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"In silico"
From Wikipedia
If the target host* of a phage therapy treatment is not an animal the term "biocontrol" (as in phage-mediated biocontrol of bacteria) is usually employed, rather than "phage therapy".
In silico
From:"Genomics,Proteomics and Clinical Bacteriology",N.Woodford and Alan P.Johnson
Phrase that emphasizes the fact that many molecular biologists spend increasing amounts of their time in front of a computer screen, generating hypotheses that can subsequently be tested and (hopefully) confirmed in the laboratory.
Phage Therapy is influenced by:
Phage therapy is influenced by:
Country : the epidemiological situation is different from country to country in terms of circulating bacteria and bacteriophages. Example: lytic phages from Italy may be no active on the same bacteria (genus and species) isolated from another country and vice versa.
Temporariness
Mutation rate
Phenotypical delay
Phage cocktail
My point of view
Country : the epidemiological situation is different from country to country in terms of circulating bacteria and bacteriophages. Example: lytic phages from Italy may be no active on the same bacteria (genus and species) isolated from another country and vice versa.
Temporariness
Mutation rate
Phenotypical delay
Phage cocktail
My point of view
Sunday, 7 February 2010
Genome Identity: M.ulcerans,M.marinum and M.smegmatis
Genome relation by Dot Plot (Gepard software)
M. ulcerans strains are characterized by the presence of a large, circular virulence plasmid called pMUM001 .
This plasmid harbours three large genes (mlsA1, mlsA2 and mlsB), encoding polyketide synthases that are required for the synthesis of the lipid toxin mycolactone that is the primary virulence factor for this pathogen.
pMUM001
Comparisons of multiple plasmid and chromosomal genes amongst ten M. ulcerans clinical isolates of diverse origins have suggested that plasmid acquisition was probably the key event that marked and permitted the recent emergence of M. ulcerans from a common Mycobacterium marinum progenitor.
M. ulcerans has undergone extensive gene loss due to DNA deletions, DNA rearrangements and pseudogene formation. Many of these changes have been mediated by some of the 213 copies of IS2404 and 91 copies of IS2606 .Neither of these insertion sequence elements (ISE) is present in M. marinum.
M. ulcerans and M. marinum are closely related to each other, as judged by 16S rRNA analysis, lipid profiles, and sequence comparisons of housekeeping and structural genes.
Despite their similarities, these two species have important phenotypic differences.
First, M. marinum grows relatively rapidly with a generation time of~ 4 h, where generation time of M. ulcerans and the M. tuberculosis-complex organisms is >20 h.
Second, similar to other pathogenic mycobacteria, M. marinum can live within host macrophages , whereas
M. ulcerans, which produces large ulcers, is possibly the only pathogenic Mycobacterium species that does not have a significant intracellular existence because it grows extracellularly.
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Genome Identity