After mosquito inoculation of a human host, cellular entry likely resembles that of other flaviviruses, whereby thevirus enters skin cells through cellular receptors, enabling migration to the lymph nodes and bloodstream. Few studies have investigated the pathogenesis of Zika virus infection. One study showed that human skin fibroblasts, keratinocytes, and immature dendritic cells allow entry of Zika virus (19). Several entry and adhesion factors (e.g., AXL receptor tyrosine kinase) facilitate infection, and cellular autophagy, needed for flaviviral replication, enhances Zika virus replication in skin fibroblasts (19). After cellular entry, flaviviruses typically replicate within endoplasmic reticulum-derived vesicles. However, Zika virus antigens were found exclusively in the nuclei of infected cells; this finding suggests a location for replication that differs from that of other flaviviruses and merits further investigation (20).