Researchers from Jupiter, Fla.-based The Scripps Research Institute have found a clue as to why the Zika virus causes severe fetal birth defects, while its cousin viruses, such as dengue and West Nile, do not. They published their findings in Proceedings of the National Academy of Sciences.
The study details the Zika virus' ability to cross the placental barrier and expose the fetus to an array of birth defects, including microcephaly. Human umbilical endothelial cells are far more susceptible to Zika infection than to other viruses, the study shows. Also, the Zika virus may be capable of exploiting a cell surface molecule known as AXL, while West Nile and dengue viruses can not.
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The Zika virus is able to bind to an intermediate molecule known as Gas6, and thereby provide a bridge between the virus and AXL. Thus, the Zika virus can then use AXL and enter host cells.
Hyeryun Choe, PhD, an associate professor at TSRI and study lead author, noted that Zika uses AXL to "efficiently slip past one of the major barrier cell types in the placenta: fetal endothelial cells."
"We don't yet understand why Zika virus uses AXL and the others don't," Dr. Choe said. "The common belief is that all flaviviruses have similar structures, but our findings suggest that Zika virus may have a different average population structure than others. This has significant scientific and clinical implications."