Zika Virus Structure Found, Important For Vaccine Development: Study

The structure of the Zika virus has been determined by scientists from Purdue University, giving some insight into treatments and vaccines for the illness. Moreover, the team could locate regions inside the virus' structure that differed from other viruses in the flavivirus family, such as West Nile, yellow fever and dengue.

"The structure of the virus provides a map that shows potential regions of the virus that could be targeted by a therapeutic treatment, used to create an effective vaccine or to improve our ability to diagnose and distinguish Zika infection from that of other related viruses," said Richard Kuhn, who led the study. "Determining the structure greatly advances our understanding of Zika - a virus about which little is known. It illuminates the most promising areas for further testing and research to combat infection."

They studied a strain of the virus from a person infected during the French Polynesia epidemic. The structure to 3.8Å, a near-atomic resolution showing important features of its structure, allowed it to look at groups of atoms and identify the chemical entities they formed.

The structure seemed to be similar to other flaviviruses, with an RNA genome in a lipid membrane inside an icosahedral protein shell. When there are subtle differences, the treatment is identified.

"Most viruses don't invade the nervous system or the developing fetus due to blood-brain and placental barriers, but the association with improper brain development in fetuses suggest Zika does," said  Devika Sirohi, co-author of the study. "It is not clear how Zika gains access to these cells and infects them, but these areas of structural difference may be involved. These unique areas may be crucial and warrant further investigation."

Almost all flavivirus structures are different in the amino acids surrounding a glycosylation site in the virus shell. The Zika virus has a site that differs from the surface of the virus. A carbohydrate molecule is part of the viral protein at this spot.

"If this site functions as it does in dengue and is involved in attachment to human cells, it could be a good spot to target an antiviral compound," said Michael Rossmann, who led the research team along with Kuhn. "If this is the case, perhaps an inhibitor could be designed to block this function and keep the virus from attaching to and infecting human cells."

The findings were published in the March 3, 2016 issue of Science.