RNA Interference

Scientists have discovered that a natural virus-fighting mechanism used by plants also exists in mammals, potentially revealing a new way to combat deadly human viruses.

Two new studies, published Oct. 11 in the journal Science, focus on a method that enables plants, insects, roundworms, and fungi to stop the spread of a virus. Until now, its existence in mammals was up for scientific debate.

Virus Attack System Blocks Infection in Plants

In response to a viral infection, plants and invertebrates turn on a virus attack system known as “RNA interference,” which refers to the genetic material found in viruses. Unlike other organisms, including humans, many viruses contain RNA instead of DNA.

The presence of a virus triggers the RNA interference system, which chops the viral RNA into small pieces. These tiny bits are then used to block—or silence—the virus' genes, preventing other copies of the virus from replicating and continuing the infection.

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In some cases, viruses have adapted to turn off this virus-fighting mechanism by creating specialized compounds called suppressor proteins. According to Shou-Wei Ding, Ph.D., and his colleagues at the University of California, Riverside, this appears to be the case in mammals.

Researchers Find RNA Interference in Mammals

During one of the new studies, the researchers infected seven-day-old mice with a Nodamura virus—a type that is carried by mosquitoes. All of the infected mice died from the virus. 

Next, the researchers modified the virus to keep it from producing a suppressor protein called B2. This protein is known to block the RNA interference system in other organisms, which enables the virus to spread.

Four weeks after the young mice were infected with the modified virus, they were still alive and healthy. The researchers also found small pieces of RNA, indicating that the mice had an active RNA interference system. In the absence of the suppressor protein, the virus-fighting system worked without a hitch.

In a related study, Ding and colleagues, along with Swiss researchers, infected mouse embryonic stem cells with a virus.

These cells, which are taken from the embryos of mice, are so young that they have not yet developed the virus-fighting system used by adult mammal cells, called a protein-based interferon immune response.

Infecting the mouse embryonic cells with a virus triggered the RNA interference system, and the same small pieces of RNA showed up in the mouse cells.

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Both studies show that mammals have the same virus-fighting system once thought to be unique among plants and invertebrates, although it likely lies dormant for most of their lives.

Ding and his colleagues suspect that the RNA interference system protects mammals at a very young age, until the interferon immune response kicks in. Because the two new studies used either young mice or very early mouse cells, researchers were able to detect the hidden virus-fighting ability.

While the interferon immune response is very quick, it lacks the virus-specific cutting carried out by the RNA interference system.

Ding now plans to turn his attention to developing new vaccines for human viruses like dengue. These vaccines would attempt to stop a virus from using suppressor proteins to block RNA interference.

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“Maybe this is what we have been missing in knowing how humans combat viral infections," Ding said in a press release. "There are many different antiviral mechanisms in our bodies, but maybe RNA interference functions as the most important antiviral defense mechanism. Maybe this is the one that really matters.”

The road from concept to approved vaccine, though, is likely to be long, with the need for more animals studies before the first humans try the vaccine.

Ding, though, is cautiously optimistic. “It is hard,” he added in an email to Healthline, “but I believe that it's possible.”