RISC complex and possible cure for AIDs

[Genecks]

Do you think it would be possible to create a RISC complex that uses a complementary mRNA strand to detect the RNA strands that code for virus structures and target those for destruction?

 

I've been reading about microRNA as of late. Supposedly, these can form complexes with RNA that target complementary RNA to degrade/destroy them.

 

Also, I've been trying to wrap my head around mitochondria and their applications.

 

So, I came to an idea:

 

What if a person could genetically alter a pre-evolutionary aspect of a mitochondrion relative that can infiltrate eukaryotic cells in order for the invader to transcribe a RISC complex that targets viral RNA?

 

I don't have the equipment nor knowledge to actually try this out, but it is at least an idea.

 

Let's attempt to take a genus of invader species, such as Rickettsia. Then, let's attempt to make it less pathogenic. From there, we will make it form RISC complexes that target the RNA that code for materials that compose the virus.

 

We would take the AIDs virus and inject it into a culture of eukaryotic cells. From there, we would take this invader species, which I will call Rickettsia bandaid, and inject it into eukaryotic cells. The prokaryote will infiltrate the host eukaryotes, create the RISC complexes that target RNA that transcribe AIDs products, and rid the cell of the AIDs virus.

 

Furthermore, if a person desires to remove Rickettsia bandaid from the body, then he or she would only need to use antibiotics.

 

This could also have other possible evolutionary aspects, such as allowing progeny to have immunity to the virus if the invader can reside in the gametes without disturbing the biological cybernetics of the living organism.

Edited February 1, 2010 by Genecks

[jimmydasaint]

Great ideas Genecks. Presumably Rickettsia species can be used due to their similarity to mitochondria (AFAIK). There should not be a problem in killing off Rickettsia using tetracyclines or chloramphenicol. However, the problem I can see is looking at genetic 'wild type' revertants. Then you may have the problem of actually contracting Rickettsial diseases and, with our Western countries being as litigious as they are, patients may cause a bit of a fuss. I know you are suggesting preliminary in vitro tests, but why not use liposome delivery targeted to virally infected cells, either by monoclonal or polyclonal antibodies?

Edited February 5, 2010 by jimmydasaint

[Lifeson]

Its a good idea, and in particular one I want to explore when I finally get my immunology Ph.d. The problem that I see with this plan is that typically when you make a virus less pathogenic, you make it inactive as well, i.e. it does nothing to the body to alter its DNA or attack its cells.

 

I did hear though that a harmless strain of the AIDS virus was used a while back in an experiment to cure a brian disorder in France and it seemed like that worked like a charm last I hear about it, so I may be wrong, or this may be a special case. If it were possible to modify the virus' DNA to not become inactive and do what you describe w/o causing major symptoms, this would be a viable treatment.

[Genecks]

So far, I've come into contact with information that says RISC complexes are not found in bacteria. This, however, could always be changed. I suggest a hypothetical scenario during which the genes that encode for RISC complexes are understood and then applied to bacterial genomes. From there, we attempt to use bacteriophages to see if the RISC complexes can be used to target and destroy the foreign DNA that enters Rickettsia bandaid.

 

I do not know too much about the RISC complex, but I suspect it could be applied to a bacterial system.

[caharris]

Didn't they find a tribe in Africa that was immune to AIDS or something like that? I vaguely remember Dawkins talking about it in a video but I may be wrong...

[dttom]

current attempts use viral vector system, but I'm concerned with the resident provirus, RNAi has to be continually effecting for its not killing the cell.