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Zika's achilles heel spotted with help from CRISPR

27 June 2016
Appeared in BioNews 857

Researchers have pinpointed a gene that, if blocked, may stop Zika and other related viruses in their tracks.

The team from the Washington University School of Medicine in St. Louis looked at over 19,000 genes in human and insect cells.

After drawing up a shortlist of nine candidate genes the researchers used CRISPR/Cas9 genome-editing technology to cut those genes out of cells. The cells were then exposed them to flaviviruses to see whether the removal of those genes affected virus survival.

Using this method the researchers found one gene, called SPCS1, which when it was removed and the cell exposed to West Nile virus, led to the virus being unable to reproduce. Both insect and human cells seemed to be unharmed by having the SPCS1 removed. The same effect was observed with other flaviviruses including Zika, dengue, yellow fever, Japanese encephalitis and hepatitis C.

Senior author Professor Michael Diamond, said that SPCS1 '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.'

Professor Diamond said that his team were now interested in the gene 'as a potential drug target because it disrupts the virus and does not disrupt the host'.

Flaviviruses infect millions of people around the world every year. Although vaccines and antiviral therapies do exist for several of the viruses, many in the developing world do not have access to them.

The study appeared as a letter in the journal Nature.

A CRISPR screen defines a signal peptide processing pathway required by flaviviruses
Nature |  17 June 2016
Potential drug target identified for Zika, similar viruses
Washington University School of Medicine in St. Louis (press release) |  17 June 2016
Potential target for Zika, flaviviruses identified
FierceBiotech |  21 June 2016
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