information

Whoever comes in this website may find a hint

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: a lytic phages from Italy may be no active on the same bacteria (genus and species) isolated from another country and vice versa.
Chronolability
Mutation rate
Phenotypical delay
Phage cocktail
My point of view

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.

Sunday 10 August 2014

Mycobacteriophages D29,L5,Bxz2 and TM4

From this work

"This phage proved to be lytic in M. ulcerans species which originated from four different continents. M. ulcerans shows genetic heterogeneity and variable phenotypic characteristics among strains of different geographic origins (Portaels et al., 1996)."

" Additionally, phage therapy could be considered for M. ulcerans infections. In Buruli ulcer, mycobacteria are typically found extracellularly, where they might be immediately accessible by lytic phages."

"Although mycolactone is a major component of the cell surface of M. ulcerans, it does not seem to be involved in the binding of phages or the injection of phage DNA, since the avirulent mycolactone-negative mutant 1615M showed the same host range as the wild-type strain."

" Interestingly, none of the tested phages formed plaques on two strains of M. marinum. In the case of TM4 and D29 at least, this was most likely due to an intracellular inhibition of phage replication, rather than a receptor–receptor binding protein mismatch, since shuttle phasmids based on these two phages are able to transfect M. marinum (Rybniker et al., 2003)."

"Host range in mycobacteria other than M. ulcerans and M. marinum

Except for Bxz2, none of the recently isolated phages formed plaques on M. tuberculosis or M. bovis BCG, showing that phages isolated in the fast-growing M. smegmatis are often confined to this mycobacterium or other fast-growing species. It is likely that environmental samples, for example from compost, may contain additional phages, and the use of slow-growing species such as M. bovis BCG should be considered when searching for wild-type phages with a broader or different host spectrum."

 Questions
All these phages grow on Mycobacterium ulcerans and on Mycobacterium smegmatis but do not grow on Mycobacterium marinum.

-The question is why?
- Have all these phages the same receptor for all mycobacteria host range or they have for each mycobacterium species a different receptor?
-Is there an intracellular inhibition of phage replication on M.marinum?