Novel tool to may lead to Zika vaccines

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Press Trust of India Houston
Last Updated : Nov 19 2016 | 3:22 PM IST
Scientists have developed a way to replicate the Zika virus, stripping it of the genes that make the virus infectious, an advance that may lower the safety risk involved in working with it and pave the way for vaccine development.
Replicons are segments of viral genome that can replicate on their own, independent of the cellular chromosome. The new Zika replicon system has deleted some of the genes that give the virus its structure.
"One of these replicons can be used to locate portions of the viral molecule that block or halt viral replication, making it a powerful tool for vaccine development," said Pei-Yong Shi, professor at University of Texas Medical Branch at Galveston in the US.
The replicon system was engineered by attaching genes that allow researchers to tag certain parts of the virus that they are interested in.
Luciferase, the chemical that gives fireflies their signature glow, was used to make targeted viral components light up - making processes like replication much easier to observe.
"The other newly-developed replicon was designed to study potential antiviral agents by differentiating between when the virus is making copies of itself and when it's altering its structure," Shi said.
"Knowing when and how the virus is mutating is important, as evolution is what makes viruses more adept at invading hosts like humans or animals or become more damaging once inside the host," he said.
The recent Zika virus outbreak has highlighted the urgent need to establish genetic tools for studying how the virus multiplies and causes disease within a newly infected person in order to develop countermeasures.
This is especially important because the Zika virus is spreading rapidly and behaves differently than many other viruses - for instance, it can be transmitted sexually and is associated with microcephaly and Guillain-Barre syndrome.
The study was published in the journal EBioMedicine.

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First Published: Nov 19 2016 | 3:22 PM IST

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