MIT scientists have designed a new medication that can identify cells that have been infected by a virus, any type of virus, then destroy those cells and effectively end the infection. The researchers, from MIT’s Lincoln Laboratory, published their breakthrough in the journal PLoS One. This new technology has the potential to eventually cure the common cold, the flu and several other illnesses.

Penicillin and other antibiotics are used to treat bacterial infections. However, they have absolutely no effect against the common cold, influenza, Ebola, and other viral infections.

In this study, the scientists tested their new medication against 15 viruses, including H1N1 influenza, a gastrointestinal virus, a polio virus, dengue fever, rhinoviruses (that cause the common cold), and various other kinds of hemorrhagic fever. It was effective against every single one of them.

The drug targets a type of RNA produced only in virally-infected cells.

Senior staff scientist, Todd Rider, said:

“In theory, it should work against
all viruses.”

The authors explain that theirs is a broad-spectrum technology – it targets a wide range of different types of viruses. Potentially, it could be effective in stopping new viral outbreaks, such as the SARS one in 2003.

Todd Rider first thought about creating a broad-spectrum antiviral about 11 years ago when he invented CANARY (Cellular Analysis and Notification of Antigen Risks and Yields). CANARY is a biosensor that can identify pathogens. A pathogen is a disease producer, such as a harmful bacterium, virus or fungus.

Rider said:

“If you detect a pathogenic bacterium in the environment, there is probably an antibiotic that could be used to treat someone exposed to that, but I realized there are very few treatments out there for viruses.”

Some antivirals do exist today. Protease inhibitors are used to control HIV infection – however, they are susceptible to resistance, and their target is narrow.

When a virus infects a cell, it takes over that cells machinery for its own purpose – to create copies of the virus. As this happens, the virus creates long strings of dsRNA (double-stranded RNA) – these do not exist in animal (including human) cells.

Human cells have proteins that stick to dsRNA, which set off a cascade of reactions that stop the viruses from replicating. However, some viruses can block the cascade reaction.

Rider wondered whether combining a dsRNA-binding protein with another one that makes cells destroy themselves (undergo adoptosis), might make the viral infection stop in its tracks. He could use, for example, a protein a cell uses when it determines it is becoming cancerous (it destroys itself). When one end of the DRACO binds to dsRNA, it could signal the other end of the DRCACO to destroy itself.

Karla Kirkegaard, professor of microbiology and immunology at Stanford University, said that combining these two elements was a good idea:

“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.”

Each DRACO has a delivery tag, taken from naturally occurring proteins, so that it can go through cell membranes and get inside a human or animal cell. If the cell has no dsRNA, though, DRACO does not signal it to die.

This study involved human and animal cell cultures in the laboratory mostly. However, they also carried out animal experiments on mice infected with the H1N1 influenza virus. When the mice were given DRACO, they were cured completely – the infection was gone. The authors add that DRACO had no toxic effect on the mice.

Further animal tests are underway and the authors say they are getting promising results. Rider would like to license the technology so that larger trials can be done on animals, and eventually humans.

Written by Christian Nrodqvist