New drug target for Zika

Scientists potentially have found a way to disrupt Zika and similar viruses from spreading in the body.

A team at Washington University School of Medicine in St. Louis has identified a single gene pathway that is vital for Zika and other flaviviruses to spread infection between cells. Further, they showed that shutting down a single gene in this pathway—in both human and insect cells—does not negatively affect the cells themselves and renders flaviviruses unable to leave the infected cell, curbing the spread of infection.

The study, published in Nature, points to a potential drug target for Zika and other flaviviruses such as dengue and West Nile that have major impacts on public health.

To identify genes that flaviviruses rely on, Diamond and his colleagues utilized a gene editing technology called CRISPR that is capable of selectively shutting down individual genes. Viruses must hijack host cells to replicate and spread, making them dependent upon the genetic material of the organisms they infect. If a cell lacks a gene that the virus requires for infection, the virus will be stopped in its tracks, and the cell will survive. Such evidence indicates that the missing gene is vital to viral spread and should be studied further.

Of the nine key genes Diamond and his colleagues identified, one called SPCS1, when disabled, not only reduces viral infection but appears to have no adverse effects on the cells the scientists studied. The researchers performed the first experiments on West Nile virus and then showed that the same results held true for other Flaviviridae family members, including Zika, dengue, yellow fever, Japanese encephalitis and hepatitis C viruses.

While the absence of this gene shut down the spread of flaviviruses, the researchers found that eliminating the gene had no detrimental effect on other types of viruses, including alphaviruses, bunyaviruses and rhabdoviruses.

For further details, see: Nature.

Posted by Dr. Tim Sandle