Zika virus (ZIKV) has evolved into a global health threat because of its unexpected causal link to microcephaly. Phylogenetic analysis reveals that contemporary epidemic strains have accumulated multiple substitutions from their Asian ancestor. Here we show that a single serine-to-asparagine substitution [Ser139→Asn139 (S139N)] in the viral polyprotein substantially increased ZIKV infectivity in both human and mouse neural progenitor cells (NPCs) and led to more severe microcephaly in the mouse fetus, as well as higher mortality rates in neonatal mice. Evolutionary analysis indicates that the S139N substitution arose before the 2013 outbreak in French Polynesia and has been stably maintained during subsequent spread to the Americas. This functional adaption makes ZIKV more virulent to human NPCs, thus contributing to the increased incidence of microcephaly in recent ZIKV epidemics.

Red light illumination with photon energy matching the direct band gap of chemical vapor deposition grown single-layer MoS2 with Au metal electrodes was used to induce a photocurrent which was employed instead of dark current for NO2 gas sensing. The resulting Au/MoS2/Au optoelectronic gas sensor showed a significant enhancement of the device sensitivity S toward ppb level of NO2 gas exposure reaching S = 4.9%/ppb (4900%/ppm), where S is a slope of dependence of relative change of the sensor resistance on NO2 concentration. Further optimization of the MoS2-based optoelectronic gas sensor by using graphene (Gr) with a work function lower than that of Au for the electrical contacts to the MoS2 channel allowed an increase of photocurrent. The limit of detection of NO2 gas at the level of 0.1 ppb was obtained for the MoS2 channel with graphene electrodes coated by Au. This value was calculated using experimentally obtained sensitivity and noise values and exceeds the U.S. Environment Protection Agency requirement for NO2 gas detection at ppb level.