Schoggins and his colleagues hope their work will ultimately help inform the design of new antiviral drugs.Overall, Schoggins and colleagues found that all viruses tested were sensitive to inhibition by a particular subset of these genes induced by interferon, with a few genes with specific effects on a single virus, and other genes have larger effects on virus more.
When the attack of the virus, a molecule more than any other to fight back. Interferon triggers the activation of over 350 genes, and despite the obvious link, the vast majority have never been tested for antiviral properties. A team of researchers led by scientists at Rockefeller University, for the first time conducted a thorough and systematic assessment of the antiviral activity of interferon-induced factors. The results, published online in the journal Nature, represents a first step toward unraveling how these molecules inhibit the natural work for viruses.
We hope this study opens the door to future work on the mechanisms of antiviral drugs, says first author John Schoggins, a postdoctoral associate at Charles M. Rice Laboratory of Virology and Infectious Disease at Rockefeller. These mechanistic studies may pave the way for the development of new drugs and so necessary to fight against a wide range of viruses that threaten the health of importance to people around the world.
And ‘fascinating evolution has provided us with a series of hundreds of molecules that can be summoned by the host during viral infection, said Schoggins. Even more interesting is that none of these factors alone are magic bullets that can eradicate the virus. In contrast, the cell is based cooperative action of many factors in the closure of the actual virus.
The scientists used a cell-based screen to measure the ability of each gene to stop the growth of the virus: One by one, the genes were delivered into cells that were then infected with the virus. In cells that lacked the genes induced by interferon delivered Schoggins and his team observed normal levels of virus replication. In cells that were induced by interferon delivered genes, have from time to time hits that could significantly affect the replication of the virus.
This study is a first step toward unraveling how these previously uncharacterized, natural, interferon-induced factor in inhibiting the virus, said Rice, who is the R. Maurice and Corinne P. Greenberg Professor and scientific director of the Rockefeller Center for the Study of Hepatitis C. In future studies, we hope to reveal the exact mechanism by which these molecules inhibit viral replication. If this can be done, then we will have a platform for the development of new drugs that can benefit the fight against viral infections
The researchers also found that two genes in combination was more potent than either gene alone, supporting the hypothesis that many long-interferon-induced factors to work combinatorics. A number of factors, the researchers found, work by interfering with the process by which the viral RNA is translated into proteins.