Fending off viruses will likely be one of the greatest challenges of our century. As the recent Ebola and Zika virus outbreaks have shown, we’re still highly vulnerable. With that in mind, a group at Stanford is trying a different approach: they want to boost our body’s defense systems instead of targeting the virus.
Scientists typically take a “one drug, one bug” approach to fighting viruses. But Jeffrey Glenn, an associate professor of medicine and of microbiology and immunology wants to develop one drug that fights multiple viruses. He founded a research center and teamed up with several other researchers, including Chaitan Khosla, a professor of chemistry and of chemical engineering. Khosla said they wanted to focus against viruses that use RNA rather than DNA as their genetic material:
“Most of the really nasty viruses use RNA,” Khosla said, including Ebola, dengue, Zika and Venezuelan equine encephalitis virus (VEEV), a mosquito-borne virus that infects horses but can also kill people.
DNA stores biological information. It is a double-stranded molecule, carrying most of the genetic instructions used in the development, functioning, and reproduction of all known living organisms and many viruses. Think of it as a blueprint for living organisms. Meanwhile, RNA is a single-stranded molecule which helps carry out DNA’s blueprint guidelines. RNA mutation rate is higher than DNA mutation rate and these viruses are also generally less stable.
Instead of developing the drug from scratch, they looked to see if something promising existed already for them to build on. They found the right candidate in a drug developed by GlaxoSmithKline. However, after a few papers published about it, the drug was shelved without a public explanation. They resurrected it and gave it a new life. After several tests, they found out how it works, and why it doesn’t work perfectly.
The drug interferes with a protein that is crucial for making the individual building blocks of RNA, the genetic code for the virus. Without RNA the virus can’t make more of itself. This was a very elegant solution which in theory, works without any significant side effects or toxicity. However, the drug was shelved because it also prevented the body’s healthy cells from dividing.
So the Stanford researchers tweaked it, adding a slightly different building block that can only be used to generate DNA, not RNA. With this change, the drug still helped the body fight off viruses, but also enabled healthy cells to divide properly. So far, all lab tests have indicated its success.
The next steps are animal tests, and if everything works out fine, then it may become a broad-spectrum antiviral strategy for humans.
Finding appeared in the journal Nature Chemical Biology.
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