Viral agents are responsible for triggering a host of unpleasant and potentially-lethal medical conditions, such as for example influenza, the common cold, hemorrhagic fevers, Ebola and even certain forms of cancer.
Fighting these viruses is proving to be extremely difficult, and doctors have been complaining about the fact that they don't have access to any potent drugs capable of fighting back for many years.
Now, investigators at the MIT Lincoln Laboratory say they managed to synthesize a new drug that has a nearly-universal effect on cells in the human body that have been infected. The compound is literally able to identify only diseased cells, and give them to order to shut down.
The most remarkable thing about this drug is that it works selectively, in the sense that it doesn't do significant damage to healthy tissue around the infected cells. Details of the study appear in the July 27 issue of the peer-reviewed scientific journal PLoS One.
During early experiments conducted at MIT, researchers found the drug to be effective against an array of no less than 15 selected viruses, including rhinoviruses that cause the common cold, H1N1 influenza, a stomach virus, a polio virus, dengue fever and several other types of hemorrhagic fever.
“In theory, it should work against all viruses,” Lincoln Laboratory’s Chemical, Biological, and Nanoscale Technologies Group senior staff scientist Todd Rider explains. He was the expert who invented the new technology.
Rider says that the approach functions in a fairly straightforward manner – the drug is designed to track down the chemical signature of a very specific type of ribonucleic acid (RNA), which is only produced in cells that have been infected by viral agents.
Because this chemical is not produce in any healthy tissue, there is no risk of the compound affecting healthy cells in the body. What this means is that – once the technology is perfected – it could have very few or no side-effects.
Infectious agents such as the 2003 Severe Acute Respiratory Syndrome (SARS) could also be counteracted using the new, broad-spectrum approach, Rider explains. He conducted the work with MIT experts Scott Wick, Christina Zook, Tara Boettcher, Jennifer Pancoast and Benjamin Zusman.
The work was funded by the National Institute of Allergy and Infectious Diseases and the New England Regional Center of Excellence for Biodefense and Emerging Infectious Diseases.
Previous funding was secured from the Defense Advanced Research Projects Agency (DARPA), Defense Threat Reduction Agency and the Assistant Secretary of Defense for Research and Engineering.