Two new studies add to the growing pool of evidence that suggests a causal link between the mosquito-borne Zika virus and a birth defect called microcephaly.
A new paper published in the New England Journal of Medicine follows the case of a pregnant women infected with Zika virus at 11 weeks into gestation demonstrates the virus' ability to affect a developing fetus at a very early stage, according to the authors.
Between the sixteenth and twenty-first weeks of pregnancy, the head circumference of the fetus decreased from the 47th percentile to the 24th percentile, and after 19 weeks, researchers detected significant brain abnormalities using ultrasonography and magnetic resonance imaging. These abnormalities occurred even without the presence of microcephaly.
"Our research also helps confirm the causal relation between the Zika virus and severe damage to the fetal central nervous system," lead author Olli Vapalahti, of the University of Helsinki in Finland, said in a statement.
In a separate study published in Cell Stem Cell, researchers from the University of California San Francisco identified AXL, a receptor protein expressed by neural stem cells, as a lever used by the Zika virus to impact brain development. They noted that, in mouse and ferrets, AXL most commonly built up in the blood vessels and cerebrospinal fluid that was in contact with neural stem stems.
If Zika does in fact use AXL proteins to produce its negative affects, this could be an explanation for why microcephaly seems to correlate with the infants of mothers infected by the virus.
"While by no means a full explanation, we believe that the expression of AXL by these cell types is an important clue for how the Zika virus is able to produce such devastating cases of microcephaly, and it fits very nicely with the evidence that's available," Arnold Kriegstein, senior study author and director of the Eli and Edythe Broad Center of Regeneration Medicine and Stem Cell Research at UCSF, said in a statement. "AXL isn't the only receptor that's been linked with Zika infection, so next we need to move from 'guilt by association' and demonstrate that blocking this specific receptor can prevent infection."