For the study, researchers used a stem cell-derived 3-D model of a first trimester fetal brain. After introducing a prototype Zika virus into the model, the researchers found Zika activated a molecule, TLR3, human cells typically use to battle viruses. This activation causes TLR3 to switch off genes that stem cells require to become brain cells and switch on genes that catalyze cell suicide. Researchers were able to limit brain cell damage in the model by inhibiting TLR3.
“We all have an innate immune system that evolved specifically to fight off viruses, but here the virus turns that very same defense mechanism against us,” said senior author Tariq Rana, PhD, professor of pediatrics at UC San Diego School of Medicine. “The good news is that we have TLR3 inhibitors that can stop this from happening.”
Though the findings are promising, the positive implications are limited because the research has only been conducted in laboratory-grown human and mouse cells. Also, the Zika virus strain used in the study originated in Uganda. The current Zika outbreak strain affecting the Americas is slightly different.
Dr. Rana and his team anticipate “other researchers will now also use this same scalable, reproducible system to study other aspects of the infection and test potential therapeutics.”
More articles on the Zika virus:
Infographic: Where in the US have Zika cases been reported? [May 5 update]
Mosquitoes infected with bacteria could slow Zika spread
Zika concerns may lead to cancellation of MLB contests in Puerto Rico
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