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The left panel shows treated and untreated cells in regards to the common cold virus (rhinovirus) while the right panel shows treated and untreated monkey cells in regards to dengue hemorrhagic fever virus  (Source: Massachusetts Institute of Technology)
Double-stranded RNA Activated Caspase Oligomerizers (DRACOs) could be the answer for terminating viruses like H1N1 influenza, stomach viruses, a polio virus, several types of hemorrhagic fever and dengue fever

Viruses like the common cold and influenza are infections that we occasionally must ride out. All anyone can really do is rest and take medications to ease the symptoms, which can range from congestion to fever to vomiting. Other viruses, such as Ebola, can be potentially fatal due to Ebola hemorrhagic fever.

While many bacterial infections can be treated with antibiotics, not many viral infections can be treated with medications. Only a "handful" can fight viruses, like the protease inhibitors to control HIV, but most other treatments only relieve the symptoms, and even that can take several days in some cases. Viruses are difficult to attack because they change and replicate in healthy cells.

But now, a team of researchers at MIT's Lincoln Laboratory may have found the cure for the common cold as well as many other viruses like H1N1 influenza, stomach viruses, a polio virus, several types of hemorrhagic fever and dengue fever. The team, led by Todd Rider, a senior staff scientist in Lincoln Laboratory's Chemical, Biological and Nanoscale Technologies Group, created therapeutic agents called Double-stranded RNA Activated Caspase Oligomerizers (DRACOs) which have successfully terminated viral infections.

Viruses infect cells by taking over the cell entirely and multiplying. While making copies of themselves, the viruses also produce long strings of double-stranded RNA (dsRNA). This is not found in animal or human cells.

To fight these infected cells, healthy human cells have proteins that bind to dsRNA, which then prompts a series of reactions that work to stop the virus from making copies of itself. The problem is that the virus can block one of the healthy cells' series of steps to prevent its replication somewhere down the line, allowing the virus to change and further reproduce once again.

To remedy this problem, Rider and his team mixed a dsRNA protein with another protein that causes cells to go through apoptosis, which is programmed cell suicide. One end of the DRACO binds to dsRNA while the other end is instructed to launch cell suicide.

Also, each DRACO consists of a "delivery tag" that they received from naturally occurring proteins. This allows it to enter any human or animal by crossing cell membranes, meaning that it can combat a broad spectrum of viruses, possibly including new outbreaks.

The team tested the DRACOs in human and animal cells cultured in the lab as well as mice infected with the H1N1 influenza virus. They found that DRACO left the mice fully cured of the infection, and that DRACO is not toxic to these animals. In addition, DRACO only targeted cells with dsRNA present while leaving healthy cells alone.

Rider and his team are now testing DRACO on other viruses in mice, and hope to eventually test it on larger animals and humans.

This study was published in PLoS One.


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RE: You Always Have To Question...
By Egglick on 8/30/2011 3:28:20 PM , Rating: 1
What part am I wrong about? The fact that the viruses will evolve and eventually find a way to become resistant to the treatment? You'd have to be pretty naive to think that they won't.

No matter what you do, there will always be doctors who over-prescribe and people who don't take the medication properly. In the short term, these treatments will probably be incredibly effective and save many lives. Some strains may be wiped out altogether, but not all of them will. In the long term, we will need to constantly alter the way the treatments work in order for them to remain effective, and we will also end up with a handful of super-resistant viruses that can get really out of hand.

Of course, that last result might be something that takes 50+ years to happen. I still think we're some years off from seeing the ramifications of our antibacterial/antibiotic use that started in the 1930's.


RE: You Always Have To Question...
By geddarkstorm on 8/30/2011 4:46:35 PM , Rating: 2
And what would they evolve and change? Do you know how this is working? It isn't going after the virus, it's going after viral infected parts of you.

Or, do you know how bacteria gain resistance to antibiotics? Antibiotics attack some part of the bacteria, and they either start overexpressing a protein that digests the antibiotic (common), pump it out of their cells, or modify the antibiotic's target (very rare) so it's no longer applicable. A virus has no control over how your cells are designed to work; they can only co-op the machinery that's already there to do their bidding. Think about how resistance actually works, for a minute; also realize it's not an all or nothing thing, it's simply changing the sliding scale of dosage higher and higher. Our medicine is also staying head of the resistance game, and bacteria don't simply gain a resistance and keep it forever--it's a constant tug of war. There will always be working antibiotics.

Bacteria and viruses are quite different in how they mutate and share genes as well. Bacteria are promiscuous, and can give each other a solution to a problem. Viruses don't, they can only pull out host factors (very rare) or modify what they already have using low fidelity replication (common, made into an art form by HIV). Since, again, this treatment does not bother with any actual part of the viruses themselves, there is nothing of their own proteins they can modify to have any effect.

There are still theoretically ways they could garner resistance, but they would be highly specific, easily circumvented, and very hard to gain. The greatest challenge would be your own immune system identifying the treatment protein and destroying it before it has a chance to act. That is the greatest barrier, and a type of resistance you could gain on the fly.


By MasterBlaster7 on 8/30/2011 5:48:31 PM , Rating: 2
Egglick...you should chop your head off now and unburden the human race of your alarmist stupidity.

That being said...viruses are also not nearly as adaptable as bacteria. There is a lot less to work with.

Yes, every time antibiotics are taken for the wrong reason it increases the chances of a resistant mutation. Additionally, every time antibiotics are taken for the right reason it increases the chances of a resistant mutation. If antibiotics are used at all, for any reason, the chances of a resistant mutation are increased. Because, if the antibiotic kills a million bacteria...it leaves 20 or so bacteria that happen to have a mutation that resists the antibiotic...if these resistant bacteria thrive...you may have a superbug. But it doesnt matter as science marches on...we will eventually get those bugs too. It really comes down to science v. mutation...and I put my money on science.

And, on a related note...this is possibly a HUGE breakthrough...right up there with the Kanzius Machine. I really hope this DRACO makes it through human trials.


By MrBlastman on 8/30/2011 10:33:38 PM , Rating: 2
Apoptosis is apopotosis man. Re-read about how the mechanisms work here. We are binding the virus to the cell and then cause the cell to kill itself--i.e. suicide. The virus dies with the cell. It doesn't get the opportunity to evolve here.

That's also the scary thing--to know that inside you your cells are dying off as a result of the treatment. However, a lot of times viruses either mutate or kill off the host cell anyways so it is pretty much a wash.


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