Researchers have discovered that small interfering RNA (siRNAs) can be triggered and suppressed by human viruses.

The findings published in Immunity, provide evidence that RNA interference (RNAi) can function as an antiviral defence in mammals, particularly in differentiated somatic cells.

The team of researchers led by Dr. Zhou Xi at the State Key Laboratory of Virology, Wuhan Institute of Virology of the Chinese Academy of Science, and Dr. Qin Cheng-Feng from Beijing Institute of Microbiology and Epidemiology, studied what happened to mammalian cells when infected with HEV71, the enterovirus that causes hand, foot and mouth disease.

It was revealed that the non-structural protein 3A of HEV71 can suppress the production of RNAi in both mammalian cell cultures and mice. In addition to this, when the 3A protein was mutated, infection with HEV71 effectively triggered an RNAi response that was able to degrade viral RNA and limit the spread of the virus.

Findings such as this reflect that RNAi can function as an antiviral immunity in mammals, as well as uncovering for the first time the detailed mechanism by which a human RNA virus evades antiviral RNAi in cell culture and animal models.

“This work defines RNAi as a novel antiviral immune pathway in mammals. Given the evolutionary conservation of RNAi in all eukaryotes, RNAi evolves from the simplest eukaryotic organisms to human beings, and keeps combating against viruses,” said Dr. Qiu Yang, the first author of the paper.

“Our study is a conceptual advance in antiviral immunity, and should inspire and attract more scientists to this field,” he added.

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