusively human pathobiont that plays a critical role in the course and pathogenesis of chronic obstructive pulmonary disease (COPD). NTHi causes acute exacerbations of COPD and also causes persistent infection of the lower airways. NTHi expresses four IgA protease variants (A1, A2, B1, and B2) that play different roles in virulence. Expression of IgA proteases varies among NTHi strains, but little is known about the frequency and mechanisms by which NTHi modulates IgA protease expression during infection in COPD. To assess expression of IgA protease during natural infection in COPD, we studied IgA protease expression by 101 persistent strains (median duration of persistence, 161 days; range, 2 to 1,422 days) collected longitudinally from patients enrolled in a 20-year study of COPD upon initial acquisition and immediately before clearance from the host. Upon acquisition, 89 (88%) expressed IgA protease. A total of 16 of 101 (16%) strains of NTHi altered expression of IgA protease during persistence. Indels and Slipped-Strand Mispairing of mononucleotide repeats conferred changes in expression of igaA1, igaA2, and igaB1. Strains with igaB2 underwent frequent changes in expression of IgA protease B2 during persistence, mediated by Slipped-Strand Mispairing of a 7-nucleotide repeat, TCAAAAT, within the open reading frame of igaB2. We conclude that changes in iga gene sequences result in changes in expression of IgA proteases by NTHi during persistent infection in the respiratory tract of patients with COPD.

  • haemophilus influenzae genome evolution during persistence in the human airways in chronic obstructive pulmonary disease
    Proceedings of the National Academy of Sciences of the United States of America, 2018
    Co-Authors: Melinda M Pettigrew, Mary C Gallo, Yong Kong, Herve Tettelin, Christian P Ahearn, Janneane F Gent, James B Munro, Adonis Dmello, Sanjay Sethi, Timothy F Murphy
    Abstract:

    Nontypeable Haemophilus influenzae (NTHi) exclusively colonize and infect humans and are critical to the pathogenesis of chronic obstructive pulmonary disease (COPD). In vitro and animal models do not accurately capture the complex environments encountered by NTHi during human infection. We conducted whole-genome sequencing of 269 longitudinally collected cleared and persistent NTHi from a 15-y prospective study of adults with COPD. Genome sequences were used to elucidate the phylogeny of NTHi isolates, identify genomic changes that occur with persistence in the human airways, and evaluate the effect of selective pressure on 12 candidate vaccine antigens. Strains persisted in individuals with COPD for as long as 1,422 d. Slipped-Strand Mispairing, mediated by changes in simple sequence repeats in multiple genes during persistence, regulates expression of critical virulence functions, including adherence, nutrient uptake, and modification of surface molecules, and is a major mechanism for survival in the hostile environment of the human airways. A subset of strains underwent a large 400-kb inversion during persistence. NTHi does not undergo significant gene gain or loss during persistence, in contrast to other persistent respiratory tract pathogens. Amino acid sequence changes occurred in 8 of 12 candidate vaccine antigens during persistence, an observation with important implications for vaccine development. These results indicate that NTHi alters its genome during persistence by regulation of critical virulence functions primarily by Slipped-Strand Mispairing, advancing our understanding of how a bacterial pathogen that plays a critical role in COPD adapts to survival in the human respiratory tract.

  • Simple sequence repeats and genome plasticity in Streptococcus agalactiae
    2010
    Co-Authors: Robert Janulczyk, Herve Tettelin, Vega Masignani, Domenico Maione, John Telford
    Abstract:

    ABSTRACT 1 Simple sequence repeats (SSRs) and their role in phase variation have been extensively studied in 2 Gram-negative organisms, where they have been associated with antigenic variation and other 3 adaptation strategies. In this study, we apply comparative genomics in order to find evidence of 4 Slipped-Strand Mispairing in the human Gram positive pathogen Streptococcus agalactiae. In two 5 consecutive screenings, 2233 (650 + 1583) SSRs were identified in our reference genome 2603V/R, 6 and these loci were examined in seven other S. agalactiae genomes. A total of 56 SSR loci were 7 found to exhibit variation, where gain or loss of repeat units was observed in at least one other 8 genome, resulting in aberrant genotypes. Homopolymeric adenine tracts predominated among the 9 repeats that varied. Positional analysis revealed that long poly-adenine tracts were overrepresented 10 in the 5’-end of ORFs and underrepresented in the 3’-end. Repeat clustering in ORFs was also 11 examined, and the highest degree of clustering was observed for a capsule biosynthesis gene and a 12 pilus sortase. A statistical analysis of O/E ratios suggested a selective pressure against long 13 homopolymeric tracts. Altered phenotypes were verified for three genes encoding surface-attached 14 proteins, in which frameshifts or fusions led to truncation of proteins and/or affected surface 1

Melinda M Pettigrew - One of the best experts on this subject based on the ideXlab platform.

  • persistence of moraxella catarrhalis in chronic obstructive pulmonary disease and regulation of the hag mid adhesin
    The Journal of Infectious Diseases, 2019
    Co-Authors: Timothy F Murphy, Melinda M Pettigrew, Aimee L Brauer, Eric R Lafontaine, Herve Tettelin
    Abstract:

    BACKGROUND Persistence of bacterial pathogens in the airways has profound consequences on the course and pathogenesis of chronic obstructive pulmonary disease (COPD). Patients with COPD continuously acquire and clear strains of Moraxella catarrhalis, a major pathogen in COPD. Some strains are cleared quickly and some persist for months to years. The mechanism of the variability in duration of persistence is unknown. METHODS Guided by genome sequences of selected strains, we studied the expression of Hag/MID, hag/mid gene sequences, adherence to human cells, and autoaggregation in longitudinally collected strains of M. catarrhalis from adults with COPD. RESULTS Twenty-eight of 30 cleared strains of M. catarrhalis expressed Hag/MID whereas 17 of 30 persistent strains expressed Hag/MID upon acquisition by patients. All persistent strains ceased expression of Hag/MID during persistence. Expression of Hag/MID in human airways was regulated by Slipped-Strand Mispairing. Virulence-associated phenotypes (adherence to human respiratory epithelial cells and autoaggregation) paralleled Hag/MID expression in airway isolates. CONCLUSIONS Most strains of M. catarrhalis express Hag/MID upon acquisition by adults with COPD and all persistent strains shut off expression during persistence. These observations suggest that Hag/MID is important for initial colonization by M. catarrhalis and that cessation of expression facilitates persistence in COPD airways.

  • changes in iga protease expression are conferred by changes in genomes during persistent infection by nontypeable haemophilus influenzae in chronic obstructive pulmonary disease
    Infection and Immunity, 2018
    Co-Authors: Mary C Gallo, Charmaine Kirkham, Samantha Eng, Remon S Bebawee, Yong Kong, Melinda M Pettigrew, Herve Tettelin, Timothy F Murphy
    Abstract:

    ABSTRACT Nontypeable Haemophilus influenzae (NTHi) is an exclusively human pathobiont that plays a critical role in the course and pathogenesis of chronic obstructive pulmonary disease (COPD). NTHi causes acute exacerbations of COPD and also causes persistent infection of the lower airways. NTHi expresses four IgA protease variants (A1, A2, B1, and B2) that play different roles in virulence. Expression of IgA proteases varies among NTHi strains, but little is known about the frequency and mechanisms by which NTHi modulates IgA protease expression during infection in COPD. To assess expression of IgA protease during natural infection in COPD, we studied IgA protease expression by 101 persistent strains (median duration of persistence, 161 days; range, 2 to 1,422 days) collected longitudinally from patients enrolled in a 20-year study of COPD upon initial acquisition and immediately before clearance from the host. Upon acquisition, 89 (88%) expressed IgA protease. A total of 16 of 101 (16%) strains of NTHi altered expression of IgA protease during persistence. Indels and Slipped-Strand Mispairing of mononucleotide repeats conferred changes in expression of igaA1, igaA2, and igaB1. Strains with igaB2 underwent frequent changes in expression of IgA protease B2 during persistence, mediated by Slipped-Strand Mispairing of a 7-nucleotide repeat, TCAAAAT, within the open reading frame of igaB2. We conclude that changes in iga gene sequences result in changes in expression of IgA proteases by NTHi during persistent infection in the respiratory tract of patients with COPD.

  • haemophilus influenzae genome evolution during persistence in the human airways in chronic obstructive pulmonary disease
    Proceedings of the National Academy of Sciences of the United States of America, 2018
    Co-Authors: Melinda M Pettigrew, Mary C Gallo, Yong Kong, Herve Tettelin, Christian P Ahearn, Janneane F Gent, James B Munro, Adonis Dmello, Sanjay Sethi, Timothy F Murphy
    Abstract:

    Nontypeable Haemophilus influenzae (NTHi) exclusively colonize and infect humans and are critical to the pathogenesis of chronic obstructive pulmonary disease (COPD). In vitro and animal models do not accurately capture the complex environments encountered by NTHi during human infection. We conducted whole-genome sequencing of 269 longitudinally collected cleared and persistent NTHi from a 15-y prospective study of adults with COPD. Genome sequences were used to elucidate the phylogeny of NTHi isolates, identify genomic changes that occur with persistence in the human airways, and evaluate the effect of selective pressure on 12 candidate vaccine antigens. Strains persisted in individuals with COPD for as long as 1,422 d. Slipped-Strand Mispairing, mediated by changes in simple sequence repeats in multiple genes during persistence, regulates expression of critical virulence functions, including adherence, nutrient uptake, and modification of surface molecules, and is a major mechanism for survival in the hostile environment of the human airways. A subset of strains underwent a large 400-kb inversion during persistence. NTHi does not undergo significant gene gain or loss during persistence, in contrast to other persistent respiratory tract pathogens. Amino acid sequence changes occurred in 8 of 12 candidate vaccine antigens during persistence, an observation with important implications for vaccine development. These results indicate that NTHi alters its genome during persistence by regulation of critical virulence functions primarily by Slipped-Strand Mispairing, advancing our understanding of how a bacterial pathogen that plays a critical role in COPD adapts to survival in the human respiratory tract.