I am trying to see the possiility of utilizing the endonuclease activity of bacteria as a therapeutic means for HIV. If I can get the HIV virus to fuse with a bacteria just like it does with T-cells, there is a possibility of lowering the virus from proliferating.
That's an interesting question Michael!
If I understand what you're asking, is your idea to sort-of trick the HIV virions into infecting bacteria instead of T-cells?
So, as I think about this, my first thought is that the surface of bacteria and the surface of human cells are quite different. Bacteria, for example, have two phospholipid bilayers and a "mess" of lipopolysaccharides on their surface. Whereas the human extracellular matrix is chemically, very different. If a TCR were placed on the surface of a bacterium, I think the virus might not be physically able to interact with it.
Also (If I understand the proposal) this would require a population of bacteria in the human blood which would cause an EPIC immune response and probably kill the patient faster than the HIV.
However, you certainly could grow T-cell receptors in genetically engineered bacteria, however getting them from the bacterial ribosome to the surface of the bacterium would be a challenge.
Thanks for your contribution. I was thinking of the possibility of utilizing the bacteriophage mechanism, but with retrovirus (HIV). I speculated an immune response ( as a side effect), however, I anticipated that administering antibiotics could help regulate such response.
Dear Michael:
Receptor mediated internalization of HIV [for that matter most of the retroviruses] are very complex. For example
Model for HIV-1 entry.: Binding of CD4 to gp120 results in exposure of a conserved coreceptor (CoR) binding site in gp120, perhaps by movement of the V3 and V1/2 loops. Coreceptor binding causes the fusion peptide of gp41 to be exposed and inserted into the membrane of the target cell in a triple-stranded coiled-coil. Formation of a helical hairpin structure in which gp41 folds back on itself is coincident with membrane fusion. see http://genesdev.cshlp.org/content/14/21/2677/F1.expansion.html
http://www.ncbi.nlm.nih.gov/pubmed/11201791
Further, most of the efforts to "mop-up: HIV viruses using cloned CD4 receptors were generally unsuccessful. Mainly because effective virus uptake require coperativity of binding between virion surface protein, co-receptors etc.
In my opinion it will be very difficult to construct a bacterial cell surface structure to accommodate all these criteria
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