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Most of that early work was carried out with Crispr molecules from a species of bacteria that lives in human skin called Streptococcus pyogenes. Once those molecules proved effective at reassembling human DNA, a number of scientists began looking at other species for Crispr systems that might be even better.

Some researchers investigated familiar species that have been studied in labs for decades. But Eugene V. Koonin and his colleagues at the National Center for Biotechnology Information instead scoured databases containing hundreds of millions of genetic sequences for those that resembled Crispr genes.

Once they discovered some candidates, they joined forces with Feng Zhang of M.I.T., who published one of the first studies on using Crispr to edit human DNA. One of the first candidates they looked at came from a species of bacteria that lives in the mouth, known as Leptotrichia shahii.

It had a group of genes that looked like Crispr genes in some ways, but with stark differences. When the researchers equipped bacteria with these genes, which they called C2c2, they found that the organisms gained a defense that had never been seen.

Many viruses do not contain DNA. Instead, their genetic information is encoded in RNA, DNA’s single-stranded cousin, which they use to hijack the genes of their hosts and cause them to make new viruses. Some of these RNA viruses, such as H.I.V. and poliovirus, attack our species. Many others attack bacteria.

Previously discovered Crispr molecules are very good at whacking apart DNA but don’t protect bacteria from an RNA virus. Dr. Zhang and his colleagues discovered that bacteria with C2c2 make molecules that can attack RNA and chop it up, destroying the invaders.

The researchers also found that they could tailor these genes to cut any RNA molecule they wanted. Now they are tinkering with the process to try to get it to work in human cells.

“There could be a lot of cool applications,” Dr. Zhang said. He hopes, for example, that C2c2 molecules could be trained to destroy RNA made only in cancer cells. Those cells would be unable to make essential proteins and die.

While it remains to be seen if these will become useful tools, Dr. Koonin said, the discovery has already revealed something important about the evolutionary history of these microbial defenses.

Some parts of C2c2 genes share a common evolutionary origin with the defense systems seen in other bacterial species. Over billions of years, Dr. Koonin said, evolution has blindly tinkered with these genes in order to generate new ways to protect against viruses.