It’s 73 A.D. and the Roman Empire is at its height, literally. They’re scaling a ramp to reach the top of an isolated plateau built for the sole purpose of escaping the Romans. Victorious, the Romans step on top of the plateau to find 960 people, already dead.
The somewhat disputed story of the Masada mass suicide is conveyed by many Jews as a victory over the Romans. Recently, history has seemed to somewhat repeat itself with scientists conveying success in events of programmed suicide.
After years of accepting that drugs are useless for virtually all viral infections (such as influenza, the common cold and deadly hemorrhagic fevers such as Ebola), a team of researchers at MIT’s Lincoln Laboratory have designed a drug that can recognize cells that have been infected by viruses and then kill those cells to terminate the infection.
Having worked in a virology lab for three years, Tyler Slater, a neuroscience major, found the MIT study particularly interesting.
“I have read many studies in my lab about different antiviral treatments against HIV,” Slater said. “In the studies we read, these antiviral drugs show limited success because HIV evolves and develops resistance to the drugs.”
However, Todd Rider, a senior staff scientist in Lincoln Laboratory’s Chemical, Biological, and Nanoscale Technologies Group, who invented the technology, said the issue of resistant viruses may be defeated with their new drug.
By targeting a specific type of RNA produced only in cells infected by viruses, Rider said, the drug “in theory … should work against all viruses.”
According to the study, when a virus pollutes a cell it hijacks the cellular machinery to make more copies of itself. During the replication process viruses create long strings of double-stranded RNA (dsRNA). Human cells naturally attack the foreign dsRNA with specific proteins that initiate a cascade of reactions that prevents the virus from replicating itself. Unfortunately, it is not uncommon for viruses to be able to overcome the proteins by blocking one of the steps further down the cascade.
This is where Rider’s team’s research differs from that of other researchers – through combining a dsRNA-binding protein with another protein that induces cells to undergo apoptosis, programmed cell suicide.
“In theory, it should work against all viruses,” Rider said about the therapeutic agents known as DRACOs (double-stranded RNA activated caspase oligomerizers).
Riley Rackliffe, an environmental science major from Taylorsville, said he clearly recalls the domino effect an untreatable viral infection had on his family over Christmas break. With 14 people staying in one home, and only his little niece sick to begin with, it was only a matter of days before everyone was infected with the virus. Rackliffe recalls helplessly watching the disease spread and having to personally endure the illness.
“I couldn’t eat, I couldn’t leave the house and the fever reduced my mental capacity,” Rackliffe said. “The hardest part was watching other people get it and not being able to do anything to help them out.”
In a paper published on July 27, 2011, in the journal PLoS One, researchers found their drug to be effective against all 15 viruses it was tested on. Such a versatile drug could reap a potentially large range of successful treatments. While Slater well understands the scientific importance of such a discovery, perhaps even more important to him is the ability to combat the lethal effects of certain viral infections that have personally impacted his life.
“This study is interesting because of its potential practical implications,” Slater said. “If the drug turns out to be both effective and safe to use, it could cure a lot of diseases including HIV. It has personal relevance to me because I have worked in a lab that studies HIV. Also [my family] has adopted siblings who were AIDS orphans.”
Information on MIT’s study was taken from mit.edu/newsoffice/2011/antiviral-0810.html; see the site for further details.