Data-driven methods predict over 35 mosquitoes are potential vectors of Zika virus, suggesting a larger geographic area and a greater human population is at risk of infection.

A global map of environmental suitability for Zika virus and the estimated population living at potential risk can help refine public health guidelines, travel advisories and intervention strategies at a crucial time in the global emergence of this arbovirus.

Fetal Zika virus’ direct infection of the brain causes neuroanatomical pathology that tracks with the brain development, following a caudal-to-rostral trajectory, even in individuals who do not develop microcephaly.

The Zika virus subgenomic flaviviral RNA binds to and inhibits the fragile X mental retardation protein, a novel Zika virus restriction factor.

Zika virus infection induces the gasdermin E-mediated pyroptosis in placental cells through TNF-α-caspase-8-caspase-3 signaling pathway, which contributes to adverse fetal outcomes in pregnant mouse model.

An ento-epidemiological model reveals that what made the Zika virus a public health problem in Feira de Santana, Brazil, was a surprisingly high attack rate coupled with a low risk of Microcephaly per challenged pregnancy.

A novel virus-inclusive single cell RNA-Seq approach enables identification of novel pro- and antiviral host factors in human cells in response to dengue and Zika virus infection.

Stochastic models able to reproduce both incidence and seroprevalence data for Zika outbreaks in the Pacific Islands estimate that the basic reproduction number (R₀) is between 1.5 and 4.1.

A combination of eight serological surveys shows a decline in seroprevalence over a two-year period following the first reports of Zika transmission in Fiji and French Polynesia.

Organoids developed from matched human placental tissue define differences in antiviral signaling between cell types comprising the maternal-fetal interface.