Researchers from Washington University in St. Louis have identified a single gene that, if switched off, stops Zika and other flaviviruses from spreading in the body.
The team used CRISPR to selectively block individual genes in human and insect cells to determine which ones the viruses required to spread infection between cells. They studied 19,000 genes and found 9 that are essential for infection to spread, said Dr. Michael Diamond, the senior author and a professor of medicine at Washington University, in a statement. Out of those 9, the team found one, known as SPCS1, that stopped the infection from spreading without harming the cell itself.
The team started with West Nile virus, but the results held true for other viruses in the family, including Zika, dengue, yellow fever, Japanese encephalitis and hepatitis C viruses. The findings are published in Nature and indicate a potential drug target for Zika and other flaviviruses.
Despite this method’s efficacy in subduing flaviviruses, it had no effect on other virus types.
“Flaviviruses appear to be uniquely dependent on this particular gene to release the viral particle,” Diamond said in the statement. “In these viruses, this gene sets off a domino effect that is required to assemble and release the viral particle. Without it, the chain reaction doesn’t happen and the virus can’t spread. So we are interested in this gene as a potential drug target because it disrupts the virus and does not disrupt the host.”
A drug to curb flavivirus infection would provide a more tangible way to combat them. While there are vaccines or treatments for some flaviviruses, such as yellow fever, there exist none for many of them. Dengue prevention depends on controlling exposure to mosquitoes, for example, while Zika-stricken El Salvador has advised women not to become pregnant for two years in light of the birth defects caused by Zika infection.