Since Zika was first spotted in Brazil last year, experts have merely inferred that this strain of the virus causes microcephaly, a birth defect in which the baby’s head size is below average.
But they haven’t been able to trace that inference to concrete proof—until now.
A team of scientists from Brazil and San Diego, California
“The media and health agencies were ahead of themselves were concluding that the Zika virus was causing microcephaly,” said study co-author Alysson Muotri, of the University of California, San Diego. “ There was a strong association , but this is experimental proof that’s only being presented now.”
Muotri and his colleagues used a sample of the Zika virus isolated from a clinical case in northeast Brazil to infect two different types of pregnant female mice at the 10- to 13-day mark, or the period of time that corresponds to when most of the women case studies in Brazil have been infected with Zika. What they found was that immediately after birth, some of the pups had experienced intrauterine growth restriction (the poor growth of a fetus while in the mother’s womb) and showed signs of microcephaly, like structural deformations in the cerebral cortex.
Not all of the mice exhibited these abnormalities, but the teams states that their evidence is sufficient to conclude that the Brazilian Zika strain causes microcephaly. Muotri also stated that a person would not have to contract an additional virus, such as dengue, to induce microcephaly or other birth defects in her newborn. Muotri’s team’s study is likely to be the catalyst for further investigations into how the virus has evolved to affect humans—as well as how vaccines can be developed to combat the disease.
The team also infected human progenitor cells with the virus, showing that the Brazilian strain leads to an increase in cell death. Combined, these analyses suggest that this particular Zika strain causes microcephaly by targeting cortical progenitor cells, prompting cell death, and thereby impeding the brain’s maturation.
Still, the researchers will need to comb through some of the experimental details—like the amount of the virus injected into the mice, the suitability of this animal model’s placenta as a comparison to the human placenta, and the timing of the dosage.
“As we learn more about the clinical data, we can adjust the timing,” Muotri said. “Probably the earlier we start, the more dramatic the effect. That’s what we expect.”
