Viral and flu infections could be inhibited by boosting natural occurring protein in the body. This natural protein called oligoadenylate synthetases-like, or OASL. It is revealed that by amplifying OASL in human cells, they were able to effectively inhibit viral replication.
OASL is a nature protein in the body that defend against pathogens.
“It was initially thought the [adaptive] immune system is all we have to protect against invasion – the one that makes antibodies and cells that can essentially destroy infected cells,” lead author Saumendra Sarkar, assistant professor of microbiology and molecular genetics at UPCI, told FoxNews.com. “But what was missing for a while is that every cell has an intrinsic ability to detect some of these invasions by pathogens… and then [they] can mount a cellular resistance.”
OASL plays an important role in a process known as RNA sensing. Hepatitis C, influenza, the childhood respiratory illness RSV, and many other viruses are known as ribonucleic acid (RNA) viruses. When these pathogens spread throughout the body, they will inject their genetic material – comprised of RNA – inside of healthy cells, taking them over and replicating to form new viruses.
Sarkar and his team discovered that OASL acts as a sensing mechanism inside of cells, detecting when foreign RNA is injected and alerting other cells to the virus’s presence. This helps to activate the innate immune system, causing other cells to sense the virus and inhibit its spread.
The only problem? It takes a lot of virus to activate OASL.
“There has to be quite a bit of virus production and replication before the system can detect it,” Sarkar said. ...There’s always a threshold for any detection – beyond the threshold, it’ll fire up the response and below the threshold, it won’t. By [boosting OASL], this firing threshold goes [down], and OASL will fire more quickly.”
To test this idea, the researchers boosted OASL in a collection of human cells, which effectively stopped viral replication. In a follow up experiment, they generated a group of mice that lacked the OASL gene, finding that the rodents were much more sensitive to viral infection.