Zika infections bear some similarity to hepatitis C, since they are both flaviviridae viruses. Researchers are looking to see if their cures could also be similar.
The headlines didn’t exactly jump off the page: “BioCryst’s Zika drug shows promise in mice.” Big deal. All kinds of companies and research labs are feverishly looking at ways to treat or prevent Zika, should it become endemic to large parts of the United States this summer.
But this one stuck out as especially interesting. Why? Because there are two striking similarities in how the company’s pre-clinical drug candidate BCX443 works in mice, and how Gilead’s Sovaldi — the “$1,000-per-day pill” that finally cured hepatitis C — work.
First, Zika and hepatitis C are both in the flaviviridae family of viruses, which also includes yellow fever, Dengue and West Nile. Second, both drugs work in the same way: by preventing the virus from synthesizing new RNA, thus stopping its replication. This is pretty cool.
A number of RNA viruses carry an enzyme called RNA-dependent RNA polymerase (RdRp), which is mercifully just called polymerase. The enzyme has only one function: to take RNA fragments, which are called base pairs, and make a string of about 600 of them hooked together. This “string” then becomes the genetic material of a newly-formed virus, which will then repeat the process.
This is one of roughly a dozen steps that is required for the virus to replicate itself, and is the same step that Sovaldi uses to bring hepatitis C replication to a screeching halt. The following picture is the structure of hepatitis C polymerase bound to an inhibitor. The method used to solve these structures is called x-raycrystallography (the “Cryst” part of the company’s name).