MIT Researchers May Have Found Cure for the Common Cold, Other Viruses
August 29, 2011 9:22 PM
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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
, 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
, 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.
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RE: neat work, though it should be noted, for those who are curious...
8/30/2011 2:01:12 PM
Actually, HIV also makes dsRNA as part of the production of its proteins and replication (see
for one of the proteins responsible for transcribing HIV dsRNA during infection).
In fact, I know of no known viral family that does not, inevitably, create dsRNA during the course of infection. That's why this is so bloody cool. It's also why your body has an entire branch of cellular immunity based on detecting dsRNA and triggering defenses (such as oligoA polymerase, DICER, interferon production, and apoptosis).
The limitation with retroviruses is when they are incorporated in your DNA (during latent, non replicating phase) they are invisible, and can't be targeted via this method. Consequently, your own immune system also cannot attack retroviruses (or any latent virus, such as Herpes) while they are not in a replicating phase.
To this end, more needs to be done to find and target cells harboring retrovirus DNA so they too can be eliminated and keep the virus from coming back out of your own genome. Sure, this new method could attack the virus once it is active again, but you'll have to perpetually do that every time it activates if we cannot eliminate the latent cells.
Interestingly enough, herpes and other latent viruses do transcribe basal factors (such as the "lasso" like RNA that herpes makes). So there is a way to eventually attack them when in their steal mode, in theory. The question is how, and that question is very much unanswered.
RE: neat work, though it should be noted, for those who are curious...
8/30/2011 6:36:56 PM
Thanks for providing that additional info. about the ubiquity of dsRNA in viral reproduction! Very interesting.
Given what you explained, it now also makes sense why they mentioned retroviruses as an example of organisms against which better therapies are needed (even thought they didn't say their therapy would be potentially effective against them).
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