There have been many concerns over the past few months about the emergence of the Zika virus. Many experts have cautioned that the virus, which has been shown to cause birth defects like microcephaly, could migrate north to the U.S. during the warm summer months.
So, with the clock ticking, researchers have been trying to learn more about it so that it can be stopped. And, fortunately, there may be some good news on that front.
A recent study conducted at the Washington University School of Medicine in St. Louis has identified several genetic pathways that is crucial for transmission of Zika virus and other flaviviruses like it. The researchers say that shutting down these pathways would render the virus incapable of moving to other cells, greatly impairing its infection ability.
Determining crucial genes
Narrowing down the number of genetic pathways that the virus could take was the primary hurtle for the researchers, but doing so has allowed them to see which avenues are crucial for Zika virus to survive.
“We wanted to find out if we could identify genes present in the host cells that are absolutely required by the virus for infection. Out of about 19,000 genes that we looked at, we only found nine key genes that the virus relies on for infection or to spread. All of them are associated with an important part of the cell that processes viral particles, which is essential to spreading infection,” said Dr. Michael Diamond, senior author of the study.
Diamond and his colleagues were able to pinpoint these pathways by using a piece of gene editing technology called CRISPR. With this tool, the researchers were able to shut down individual genes and see if they played a primary role in the virus’ survival.
Stopping the domino effect
One problem that the researchers ran into was figuring out the potential side effects of disabling genes. While shutting one down might cease the spread of Zika virus to other cells, it could also come at a cost, including cell death. Fortunately, not all of the genes that were identified carried such a risk.
Of the nine genes that the researchers found, one stood out as a particularly good drug target for future trials. This gene, called SPCS1, not only shuts down the transmission pathway for Zika when it is disabled, but it also does so with no adverse effect to the host’s cells.
Additionally, they found that disabling this gene not only contained infection rates for Zika virus, but for other types of flaviviruses. Researchers found similar results when they tested for dengue, yellow fever, Japanese encephalitis, and hepatitis C viruses, giving hope that therapies focused on this genetic pathway could be widely beneficial.
“Flaviviruses appear to be uniquely dependent on this particular gene to release the viral particle. 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,” said Diamond.