The research team of Professor Kim Young-joon (Biochemistry) recently discovered that the OASL1 gene could be a potential therapeutic target for boosting the immune response during viral infections. The article, based on their research with mice, “OASL1 inhibits translation of the type I interferon–regulating transcription factor IRF7,” was published February 17th in the online version of Nature Immunology. When a virus invades a cell, the infected cell produces a protein called interferon, which communicates the presence of the virus to other cells, activating an immune response. This response, which consists in inhibiting protein synthesis, destroys both the virus and infected host cells. In order to isolate the gene that regulates the production of interferon, Professor Kim’s team focused on OASL1, whose function was previously unknown. Experimenting on mice infected with the herpes simplex virus (HSV-1), the team showed that mice which were genetically modified not to express OASL1 produced more interferon than the control group. That is, the mice in the experimental group were resistant to viral infection because of the greater presence of interferon. “The study has found that a very strong antiviral immune reaction can be induced by inhibiting the OASL1 function,” said Professor Kim. “Even after eradicating the virus, side effects such as excessive immune reactions were not observed.” Since OASL1 is presumed to function in the same manner in most animals, including humans, cattle, and pigs, the findings of this research will be applied to the development of treatments for viral infections.