Researchers at the McGill University have devised a method that will boost the natural defence mechanism of an organism that will make the cells immune to viruses like influenza.
The research was conducted by post-doctoral fellows Dr. Rodney Colina and Dr. Mauro Costa-Mattioli, working in collaboration with Dr. Nahum Sonenberg, a Howard Hughes Medical Institute International Scholar at McGill.
They developed this process, which could lead to the creation of new anti-viral therapies in humans.
The process involves destroying two genes in mice that inhibit the production of the protein interferon (the cell's first line of defence against viruses).
In the absence of these repressor genes, the mouse cells produced interferon in a much higher level, effectively blocking viruses from reproducing. This process was tested on influenza virus, encephalomyocarditis virus, vesicular stomatitis virus and Sindbis virus.
"People have been worried for years about potential new viral pandemics, such as avian influenzas. If we might now have the means to develop a new therapy to fight flu, the potential is huge," Nature quoted Dr. Sonenberg, as saying.
Viruses are sub-microscopic infectious agents which can reproduce only by seizing a cell's reproductive machinery, a process often leading to disease and even the death of the host organism. Interferon, particularly, the type 1 interferons (IFN-a and IFN-ß) repress propagation of virus.
The interferon regulatory protein 7 (Irf7), which researchers believe to be the "master-regulator" of interferon production in the body control the production of type 1 interferon. It was found that protein synthesis of Irf7 is controlled by the repressor genes called 4E-BP1 and 4E-BP2.
"In a sense, it's quite a simple story. When you get rid of the repressors, you have more of the key protein Irf7 present, which induces an anti-viral state in the cell. You're basically removing the brakes," explained Dr. Costa-Mattioli.
Dr. Costa-Mattioli said they did not detect any abnormalities or negative side-effects resulting from enhanced interferon production in the mice.
Dr. Sonenberg explained that this process to destroy genes is not possible in humans; however, the researchers are optimistic that new pharmaceutical therapies will develop from their research.
"If we are able to target 4E-BP1 and 4E-BP2 with drugs, we will have a molecule that can protect you from viral infection. That's a very exciting idea. We don't have that yet, but it's the obvious next step," said Dr. Costa-Mattiolo said.
The findings of this research are published in the journal Nature.