US and Swiss researchers said Thursday they have discovered a promising new approach called RNA interference (RNAi) to combating deadly human viruses, a development that could help create vaccines against deadly infections such as HIV, hepatitis C and dengue.

Researchers from the University of California, Riverside, led by Professor Shou-Wei Ding, found that like plants and invertebrate animals, mammals use the RNAi process to destroy viruses within their own cells.

Until now, scientists were unable to prove that mammals use RNAi for killing viruses, and Ding said it's because viruses have been outwitting that innate protection in our cells by using proteins to suppress our virus-killing mechanism.

Remove the suppressor protein from the virus and the subject's body will quickly eliminate the virus using the RNAi process, which sends out small interfering RNAs (siRNAs) to kill the disease, Ding said.

In their study in the journal Science, the researchers infected suckling mice, just seven days old, with a mosquito-transmissible virus called Nodamura and found these animals died in several days, but when they removed the suppressor protein called B2 from the virus, the infected mice began producing huge armies of the virus- attacking siRNAs and lived, unaffected by the otherwise lethal infection.

"Many have tried to do this, that is, find the viral siRNAs in mammals, but they could not find the key," said Ding. "The key was our prior knowledge of the B2 protein in the Nodamura virus, a virus few people know about."

"Second, our study examined the host antiviral immunity during the infection of mice, unlike many previous studies that were conducted only in cell culture. Our results show that the in vivo response is much stronger and easier to detect than the in vitro response," Ding told Xinhua.

In a second study in Science, Researchers from Swiss Federal Institute of Technology, led by Professor Olivier Voinnet, and Ding's lab, investigated whether an antiviral RNAi response could be produced not in live animals, but in undifferentiated mouse embryonic stem cells. They infected the cells with two viruses and observed that siRNA molecules did indeed accumulate.

"Numerous attempts to develop vaccines against HIV, hepatitis C and dengue viruses have failed and effective therapeutic treatment is not available for many emerging and re-emerging human viral diseases. These observations indicate that there are important gaps missing in our current understanding of human immune responses to viral infection," Ding said.

"We believe that one such gap is the new mammalian antiviral immunity mechanism shown ... in our paper and the accompanying paper from collaboration between my lab and the Voinnet lab in Switzerland," he added.