Scientists at MIT are developing a new drug that may fight viruses as effectively as antibiotics like penicillin dispatch bacteria. In lab tests using animal and human cells, the new therapy was effective against 15 viruses, including the common cold, dengue fever, a polio virus, a stomach virus and several types of hemorrhagic fever. Perhaps the most important virus it worked on was the H1N1 influenza.
The end result is a drug called DRACO (for double-stranded RNA activated caspase oligomerizers). Basically, when one end of DRACO binds to dsRNA, it signals the other end of DRACO to initiate apoptosis, killing cells before a virus has a chance to replicate.
Todd Rider, a senior staff scientist in Lincoln Laboratory's Chemical, Biological, and Nanoscale Technologies Group at MIT stated:
"In theory, it should work against all viruses."
The broad spectrum treatment is designed to trigger cell-suicide in cells that have been invaded by any virus, thereby halting infection, while leaving healthy cells alone. In lab experiments, DRACO completely cured mice infected with the H1N1 flu virus. The researchers think the treatment could potentially be used to thwart outbreaks of new viruses like SARS.
The scientists are currently testing DRACO against more viruses in mice and said they hope to license the technology for trials in larger animals someday in humans.
The drug works by using human cells' natural defense systems against viral infection. When a virus infects a healthy cell it takes over the cell's machinery for its own purposes to replicate. In the process, the virus produces long strands of double stranded RNA, or dsRNA, which is the mark of an infected cell.
Eventually, once the virus has finished replicating, it will kill off its host cell and move on.
Karla Kirkegaard, professor of microbiology and immunology at Stanford University continues:
"Viruses are pretty good at developing resistance to things we try against them, but in this case, it's hard to think of a simple pathway to drug resistance."
Human cells have proteins that attach to dsRNA and trigger a cascade of reactions that stop viruses from copying themselves. Rider had the idea to combine one of these proteins with yet another protein that induces cells to commit suicide, a process known as apoptosis. It worked.
At the start of the H1N1 pandemic, officials could already see the virus was easily transmissible, cases were accumulating fast, and it took only a few weeks for the virus to reach nearly every corner of the world. But while researchers knew from past pandemics that a new flu virus like H1N1, against which humans have no immunity, could spread quickly, what they could not immediately gauge was whether it could also be deadly.
Some past pandemics had been relatively mild, while others, such as the 1918 flu, which killed as many as 100 million people worldwide, had not. At the outset, there was no way to know which kind of virus H1N1 would turn out to be.
In hindsight, the 2009-10 pandemic looks relatively mild, and was certainly much milder than the initial media panic might have led us to expect. Still, a closer inspection of H1N1 shows that it was no trifle. Unlike seasonal flu, which tends to kill the elderly and those with underlying health conditions, H1N1 proved disproportionately dangerous to the young, the healthy and the pregnant.
Written by Sy Kraft