Congenital Zika Syndrome (CZS), a collection of developmental malformations in infants associated with Zika virus (ZIKV) infection, is linked to poor diet among the children's mothers, a new study says.
The syndrome causes conditions impacting infants for the rest of their lives, such as smaller (microcephaly) and unfolded (lissencephalic) brains, abnormalities in the retina, enlarged blood vessels in the heart, a lack of connections between the brain's hemispheres, the study published in the journal Science Advances, noted.
"We knew that areas of Brazil with the lowest socioeconomic status had the highest level of developmental impairment in babies due to CZS, which is why we looked at the possible link between ZIKV, and one of the potentially most important co-factors, nutrition," said study co-author Zoltan Molnar of the University of Oxford in the UK.
According to the study, developmental impairment caused by ZIKV congenital infection is worsened by environmental co-factors like diets poor in protein -- explaining why the devastating effects of CZS vary across ZIKV endemic regions.
In the current study, the scientists used a mouse model to replicate the effects of Zika infection in mice that had a low-protein diet.
They found that several of the symptoms found in humans appeared in the undernourished mice in a similar way.
"When we replicated the effects seen in humans who had poor diets in mice, we saw similar effects in the foetuses, such as placental damage, as well as poor embryonic body growth, and a reduction in brain size of newborns born to undernourished pregnant mouse," Molnar said.
"The mouse mothers were clearly less able to fight against ZIKV, which was shown by a robust and persistent ZIKV infection in the spleens of undernourished mothers, in contrast to healthy mice. Our undernourished mouse model helped us to identify the cellular mechanisms that are responsible for the differences in humans," he added.
While improving the diet may not protect against ZIKV infections by itself, it can determine the severity of the syndrome, the researchers said.
"While we need more work to translate these findings to human disease, our mouse model helped us to identify significant differences in the regulation patterns of key molecular pathways, and particular genes identified within developing brains reflect how a poor nutritional status increases the adverse effects of ZIKV infection," Molnar said.
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