Zika virus (ZIKV) is a mosquito-borne flavivirus first
identified in 1947 (ref. 1). Little was known about ZIKV
when fetal abnormalities and Guillain–Barre´ syndrome
were reported coincident with epidemic spread of Asian-lineage
ZIKV in South America2–4. Animal models are essential for
quickly understanding ZIKV transmission and pathogenesis, as
well as for evaluating candidate vaccines and therapeutics.
ZIKV infects immunocompromised mice5, providing evidence
suggesting that ZIKV causes microcephaly by attacking neuronal
progenitor cells and leads to intrauterine growth restriction6–9.
However, mouse models do not mimic key attributes of human
infection and fetal development such as infection in an
immunocompetent state or the same type of remodelling of the
spiral arteries and arterial vasodilation10. This remodelling of the
arteries that occurs in humans and nonhuman primates, but
not in mice, leads to high blood flow to the fetus, altering the
potential transmission of viruses.