ArticleClinical and vaccine immunology : CVI2008
Independent loss of immunogenic proteins in Mycobacterium ulcerans suggests immune evasion.
Article in Clinical and vaccine immunology : CVI, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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17 citing papers in PubMed, 37 citations in OpenAlex.
- Cracking the antigenic code of mycobacteria: CFP-10/ESAT-6 tuberculosis skin test and misleading results.Journal of clinical tuberculosis and other mycobacterial diseases · 2024Article
- ProfilingFuture science OA · 2023Review
- The immunology of other mycobacteria: M. ulcerans, M. leprae.Seminars in immunopathology · 2020Review
- Buruli ulcer: The Efficacy of Innate Immune Defense May Be a Key Determinant for the Outcome of Infection WithFrontiers in microbiology · 2020Review
- Locally Confined Clonal Complexes of Mycobacterium ulcerans in Two Buruli Ulcer Endemic Regions of Cameroon.PLoS neglected tropical diseases · 2015Article
- Genotyping Tools forMycobacterial diseases : tuberculosis & leprosy · 2014Article
- Article
- Comparative genomics analysis of Mycobacterium ulcerans for the identification of putative essential genes and therapeutic candidates.PloS one · 2012Article
- Single nucleotide polymorphism typing of Mycobacterium ulcerans reveals focal transmission of buruli ulcer in a highly endemic region of Ghana.PLoS neglected tropical diseases · 2010Article
- Molecular characterization of heterologous HIV-1gp120 gene expression disruption in mycobacterium bovis BCG host strain: a critical issue for engineering mycobacterial based-vaccine vectors.Journal of biomedicine & biotechnology · 2010Article
- Lack of insertional-deletional polymorphism in a collection of Mycobacterium ulcerans isolates from Ghanaian Buruli ulcer patients.Journal of clinical microbiology · 2009Article
- Single nucleotide polymorphisms on the road to strain differentiation in Mycobacterium ulcerans.Journal of clinical microbiology · 2009Article
- Computational resources in infectious disease: limitations and challenges.PLoS computational biology · 2009Review
- Genomic diversity and evolution of Mycobacterium ulcerans revealed by next-generation sequencing.PLoS pathogens · 2009Article
- Large sequence polymorphisms unveil the phylogenetic relationship of environmental and pathogenic mycobacteria related to Mycobacterium ulcerans.Applied and environmental microbiology · 2009Article
- Buruli ulcer: reductive evolution enhances pathogenicity of Mycobacterium ulcerans.Nature reviews. Microbiology · 2009Review
- Differential gene repertoire in Mycobacterium ulcerans identifies candidate genes for patho-adaptation.PLoS neglected tropical diseases · 2008Article
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The highly immunogenic mycobacterial proteins ESAT-6, CFP-10, and HspX represent potential target antigens for the development of subunit vaccines and immunodiagnostic tests. Recently, the complete genome sequence revealed the absence of these coding sequences in Mycobacterium ulcerans, the causative agent of the emerging human disease Buruli ulcer. Genome reduction and the acquisition of a cytopathic and immunosuppressive macrolide toxin plasmid are regarded as crucial for the emergence of this pathogen from its environmental progenitor, Mycobacterium marinum. Earlier, we have shown the evolution of M. ulcerans into two distinct lineages. Here, we show that while the genome of M. marinum M contains two copies of the esxB-esxA gene cluster at different loci (designated MURD4 and MURD152), both copies are deleted from the genome of M. ulcerans strains belonging to the classical lineage. Members of the ancestral lineage instead retained some but disrupted most functional MURD4 or MURD152 copies, either by newly identified genomic insertion-deletion events or by conversions of functional genes to pseudogenes via point mutations. Thus, the esxA (ESAT-6), esxB (CFP-10), and hspX genes are located in hot-spot regions for genomic variation where functional disruption seems to be favored by selection pressure. Our detailed genomic analyses have identified a variety of independent genomic changes that have led to the loss of expression of functional ESAT-6, CFP-10, and HspX proteins. Loss of these immunodominant proteins helps the bacteria bypass the host's immunological response and may represent part of an ongoing adaptation of M. ulcerans to survival in host environments that are screened by immunological defense mechanisms.
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